In recent years, the incidence of psychiatric disorders has been steadily increasing, posing significant challenges to both individual health and social stability. Emerging evidence has highlighted a close association between immune cells and the onset and progression of various psychiatric conditions. Traditional approaches for inferring causality, such as randomized controlled trials and observational studies, are often limited by feasibility, bias, and confounding factors. Mendelian randomization (MR), which leverages genetic variants as instrumental variables, provides a powerful alternative for assessing causal relationships between immune cells and psychiatric disorders. This review summarizes recent advances in MR studies investigating the causal links between immune cell profiles and psychiatric disorders, including anxiety, depression, and schizophrenia. By integrating current evidence from MR studies, this review aims to provide new insights and reference points for future research exploring the relationship between immune cells and psychiatric disorders.

This meta-analysis was conducted to investigate the efficacy and safety of omalizumab in the treatment of allergic rhinitis in adults.
Randomized controlled trials (RCTs) on omalizumab in the treatment of allergic rhinitis in adults were collected by searching PubMed, Cochrane Library, Embase, Web of Science, CNKI, VIP, and Wanfang Data. The search period was from the establishment of each database to October 2024. Stata 15.0 software was used for data analysis. The control group received a placebo or other anti-allergy drugs, while the experimental group received omalizumab, with or without specific immunotherapy.
A total of 8 RCTs were involved in this meta-analysis. The combined analysis exhibited that the effective rate was higher in the omalizumab group than in the control group (RR=1.15; 95% CI, 1.06–1.24) for allergic rhinitis. IgE levels (SMD=−2.82; 95% CI, −4.03 to −1.62) and DNSS (SMD=−1.99; 95% CI, −3.04 to −0.94), DOSS (SMD=−2.95; 95% CI, −4.65 to −1.25) were lower in the omalizumab group compared with the control group. No significant difference was observed in the incidence of adverse events between the two groups (RR=1.15; 95% CI, 0.69–1.93).
Omalizumab is effective and safe in the treatment of adult allergic rhinitis.

The aim of this study was to evaluate the clinical and inflammatory outcomes of minocycline hydrochloride combined with tinidazole in patients with chronic periodontitis.
PubMed, Cochrane Library, Embase, CNKI, WanFang Data, and VIP were searched through December 2025 for randomized and nonrandomized controlled studies. Randomized trials were assessed using the Cochrane Risk of Bias tool, while the cohort study was assessed using ROBINS-I. Meta-analysis was conducted using RevMan 5.3. Random-effects models were applied when substantial heterogeneity was present, and sensitivity analyses were performed by excluding the cohort study.
Fourteen studies were included. Compared with the control treatment, combination therapy was associated with greater improvements in gingival index (MD=−0.71; 95% CI, −0.77 to −0.65), probing pocket depth (MD=−0.87; 95% CI, −1.07 to −0.66), clinical attachment level (MD=−0.77; 95% CI, −1.06 to −0.49), plaque index (MD=−0.38; 95% CI, −0.45 to −0.32), and sulcus bleeding index (MD=−0.68; 95% CI, −0.96 to −0.40). Changes were also observed in several inflammatory and immune-related indicators, whereas CRP did not differ significantly between the groups. Substantial heterogeneity was present for most outcomes.
Overall, minocycline hydrochloride combined with tinidazole may provide additional short-term benefits for patients with chronic periodontitis. Nevertheless, these findings should be interpreted cautiously because of methodological limitations, substantial heterogeneity, incomplete safety reporting, and short follow-up periods.

Periodontitis is a chronic inflammatory disease driven by dysregulated immune responses to microbial biofilms, in which excessive pro-inflammatory cytokine production contributes to periodontal tissue destruction. Although laser-assisted periodontal flap surgery has been proposed as an adjunctive therapy, its effects on inflammatory mediator regulation remain unclear. This meta-analysis evaluated the effects of laser-assisted periodontal flap surgery on tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and C-reactive protein (CRP), and their association with clinical outcomes in patients with Stage 3–4, Grade B/C chronic periodontitis.
Randomized controlled trials comparing laser-assisted periodontal flap surgery with conventional flap surgery were systematically retrieved from major English and Chinese databases. Primary outcomes included changes in inflammatory biomarkers measured in gingival crevicular fluid or serum; while probing depth (PD), clinical attachment level (CAL), gingival index, and postoperative pain were secondary endpoints. Meta-analyses used fixed- or random-effects models according to heterogeneity, with sensitivity analyses conducted to assess result robustness.
Twelve randomized controlled trials were included. Laser-assisted therapy significantly reduced early postoperative (24-hour) TNF-α (MD=−0.88, 95% CI −1.01 to −0.75) and IL-6 (MD=−1.41, 95% CI −1.81 to −1.02) compared with conventional surgery, while CRP showed no significant difference. Clinically, adjunctive laser therapy improved short-term probing depth reduction at 3 and 6 months, whereas CAL improvements were not consistently sustained.
Laser-assisted periodontal flap surgery significantly downregulates key inflammatory cytokines in the early postoperative period and may improve short-term outcomes. However, long-term periodontal attachment stability remains uncertain, warranting further well-designed studies with standardized biochemical and clinical assessments.

