Non-small cell lung cancer (NSCLC) and pancreatic ductal adenocarcinoma (PDAC) figure prominently in the list of prevalent and resistant cancers that reveal significant differences in response to immunotherapy. Neoantigens, specific antigens resulting from tumor mutations, play an important role in provoking immune responses and the success of immunotherapy. This review scrutinizes the quantitative and qualitative differences in neoantigens in NSCLC and PDAC and their impact on the efficacy of immunotherapy. The evidence suggests that the higher mutational burden, greater diversity, and different quality of neoantigens in NSCLC compared with PDAC are among the key drivers contributing to the enhanced susceptibility to immunotherapy in this cancer. These differences could pave the way for the development of personalized therapies and novel strategies to improve treatment outcomes in resistant cancers.

Ataxia Telangiectasia (AT) is a rare autosomal recessive disease with features of progressive cerebellar atrophy, immunodeficiency, and enhanced cancer susceptibility due to mutations in the ataxia telangiectasia mutated (ATM) gene. However, despite evidence from patients with AT in consanguineous Iranian families, limited information is still available on the genotype-phenotype association. This paper presents a familial case series of AT in Yazd, Iran, with a novel homozygous ATM mutation.
This report examines a consanguine family in Yazd, Iran, with four members presenting with symptoms characteristic of AT, including progressive neurological decline, cerebellar atrophy, immunodeficiency, elevated alpha-fetoprotein, and recurrent infections.
Genetic analysis confirmed a novel homozygous mutation of the ATM gene (c.1834C>A; p.Leu612Ile), which is a non-conservative substitution. It is predicted to result in loss of function, and parents were carriers of the mutation. Treatment included intravenous immunoglobulin, prophylactic antibiotics, and supportive care. One of the patients died due to severe infection despite intervention.
This case series highlights the impact of consanguinity on the occurrence of AT and the supporting role of genetic testing in diagnosing ATM mutations. The results emphasize the need for improved genetic counseling, family planning, early immunological therapy, and culturally tailored public health strategies to effectively manage AT in consanguineous populations.

Acute calculous cholecystitis (ACC) often triggers transient perioperative elevations in liver enzymes and systemic inflammation, yet existing complication-prediction tools seldom incorporate dynamic biomarker changes. Our goal was to establish and develop, using internal validation, a multivariable risk model that incorporates perioperative variations in liver function tests (LFTs) and the Systemic Immune-Inflammation Index (SII) in order to predict Clavien–Dindo grade ≥II complications following cholecystectomy for ACC. In this retrospective cohort study at a tertiary academic center (January 2022–December 2024), we analyzed 260 adult patients undergoing laparoscopic or open cholecystectomy for ACC.
We calculated Δ-values (day 1 minus baseline) for alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin, and SII (platelet × neutrophil/lymphocyte). Multivariable logistic regression with backward stepwise selection was used to derive the final model, which included ΔALT, ΔAST, Δbilirubin, ΔSII, age, American Society of Anesthesiologists (ASA) status, and operative duration. Internal validation employed 1 000 bootstrap replications.
The model demonstrated good discrimination (optimism-corrected area under the curve, 0.82; 95% CI, 0.77–0.87) and excellent calibration (slope, 0.95; intercept, –0.02). Significant predictors included ΔALT, ΔAST, Δbilirubin, and ΔSII, along with age, ASA III status, and longer operative duration. The decision-curve analysis demonstrated net benefit across threshold probabilities of 5% to 40%, with 15 additional true positives per 1 000 at the 20% threshold.
Integrating dynamic perioperative changes in LFTs and SII with key clinical factors yields a robust risk prediction model for postoperative complications after ACC surgery.

This study aimed to explore the effects of different dexmedetomidine (DEX) administration routes on anesthesia quality in pediatric patients undergoing endoscopic low-temperature plasma adenotonsillar ablation.
We selected 120 children with obstructive sleep apnea hypopnea syndrome scheduled for surgery between May and December 2023. Participants were divided into four groups (n=30 each): a control group (Group S) receiving standard anesthesia without DEX; a local anesthesia group (Group L) receiving ropivacaine infiltration with 0.3 µg·kg⁻¹ DEX; an intravenous group (Group T) receiving 0.6 µg·kg⁻¹ DEX infusion post-induction; and a nasal drip group (Group N) receiving 0.6 µg·kg⁻¹ DEX intranasally upon room entry. We compared operation/extubation/recovery times, and scores from the Observer Assessment of Alertness and Sedation (OAA/S), Objective Pain Scale (OPS), and Pediatric Anesthesia Emergence Delirium (PAED) scales. Rescue sedation and safety were also assessed.
Group T showed lower heart rates at specific timepoints, while Group L had lower blood pressures. Recovery time (Steward score ≥4) was longer in Groups L and T compared to Group S, but not in Group N. Groups T and N showed increased OAA/S scores post-awakening, with Group N having the highest scores. OPS and PAED scores decreased in all DEX groups, with Group N demonstrating the lowest scores, followed by Group L and then Group T. No significant differences were found in operation time, extubation time, or the incidence of rescue sedation/complications among groups.
Intranasal DEX emerged as the optimal route, providing effective analgesia and sedation without prolonging recovery time.

T helper 1 (T_H1) and T helper 2 (T_H2) cells can secrete various proinflammatory and anti-inflammatory factors, which can serve as indicators for predicting the severity of pneumonia. However, they are rarely used in combination with procalcitonin (PCT) and high-sensitivity C-reactive protein (hsCRP) detection to predict the severity of pneumonia. The purpose of this study is to investigate the combination of serum T_H1/T_H2 cytokines, PCT, and hsCRP for predicting the severity of community-acquired pneumonia (CAP).
This study observed 58 inpatients with CAP. Analyses were conducted on the serum levels of T_H1/T_H2 cytokines, PCT, and hsCRP; imaging examination results; underlying diseases; pathogens; and the pneumonia severity index (PSI).
The severe pneumonia group showed significantly higher PSI scores, age, and complication rates. Serum IL-2 was notably elevated in severe cases, while a combination of PCT, IL-4, TNF-α, and IFN-γ effectively predicted severe pneumonia, with an AUC of 0.712. Specific alterations in cytokines and biomarkers were identified as risk factors for higher PSI, complications, and prolonged hospitalization.
The combined detection of PCT, IL-4, TNF-α, and IFN-γ provides a potential tool for predicting severe CAP, and distinct biomarker profiles are associated with different clinical outcomes.

Allergic rhinitis (AR), as a chronic disease, seriously affects the quality of life of patients while concurrently exerting a significant economic and healthcare burden on the medical system. However, the existing treatment methods have certain limitations, and more effective treatment strategies are needed. To this end, we proposed an ovalbumin-induced guinea pig model of AR to investigate the potential impact of activated polyethylene glycol (PEG) with varying molecular weights and concentrations in local nasal treatment.
The therapeutic effect was evaluated by behavioral score, serological detection, and histopathological observation.
The behavioral assessment demonstrated significant alleviation of sneezing frequency, nasal pruritus, and clear nasal discharge in the activated PEG-600 treatment groups relative to the sham group. However, statistical analysis revealed no appreciable intergroup differences between the activated PEG-3400 treatment groups and the sham group. Histopathological evaluation disclosed a marked reduction in eosinophilic infiltration in the activated PEG-600 group, accompanied by preservation of nasal mucosal structural integrity and notable attenuation of inflammatory infiltration. In contrast, the activated PEG-3400 group exhibited comparatively limited therapeutic efficacy, demonstrating only a subtle reduction in inflammatory cell counts and more pronounced disorganization of mucosal epithelial architecture compared to the PEG-600-treated group. Serum immunological profiling indicated that while local inflammatory markers showed evidence of mitigation, systemic immune parameters remained unaffected by either activated PEG formulation.
These findings underscore the differential efficacy profile between PEG-600 and PEG-3400 derivatives in ameliorating AR symptoms, among which PEG-600 exhibits superior anti-inflammatory effects.

Ulcerative colitis (UC) is a chronic immune-mediated disease with a growing global burden. In this study, bioinformatics analysis and machine learning methods were employed to screen the potential immune microenvironment-related feature genes.
We identified 4 immune-related genes that are consistently dysregulated in UC and correlate with immune infiltration, including APOBEC3B (Apolipoprotein B mRNA Editing Enzyme Catalytic Subunit 3B), CXCL11, PLA2G2A, and TMEM173. Their diagnostic performance was verified in an external cohort and in our clinical samples.
Then, the proportion of ambiguous clustering (PAC) successfully classified UC patients into 2 molecular subtypes, including subtype 1 (metabolism-related subtype) and subtype 2 (immune-related subtype). The single sample gene set enrichment analysis (ssGSEA) algorithm revealed that subtype 2, with a higher score, of the majority of immune cells presented a worse inflammatory response.
In addition, we assessed scores of partial novel drugs querying the cMAP database and found that the efficacy of clinical small-molecule compounds presented different results across UC subtypes. These findings identify biomarkers, establish a concise immune-based classification of UC, and support subtype-guided therapy.