 To evaluate whether adjunctive Modified GuiPi Decoction provides additional benefit to standard immunosuppressive therapy in adult patients with chronic immune thrombocytopenia (ITP).
This retrospective cohort study included 120 adult patients aged 18–65 years, diagnosed with ITP according to the 2016 Chinese Expert Consensus. Patients received either standard therapy (cyclosporine A plus prednisone; comparison group, n = 60) or standard therapy plus Modified GuiPi Decoction (treatment group, n = 60) between July 2022 and July 2024.
After 12 weeks of treatment, the treatment group showed significantly greater improvement in fatigue severity score (mean reduction: 3.2 vs 1.8) and quality-of-life index (mean increase: 15.4 vs 9.1) compared to the comparison group. However, no significant between-group difference was observed in platelet count recovery (mean increase: 45.3 × 10⁹/L vs 53.1 × 10⁹/L), with the comparison group showing a numerically larger rise. Mild ALT/AST elevations were more pronounced in the treatment group.
In adult ITP patients, adjunctive Modified GuiPi Decoction may offer symptomatic and quality-of-life benefits beyond standard therapy, but did not demonstrate superior hematological response. Caution is warranted regarding potential hepatotoxicity.

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.

This study aimed to assess the clinical symptoms associated with UFs and to evaluate dynamic, longitudinal changes in serum inflammatory markers before and after treatment in women diagnosed with UFs compared with healthy controls.
In this retrospective observational study, 90 women including 60 women diagnosed with UFs and 30 age-matched healthy controls. Uterine fibroids were confirmed by ultrasonography and histopathology. Serum levels of tumor necrosis factor α (TNF-α), interferon β (IFN-β), IFN-γ, C-reactive protein (CRP), and basic fibroblast growth factor (FGF) were measured using standardized enzyme-linked immunosorbent assay kits. Lymphocyte subsets were analyzed via flow cytometry. Patients with UFs underwent medical or surgical treatment based on clinical indications, and inflammatory markers were reassessed 3 months posttreatment.
There were various symptoms such as pelvic pain (66.67%), abnormal bleeding (66.67%), organ-compression symptoms (45%), infertility (26.67%), and miscarriage (18.33%) compared with controls. Women diagnosed with UFs showed a higher lymphocyte count, proinflammatory mediators, and decreased level of interleukins as compared with the healthy population of females.
The observed dynamic pretreatment and posttreatment shifts in serum inflammatory markers suggest involvement of adaptive immunity and angiogenic pathways, highlighting the potential role of inflammatory regulation in improving reproductive outcomes, including preparation for assisted reproductive technologies.

This prospective single-arm study examined associations between peripheral immune-inflammatory biomarkers and changes observed during cognitive rehabilitation in patients with early Alzheimer disease.
Seventy-two patients completed a 12-week structured cognitive rehabilitation program delivered three times weekly. Baseline plasma/serum glial fibrillary acidic protein (GFAP), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and C-reactive protein (CRP) were measured. Cognitive and functional outcomes were assessed before and after the program. Correlation and multivariable linear regression analyses examined associations between baseline biomarkers and pre–post changes.
After 12 weeks, scores on global cognition, memory, digit span, and semantic fluency increased, whereas Trail Making Test completion times and Activities of Daily Living dependency scores decreased. Among 60 participants with repeat biomarker measurements, GFAP, IL-6, TNF-α, and CRP levels were lower at follow-up. Baseline GFAP, IL-6, TNF-α, and CRP were inversely correlated with change in Montreal Cognitive Assessment score; GFAP showed the strongest correlation (r=−0.48). After adjustment for age, education, and baseline cognition, baseline logGFAP, logIL-6, and TNF-α remained associated with smaller Montreal Cognitive Assessment score changes.
In this uncontrolled cohort, cognitive rehabilitation was associated with short-term cognitive, functional, and biomarker changes. Higher baseline inflammatory biomarker levels were associated with smaller pre–post changes, with GFAP showing the strongest association. These exploratory findings do not establish efficacy or causality and require confirmation in randomized controlled studies.