Traditional radical cystectomy has a high recurrence rate, a high probability of metastasis, and a reduced quality of life for patients. This study aimed to explore the efficacy of combining immunotherapy and surgical resection for high-risk muscle-invasive bladder cancer.
In a retrospective study, 231 patients with high-risk muscle-invasive bladder cancer admitted to Yueyang People’s Hospital between January 2019 and May 2024 were selected. After exclusions, 200 cases were analyzed and divided into two groups according to the treatment modality: the control group (surgical resection alone, n=100) and the intervention group (combination of immunotherapy and surgical resection, n=100). The cellular immune function indexes (CD3⁺, CD4⁺/CD8⁺, and natural killer cell levels), tumor markers (carcinoembryonic antigen, carbohydrate antigen 125, cytokeratin 21-1, and neuron-specific enolase), serum cytokines (basic fibroblast growth factor, vascular endothelial growth factor, and tumor necrosis factor-α), pathological complete remission (pCR), 1-year survival, and Functional Assessment of Cancer Therapy-Bladder (FACT-BL) quality-of-life scores were assessed in the two groups.
After 1 year of treatment, the indicators of the two groups of patients were statistically significant in comparison with each other. Patients in the intervention group had substantial improvements in immune function indexes, pCR, 1-year survival rate, and FACT-BL scores in comparison with the control group. Tumor markers and serum cytokines were lower than those in the control group.
The combination of immunotherapy and surgical resection can enhance clinical efficacy, providing a scientific basis for optimizing the clinical treatment plan.

Lung cancer remains a major cause of cancer-related mortality worldwide, with current treatments such as surgery, chemotherapy, and immunotherapy facing limitations, including severe side effects and high costs. Hyperthermia (H) has emerged as a promising strategy to enhance tumor sensitivity to treatments and reduce toxicity. This study investigates the effects of H in enhancing the anti-tumor efficacy of pemetrexed (PEM) and altering the expression profile of hsa-MiR-548c-3p (tumor suppressor) in the A549 cell line.
A549 cells were cultured in DMEM medium and divided into four groups: Control, and treatment with H, PEM, and a combination of H and PEM. Subsequently, cell viability, apoptosis percentage, release rate of LDH, production of ROS, and the expression level of hsa-MiR-548c-3p, CASP 8 and 9, and TYMS genes were measured.
Results revealed that the combination of H and PEM treatment had greater antitumor effects compared to the other groups. The combination of H and PEM significantly reduced cell viability, increased the percentage of apoptosis, LDH release, and ROS production, and upregulated hsa-MiR-548c-3p, CASP 8, and 9, while downregulating TYMS.
The findings suggest that H enhances the chemotherapeutic efficacy of PEM by upregulating hsa-MiR-548c-3p expression and promoting apoptosis in lung cancer cells, making it a promising complementary approach for overcoming drug resistance.

Alternaria alternata is one of the most potent fungal allergens associated with allergic respiratory diseases, particularly asthma. Sensitization to A alternata has been linked to poor asthma control and increased morbidity, yet its prevalence varies widely across populations due to environmental and methodological differences. This study aimed to determine the prevalence and demographic predictors of A alternata sensitization among patients with moderate to severe asthma.
A cross-sectional study was conducted from March to September 2024 among 80 patients with physician-diagnosed moderate or severe asthma in Shiraz, Iran. Participants underwent skin prick testing (SPT) for A. alternata. Demographic and clinical data were collected and analyzed using descriptive statistics, χ² tests, and logistic regression.
Among the 80 patients (mean age 29.03 ± 20.45 years; 53.8% male), 28.8% tested positive for Alternaria sensitization. Sensitization was significantly more prevalent in patients younger than 18 years (44.1%) compared to adults (17.4%). No significant difference was observed based on sex. Although sensitization was more frequent in patients with severe asthma (40.6%) than moderate asthma (20.8%), this trend was not statistically significant. Logistic regression identified younger age as the only independent predictor of sensitization.
Alternaria alternata sensitization is common among individuals with moderate to severe asthma, particularly in younger patients. These findings underscore the importance of routine fungal allergen screening in asthmatics, especially children, to inform targeted management strategies and potentially reduce asthma-related morbidity.

This study aimed to investigate whether propofol-remifentanil anesthesia offers superior perioperative outcomes compared to propofol-fentanyl in pancreatic cancer surgery patients, with a focus on its effects on apoptotic molecules, plasma CXCL10/CXCL13 levels, and postoperative recovery.
A total of 150 pancreatic cancer patients were divided into 2 cohorts receiving either propofol-fentanyl (control group, n=75) or propofol-remifentanil (study group, n=75) anesthesia. We measured perioperative hemodynamics (cardiac index [CI], mean arterial pressure [MAP], heart rate [HR]), T-cell subsets, postoperative recovery indices (eye-opening time, extubation time, spontaneous respiration recovery time), sedation and analgesia levels (via Ramsay sedation score [RSS] and visual analog scale [VAS]), plasma CXCL10/CXCL13 levels, and apoptosis-related proteins (Survivin, Bax, Caspase-4, Bcl-2) using enzyme-linked immunosorbent assays (ELISAs). Adverse reactions were also recorded.
The study group exhibited significant advantages in hemodynamic stability and immune preservation. Despite similar baseline cardiovascular parameters, the remifentanil group maintained better CI, MAP, and HR stability during and after surgery. Flow cytometry analysis revealed better preservation of T-cell immunity (CD4⁺, CD3⁺, CD4⁺/CD8⁺ T cells) at 24 hours post-surgery. The intervention group also demonstrated accelerated postoperative recovery with significantly reduced emergence times (eye-opening, extubation, spontaneous respiration). Notably, the study group had more favorable inflammatory profiles (lower CXCL10/CXCL13 levels) and enhanced apoptotic responses (modulated Bax, Caspase-4, Survivin, and Bcl-2 expression). Clinical outcomes were superior in the study group, with significantly fewer adverse events (2 vs. 9 patients).
Propofol-remifentanil anesthesia provides effective sedation and analgesia in pancreatic cancer surgery, modulates key biological pathways related to apoptosis and inflammation, and improves postoperative recovery. These findings suggest that the choice of anesthesia regimen may have significant implications for perioperative outcomes and potentially long-term prognosis in pancreatic cancer patients. Future research should further explore the underlying mechanisms and long-term clinical benefits of this anesthesia strategy.

Background: Bronchial asthma (BA) involves immune imbalance and airway remodeling (AR), with CB2 receptors playing a role in inflammation regulation. This study explores the therapeutic potential of a CB2 receptor inverse agonist in BA rats and its mechanisms via the TLR4/NF-κB pathway.

Methods: Twenty-seven rats were divided into control (CG), model (MG), and intervention (IG) groups. BA models were induced in MG and IG via ovalbumin sensitization. IG received a CB2 receptor inverse agonist, while CG and MG received saline. Th1/Th2 cytokines, Th1/Th2 cell subpopulations, AR parameters, and TLR4/NF-κB expression in lung tissue were analyzed.

Results: Compared to CG, MG showed Th1/Th2 imbalance, increased AR indices, upregulated TLR4/NF-κB expression, shorter asthma latency, and prolonged total asthma attack duration (tAAD). IG exhibited restored Th1/Th2 balance, decreased TLR4/NF-κB expression, prolonged asthma latency, and reduced tAAD (P < 0.05).

Conclusion: CB2 receptor inverse agonist shows potential for BA prevention and treatment by regulating Th1/Th2 balance, inhibiting AR, and modulating the TLR4/NF-κB pathway.

Intervertebral Disc Degeneration (IVDD) is a complex biological process marked by changes in gene expression that final result in structural and functional problems in the intervertebral disc. This study was undertaken to obtain a thorough comprehension of the molecular mechanisms that drive IVDD.

The present work incorporated and examined two sets of gene expression data related to IVDD, obtained from the Gene Expression Omnibus database. An investigation of functional enrichment was conducted utilizing gene ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis to clarify the biological processes and signaling pathways linked to these differentially expressed genes (DEGs). A protein-protein interaction (PPI) network was constructed, and Biomarkers were identified by selecting 13 hub genes using LASSO and SVM-RFE algorithms. An analysis of immune infiltration was conducted using ssGSEA, and the identification of transcription factor targets and medicines was investigated. The expression of ADM, ITGB5, RTN4, SLPI, and CSNK1E was validated using qPCR and Western blot approaches in an IL-1β-induced HNPCs model.