MicroRNAs (miRs) play a crucial role in the pathogenesis, progression, and prognosis of cancer, including non-small-cell lung cancer. The purpose of this present study was to investigate the correlation between ‎MIR141‎ expression in peripheral blood mononuclear cells and serum levels of interleukins (IL-6 and IL-8) and CXCL10 in non-small-cell lung cancer patients.
Forty-six patients diagnosed with primary non-small-cell lung cancer and 30 age- and gender-matched healthy controls were recruited in this prospective cohort study. Two 3-mL samples of systemic blood were collected into tubes either containing or without an anticoagulant from all patients before treatment and from healthy controls. PBMCs were isolated, total RNA extracted, and microRNA expression measured using real-time quantitative polymerase chain reaction. Serum cytokine levels were measured by enzyme-linked immunosorbent assay.
MIR141‎ expression in peripheral blood mononuclear cells was significantly higher in non-small-cell lung cancer patients (4.124 [3.259–4.944]) compared to healthy controls (2.181 [1.036–2.946]). The area under the Receiver operating characteristic (ROC) curve, AUC for MIR141,‎ was 0.695 (95% CI, 0.603–0.787), indicating statistically significant diagnostic performance. Serum levels of IL-6, IL-8, and CXCL10 were also markedly elevated in non-small-cell lung cancer patients compared to healthy controls.
Increased expression of MIR141 in peripheral blood mononuclear cells is associated with non-small-cell lung cancer and elevated systemic inflammatory mediators. These findings suggest that peripheral blood MIR141 may serve as a promising non-invasive biomarker for the diagnosis of non-small-cell lung cancer.

Pneumocystis jirovecii pneumonia (PJP) is a common opportunistic infection in immunocompromised children, often causing acute fulminant pneumonia with respiratory failure. The prognosis of PJP in human immunodeficiency virus (HIV)-negative children with acute respiratory distress syndrome (ARDS) remains unclear.
This retrospective review (2015–2021) included 20 HIV-negative children with ARDS and PJP. Among them, 17 had hematological malignancies or solid tumors, and 3 had renal disease; 15 survived, 5 did not. Both groups had very low CD4⁺ T cell counts (<0.2×10⁹/L), severe ARDS (partial pressure of oxygen in arterial blood / fraction of inspired oxygen [PaO₂/FiO₂] ratio <150), and elevated lactate dehydrogenase (LDH) and (1,3)-β-D-glucan (BDG) levels. In non-survivors, anti-PJP therapy was initiated approximately 7 days later than in survivors.
Single-cell sequencing revealed CD4⁺/CD8⁺ T cell ratios of 0.16 (survivors) vs 2.13 (non-survivors), with a higher ratio of regulatory T cells (Tregs) to CD4⁺ T cells in non-survivors (33% vs. 10.6%). Non-survivors showed enrichment of neutrophil degranulation and activation pathways and expressed more proapoptotic and proinflammatory signals (e.g., FAS_FASLG, interferon-γ).
Early treatment initiation is critical. Prolonged CD8⁺ T cell deficiency, high Treg expression with proapoptotic genes, and excessive inflammation may predict poor prognosis.

The research intended to elucidate the synergistic effects of eosinophils (Eos) and mast cells (MCs) on human nasal epithelial cells (HNEpCs) in the context of allergic rhinitis (AR), focusing on inflammation, tight junction protein expression, and DNA damage.
Cell proliferation capacity was measured using the Cell Counting Kit-8 (CCK-8) method, apoptosis was examined via the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, and inflammatory cytokine levels were assayed via enzyme-linked immunosorbent assay. Western blotting evaluated the protein abundance of tight junction proteins (ZO-1, Occludin) and CD40L/CD40. Immunofluorescence was used to detect phosphorylated histone H2AX (γH2AX) (DNA damage), as well as subcellular ZO-1/Occludin distribution. Co-immunoprecipitation (Co-IP) was used to analyze the CD40L-CD40 interaction between Eos and MCs.
Eos and MCs significantly reduced HNEpC viability and enhanced apoptosis, with the most pronounced effects in the AR+Eos+MC group. Inflammatory cytokine levels were markedly elevated in the Eos+MC and AR+Eos+MC groups, with the highest concentrations observed in the AR+Eos+MC group. Western blot and immunofluorescence analyses showed decreased expression of ZO-1 and Occludin in treatment groups compared to Control, along with a shift in their localization from the cell membrane to the cytoplasm. γH2AX expression, indicating DNA damage, was significantly elevated, with the highest levels observed in the AR+Eos+MC group. Co-IP analysis confirmed enhanced CD40L-CD40 interaction involving Eos and MCs within the Eos+MC and AR+Eos+MC groups.
Eosinophils and MCs synergistically promote inflammation, disrupt the nasal epithelial barrier, and exacerbate DNA damage. The CD40L-CD40 pathway serves an essential function in their interaction, providing a potential therapeutic target for AR.