A profound correlation between IVDD and 112 DEGs was observed. The functional enrichment analysis demonstrated their participation in the organization of the extracellular matrix, translation in the cytoplasm, and the PI3K-Akt signaling pathway. An immunological infiltration examination revealed reduced infiltration of suppressor cells and monocytes derived from myeloid cells in the IVDD group. A total of thirteen hub genes were identified as promising indicators. An in vitro validation showed a notable decrease in the expression of ADM, ITGB5, RTN4, SLPI, and CSNK1E in the IVDD group as compared to the control group.

This thorough investigation provides deep understanding of the molecular processes that cause IVDD and reveals possible targets for treatment. The confirmation of important genes and their interactions with drugs in a laboratory setting strongly supports the results and lays the groundwork for future drug development and therapy approaches targeting IVDD.

Allergy and lung cancer are two distinct health concerns. While allergies are typically associated with heightened immune activity, such immune responses may also influence the tumor microenvironment. This study aimed to investigate a potential link between allergic conditions and the risk of lung cancer.
We conducted a case-control study analyzing 82 histologically confirmed lung cancer patients and 82 healthy controls from 2019 to 2022. Data were collected through structured questionnaires assessing asthma, allergic rhinitis (AR), food/drug allergies, and chronic urticaria. Statistical analyses included independent samples t-tests and chi-square tests, with significance set at a predetermined threshold.
We observed a significant inverse association between AR and lung cancer (8.54% vs 47.56% in controls; OR=0.14, 95% CI: 0.06–0.32). No significant associations were found for asthma (7.32% vs 3.66%), chronic urticaria (3.66% vs 3.66%), drug allergy (4.88% vs 1.22%), or food allergy (2.44% vs 6.10%). The association between AR and lung cancer remained robust after adjustment for demographic factors.
AR demonstrated a strong negative association with lung cancer, suggesting potential protective mechanisms distinct from other allergic conditions. These findings support the growing evidence for allergy-cancer immunomodulatory interactions and highlight the need for mechanistic studies on AR-specific pathways in oncogenesis.

Pediatric rhinitis is a common recurrent disorder that may progress to asthma or sinusitis in severe cases. This study aimed to compare the efficacy of different doses of glucocorticoid nasal spray combined with loratadine for rhinitis in children, and provide evidence for optimizing clinical treatment.
A total of 150 children with rhinitis admitted from June 2022 to June 2024 were divided into three groups: group I (low-dose group, n=50), group II (medium-dose group, n=50), and group III (high-dose group, n=50). Patients in all three groups were treated with a glucocorticoid nasal spray with loratadine combined with antihistamines. The immune function, serum inflammatory factor level, quantitative Lund-Kennedy score by nasal endoscopy, nasal symptom score, Quality of Life Questionnaire (RQLQ) scores, clinical efficacy, incidence of adverse events, and treatment compliance were assessed.
Post-treatment, all indices improved in the three groups. The percentages of CD4⁺ and CD8⁺ T cells, IL-10 content, and clinical efficacy in groups II and III were significantly higher than those in group I, while the immunoglobulin E (IgE), IL-6 and IL-17 content, the quantitative Lund-Kennedy score of nasal endoscopy, the children’s nasal symptom scores, the RQLQ scores, and the incidence rate of adverse events were below in group I. No significant differences were found between groups II and III in all indices, nor in treatment compliance across the three groups.
Loratadine combined with a glucocorticoid nasal spray therapy effectively improves clinical outcomes, inflammation, immune function, symptoms, and quality of life in rhinitis in children, with high clinical application value.

Osteoarthritis (OA) is the most common form of arthritis, characterized by pathological changes in joint components. Increasing evidence suggests that helper T (T_H) lymphocytes play a pivotal role in the inflammatory processes associated with OA. Curcumin, the primary polyphenolic compound found in Curcuma longa, exhibits potent antioxidant and anti-inflammatory properties. This study aimed to evaluate the effects of curcumin on the gene expression of key transcription factors of T_H1 and T_H2 cells and to explore their associations with clinical and immunological parameters in patients with knee OA.
This mechanistic sub-study presents a secondary molecular analysis of RNA biospecimens from a previously completed double-blind, placebo-controlled clinical trial involving 30 patients with knee OA. Participants were randomly assigned to receive either 80 mg/day of nano-micelle curcumin or a placebo for 3 months. Expression levels of T-box transcription factor 21 (T-bet) and GATA binding protein 3 (GATA3), the key transcription factors of T_H1 and T_H2 cells, respectively, were quantified using SYBR Green-based real-time PCR. Their associations with changes in visual analogue scale (VAS) score, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and percentages of CD4⁺ and CD8⁺ T cells were analyzed.
Curcumin administration significantly reduced T-bet gene expression compared to baseline and showed a positive correlation with the frequency of CD8⁺ T cells, while GATA3 expression remained unchanged.
These findings may provide a novel molecular perspective on curcumin's potential to influence CD8⁺ T cell dynamics by modulating T_H1-associated transcriptional programs.

Non-alcoholic fatty liver disease (NAFLD) is a major hepatic manifestation of metabolic syndrome and encompasses a spectrum ranging from simple steatosis to non-alcoholic steatohepatitis (NASH). This study aimed to evaluate the contribution of immunological, inflammatory, and metabolic parameters-including cytokine levels, immune cell profiles, and microRNA (miR) expression-in the progression from NAFLD to NASH among individuals with features of metabolic syndrome.
An observational study was conducted between January 2022 and December 2024, enrolling 300 adult patients with radiologically or histologically confirmed NAFLD. Patients underwent comprehensive anthropometric, biochemical, and immunological assessments, including cytokine profiling (interleukin [IL]-6, IL-17, tumor necrosis factor-α [TNF-α], transforming growth factor-β1 [TGF-β1]), immune cell phenotyping (T helper 17 [T_H17], regulatory T cells [Tregs], monocytes), and miR quantification (miR-122, miR-34a). Liver biopsy was performed in 95 selected cases.. The nursing team also assists in coordinating multidisciplinary care and ensuring follow-up compliance, which are vital for long-term disease management and reducing progression to NASH.
Significant elevations were observed in metabolic parameters (body mass index [BMI], homeostatic model assessment for insulin resistance [HOMA-IR]), hepatic enzymes (alanine aminotransferase [ALT], aspartate aminotransferase [AST]), inflammatory markers (high-sensitivity C-reactive protein [hs-CRP], ferritin), and oxidative stress markers (malondialdehyde [MDA]). Adipokines (↑leptin, ↓adiponectin), hepatokines (↑fibroblast growth factor 21 [FGF21], ↑fetuin-A), and cytokines (↑IL-6, ↑TNF-α, ↑IL-17) were markedly altered in patients with biopsy-proven NASH.
This study reinforces that pro-inflammatory cytokines, altered immune cell profiles, and dysregulated miRs serve as promising biomarkers for early identification and potential therapeutic targeting in metabolic syndrome-associated steatohepatitis.

Anaphylaxis is a severe, rapidly progressing, and potentially life-threatening emergency requiring prompt, evidence-based intervention. This study assessed pre-hospital emergency healthcare professionals’ knowledge of anaphylaxis diagnosis, acute management, and treatment protocols in line with current clinical guidelines.
A descriptive cross-sectional study was conducted between February and April 2025 among physicians, paramedics, and emergency medical technicians (EMTs) working in Emergency Medical Services (EMS) stations. Data were collected via a 21-item Google Forms survey covering demographics and key knowledge domains based on established pediatric anaphylaxis guidelines.
A total of 322 professionals participated: paramedics (n = 214, 66.5%), EMTs (n = 73, 22.7%), and physicians (n = 35, 10.9%). Although most reported prior anaphylaxis training (90.0%) and clinical encounters (87.6%), only 52.2% correctly identified all three diagnostic criteria. Regarding pharmacologic management, 81.7% recognized epinephrine as first-line treatment, with physicians performing best (94.3%) compared to paramedics (81.8%) and EMTs (75.3%). Similarly, 81.1% correctly identified the intramuscular route, with physicians again demonstrating superior knowledge (95.5%). However, major deficiencies were noted in appropriate patient positioning (52.2%) and epinephrine auto-injector use (50.6%), with significant inter-professional differences across both domains.
Substantial knowledge gaps exist among pre-hospital emergency providers regarding anaphylaxis diagnosis, patient positioning, and auto-injector administration. Targeted training and standardized protocols are urgently needed to enhance competency and improve patient safety in pre-hospital anaphylaxis management.