Gastric cancer is among the most prevalent malignancies worldwide, with a poor prognosis in advanced stages. Overexpression of human epidermal growth factor receptor 2 (HER2, also known as ERBB2) and heat shock protein 90 alpha (HSP90AA1, also known as HSP90α) has been associated with tumor progression. Anethum graveolens, a medicinal plant from the Apiaceae family, has demonstrated anticancer properties in previous studies. This study aimed to evaluate the effects of A graveolens methanolic extract on apoptosis and the expression of HER2, HSP90α, tumor protein p53 (TP53), and caspase-3 genes in the human gastric adenocarcinoma cell line (AGS).
A methanolic extract of the aerial parts of A graveolens was prepared. Cytotoxicity was assessed in AGS and human gingival fibroblast (HUGU) cell lines using the -(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Gene expression was measured by real-time PCR, and apoptosis was evaluated using Annexin V/propidium iodide (PI) staining followed by flow cytometry.
The methanolic extract exhibited dose-dependent cytotoxicity, with a half-maximal inhibitory concentration (IC50) of 1280 μg/mL in AGS cells. Gene expression analysis revealed significant downregulation of HER2 and upregulation of HSP90α, TP53, and caspase-3 in treated AGS cells compared to controls. Apoptosis rates were significantly higher in treated AGS cells, confirming the proapoptotic effect of the extract. A graveolens exerts cytotoxic and proapoptotic effects in AGS cells and modulates key genes involved in gastric cancer progression.
These findings suggest its potential as a natural therapeutic candidate for gastric cancer, warranting further preclinical and clinical investigations.

Long noncoding RNA SSTR5 antisense RNA 1 (lncRNA SSTR5-AS1) is increased in a variety of tumors, but its molecular mechanism in ovarian cancer (OC) remains unreported.
lncRNA SSTR5-AS1 and signal transducer and activator of transcription 3 (STAT3) expressions in SKOV3 and A2780 cells were interfered (n=3), and the cells were treated with ferroptosis inhibitor Ferrostatin-1. lncRNA SSTR5-AS1 and STAT3 expressions were discovered. The interaction between them was detected by immunoprecipitation assay. The cell malignant progression was evaluated through Transwell and scratch healing assays. Ferroptosis was measured through kits and fluorescent probes; the expression levels of immunosuppressive factors and STAT3/solute carrier family 7 member 11 (SLC7A11) signaling pathway were discovered through Western blot. A transplanted tumor model (n=6 mice per group) was established to evaluate ferroptosis, immunosuppressive factors, and tumor growth in tumor tissues.
lncRNA SSTR5-AS1 was up-regulated on OC cells. LncRNA SSTR5-AS1 and STAT3 bind to each other, and knockdown of lncRNA SSTR5-AS1 can reduce p-STAT3/STAT3 and SLC7A11 protein levels (one-way ANOVA). Knocking down lncRNA SSTR5-AS1 and STAT3 suppressed cell viability, migratory rate, and invasive cell number; increased reactive oxygen species (ROS) and Fe2+ levels; and reduced immunosuppressive factors and ferroptosis proteins. Ferrostatin-1 significantly reversed the effect of knockdown of lncRNA SSTR5-AS1 on ferroptosis. In transplanted tumor tissues, downregulation of lncRNA SSTR5-AS1 can reduce tumor size and volume, show obvious iron deposition, and reduce the secretion of immunosuppressive factors.
Knockdown of lncRNA SSTR5-AS1 induces ferroptosis and reduces the secretion of immunosuppressive factors through the STAT3/SLC7A11 pathway, thereby antagonizing OC.

 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.

Good’s syndrome (GS) is a rare immunodeficiency disorder associated with thymoma, characterized by hypogammaglobulinemia and impaired cellular immunity. Due to its variable clinical presentation and lack of clear diagnostic criteria, GS is often underrecognized or diagnosed with delay.
We report 7 patients diagnosed with GS, including 2 previously reported cases and 5 new cases. Clinical, immunological, and radiological data were analyzed to characterize the spectrum of disease manifestations and outcomes.
The study comprised 6 men and 1 woman, with a mean age of 48 years at thymoma diagnosis and 50 years at immunodeficiency detection. Two patients were diagnosed with thymoma and immunodeficiency simultaneously, while in 5 patients thymoma preceded GS diagnosis by 1 to 2.5 years. Common clinical features included recurrent sinopulmonary infections and autoimmune manifestations, such as myasthenia gravis and lichen planus. Opportunistic infections, including cytomegalovirus and mycobacterial infections were observed. Immunological profiles demonstrated hypogammaglobulinemia, reduced B-cell markers (CD19, CD20), and variable T-cell subsets. Intravenous immunoglobulin replacement therapy led to clinical improvement in most cases. Two patients succumbed to complications related to severe infections.
GS presents with diverse clinical and immunological features, necessitating a high index of suspicion in patients with thymoma and recurrent infections. Early recognition and individualized immunoglobulin replacement therapy are critical for improving outcomes. Our series highlights the need for ongoing monitoring and management of immunodeficiency in thymoma patients.