Chemokines and their receptors play a central role in mediating the migration of pathogenic T cells into the central nervous system of patients with multiple sclerosis (MS). Vitamin D and curcumin are known to possess anti-inflammatory and immunomodulatory properties; however, their combined effects on T-cell chemokine receptor expression in MS remain poorly defined.
In this study, we investigated the in vitro effects of vitamin D, curcumin, and their combination on CD4⁺ and CD8⁺ T cells expressing CXCR3, CCR6, and CCR4 in patients with relapsing-remitting MS (RRMS). Peripheral blood mononuclear cells were collected from patients in relapse (n=10), remission (n=14), and healthy controls (n=15) and analyzed using flow cytometry.
Relapse patients exhibited elevated frequencies of CXCR3⁺CD4⁺ T cells compared to healthy controls, which normalized following treatment. Increased CCR6⁺CD4⁺ T cells and CXCR3⁺CD8⁺ T cells were also observed in patients, with a significant reduction achieved only after combined treatment with vitamin D and curcumin. The combined treatment further decreased the mean fluorescence intensity of CXCR3 and CCR6 on T cells in relapse patients, while vitamin D alone specifically reduced CCR4⁺CCR6⁺CD4⁺ T cells, a T_H17-like subset enriched during relapse.
These findings indicate that vitamin D and curcumin, particularly in combination, modulate T-cell activity by downregulating chemokine receptor expression and may represent a promising adjunctive approach for controlling immune cell migration in MS.

Autoimmune hepatitis (AIH) is a chronic immune-mediated liver disease that can progress to cirrhosis and liver failure if untreated. Current therapies, mainly corticosteroids, are effective but limited by adverse effects and incomplete responses, prompting the search for safer alternatives. Peiminine, an alkaloid derived from Fritillaria species, has demonstrated anti-inflammatory and antioxidant properties in several disease models. This study evaluated its efficacy in a concanavalin A (ConA)–induced mouse model of AIH.
Male C57BL/6 mice were divided into six groups, including ConA-injured animals, and treatment groups receiving peiminine (3 mg/kg, i.p.), prednisolone (10 mg/kg, i.p.), or their combination.
ConA injection caused sharp increases in ALT (↑ 5.4-fold), AST (↑ 4.8-fold), and ALP (↑ 3.9-fold), alongside marked elevations in MPO activity, nitric oxide, and pro-inflammatory cytokines (TNF-α, IL-6, IFN-γ). Peiminine significantly reversed these alterations—reducing ALT, AST, and ALP by 65% to 75% and restoring IL-4, TGF-β, and SOD activity toward normal values. Pre-treatment provided stronger protection than post-treatment, and outcomes were comparable to those of prednisolone, with combination therapy yielding the greatest improvement across all indices.
These findings indicate that peiminine mitigates immune-mediated hepatic injury by modulating cytokines, reducing oxidative stress, and maintaining liver integrity. Peiminine may represent a promising preventive or adjunct therapy for AIH, warranting further mechanistic and long-term investigations.

Exhausted T cells are phenotypically and functionally heterogeneous, from progenitor- to terminally-exhausted T cells. We evaluated gene expression profile of CD8⁺ T cells in acute leukemia to characterize the phenotype of exhausted T cells.
Blood samples were collected from acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) patients prior to treatment and from control subjects. Additionally, samples were obtained from ALL patients after induction therapy. TCF7, NFATc1, IRF4, and BATF gene expression was then evaluated in isolated CD8⁺ T cells.
CD8⁺ T cells from ALL patients showed higher expression of TCF7 and NFATc1 compared to the control group. The two study groups did not have a significant difference in the expression of BATF and IRF4. When compared to the control group, CD8⁺ T cells of AML patients showed an elevated expression level of NAFTc1 and IRF4. Significant differences were not found between the two study groups in AML when it came to the expression of BATF and TCF7.
To our findings, the majority of CD8⁺ T cells found in ALL patients consist of progenitor-exhausted T cells.

Chédiak-Higashi syndrome (CHS) is a rare autosomal recessive disorder characterized by severe immunodeficiency, partial albinism, recurrent infections, and progressive neurologic dysfunction. Unless patients undergo successful hematopoietic cell transplantation (HCT), a majority of them die during childhood because of an accelerated phase of immune dysfunction and hemophagocytic lymphohistiocytosis (HLH). Herein, we aim to describe the laboratory diagnosis, clinical manifestations, and genetic findings in three patients with CHS.
Three patients with partial albinism associated with CHS were included in this study. Immunological screening tests were done. Leukocyte granules in peripheral blood smear (PBS) and hair shafts were examined. Subsequently, genetic analyses were performed by Whole Exome Sequencing (WES) followed by Sanger sequencing for all patients and their parents.
Initial immunology screening tests were within normal limits. Light microscopy studies of patients’ PBS showed giant granules in the leukocyte cytoplasm. Furthermore, there were evenly distributed melanin granules in the patients' hair shafts. Variant analysis of the LYST gene identified three splicing site defects: one known variant, c.7060-1G>A in intron 24, and two novel variants, c.2363+2T>C in intron 5, and c.10702-3A>G in intron 47.
Hair shaft assay and PBS are rapid and suitable tests in early diagnosis and differentiation in CHS patients. WES results revealed 2 novel splice site variants that might contribute to earlier and more accurate diagnosis. This facilitates early enrolment of CHS patients in the HCT protocol-the optimal treatment path-and enables prenatal diagnosis for affected families.

 Atopic dermatitis (AD) is a chronic inflammatory skin disease with heterogeneous immune dysregulation. Although interleukin-17 (IL-17) signaling is implicated in AD, IL-17-related diagnostic biomarkers and molecular subtypes remain unclear. This study aimed to identify IL-17-associated biomarkers, characterize immune infiltration and subtypes, and explore upstream regulatory mechanisms.
Gene expression datasets (GSE121212, GSE6012) were acquired from the Gene Expression Omnibus database, and an IL-17-related gene set was collected from the Gene Set Enrichment Analysis website (GSEA)(http://www.gsea-msigdb.org/gsea/msigdb/search.jsp). Differential expression (limma) and Weighted Gene Co-expression Network Analysis were integrated to identify candidate genes, followed by feature selection using Least Absolute Shrinkage and Selection Operator and random forest. We evaluated immune cell infiltration by applying the CIBERSORT algorithm alongside single-sample Gene Set Enrichment Analysis. GSEA was applied to investigate underlying biological processes. AD patients were clustered into subtypes relying on IL-17 scores using ssGSEA.
Our integrated analysis identified IL4R and PRSS22 as key IL-17-related diagnostic biomarkers for AD, demonstrating excellent diagnostic accuracy across both training and validation cohorts. Immune-infiltration analyses revealed altered immune-cell composition and correlations observed between the identified biomarkers and specific immune cells. Two distinct AD subtypes were identified based on IL-17 scores, exhibiting immune infiltration patterns and enriched biological pathways. A ceRNA network highlighted potential regulatory mechanisms involving these biomarkers.
IL4R and PRSS22 are robust IL-17-related diagnostic biomarkers for AD, with high predictive power across cohorts. Immune infiltration profiling and IL-17 score-based subtyping reveal AD heterogeneity. These findings provide a foundation for improved diagnosis, molecular stratification, and potential therapeutic targeting in AD.

Cognitive dysfunction (CD) is a common neuropsychiatric manifestation of systemic lupus erythematosus (SLE), but its early identification lacks objective serological markers. This study aimed to explore the predictive value of combined serum interleukin-6 (IL-6), intercellular adhesion molecule-1 (ICAM-1), and neurofilament light chain (NfL) for CD in SLE patients.
A total of 108 SLE patients (January 2018–December 2019) and 50 healthy controls were enrolled. SLE patients were divided into CD group (MoCA score <26, n=49) and non-CD group (MoCA score ≥26, n=59). Serum IL-6, ICAM-1, and NfL levels were detected by ELISA. Logistic regression and ROC curve analyses were performed to evaluate risk factors and predictive efficacy.
Serum IL-6, ICAM-1, and NfL levels were significantly higher in SLE patients than in controls (p<0.05), and further elevated in the CD group. These three markers were independent risk factors for SLE-related CD. The AUC of combined detection (0.852) was significantly higher than individual markers (0.734, 0.712, 0.677).
Serum IL-6, ICAM-1, and NfL have certain predictive value for CD in SLE patients, and the combined detection of these three indicators offers higher predictive value.

Chronic Granulomatous Disease (CGD) is a defect or abnormality in the immune system that produces severe and persistent signs and symptoms in affected individuals.
Phenotypic diversity and genetic heterogeneity exist among patients with inborn errors of immunity (IEI). Symptoms may vary even when the mutations are identical; conversely, patients with different mutations may have similar clinical features. The expression of phenotype may be determined by the gene sequence, epigenetic changes, and sometimes environmental factors. Some of these outcomes are influenced by the individual’s past immunological exposure.
This study discusses two CGD cases, a father and son; after the diagnosis of CGD in the child and confirmation of the genetic mutation, the same mutation was also identified in the father.
Therefore, physicians should have more awareness that a single genetic mutation can have different clinical manifestations.