Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 19 4 2020 08 25 452 455 Maryam Joudi Department of Immunology and Allergy, Allergy Research Center, Mashhad University of Medical Sciences, Mashhad, Iran Mohammad Hosein Eshaghi Ghalibaf Student Research Committee, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran Atefeh Ghorbanzadeh Student Research Committee, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran Samira Zabihyan Department of Neurosurgery, Mashhad University of Medical Sciences, Mashhad, Iran Nasrin Moazzen Department of Pediatric Immunology and Allergy, Akbar Medical Center, Mashhad University of Medical Sciences, Mashhad, Iran Maryam Khoshkhui Department of Immunology and Allergy, Allergy Research Center, Mashhad University of Medical Sciences, Mashhad, Iran 2019 02 12 2020 03 10 Brain tumors are the rarest cause of cerebrospinal fluid rhinorrhea. Non-traumatic cerebrospinal fluid rhinorrhea is also a relatively rare condition. It may be misdiagnosed as allergic rhinitis or chronic sinusitis and lead to unsuitable treatment. We described a 34-year-old man who came to our allergy clinic with a chief complaint of clear rhinorrhea from his left nostril with more than four years of duration. Onlyhypertrophy of left inferior concha was found in the clinical examination. His rhinorrhea aggravated when bending forward. So we were suspicious of CSF rhinorrhea. MRI was done for him and demonstrated a large tumor in the pineal region. The patient underwent surgery with resection of the mass via an infratentorial-supracerebellar approach. This case showed the role of maintaining differential diagnosis for a common complaint; rhinitis which is seen as usual. https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2308

Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 19 4 2020 08 25 323 336 Amir Hossein Mansourabadi Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran Ladan Gol Mohammad pour Afrakoti Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran Abbas Shabanian Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran AND Students Scientific Research Center, Tehran University of Medical Sciences, Tehran, Iran Reza Shabanian 3 Department of Pediatric Cardiology, Children’s Medical Center Hospital, Tehran University of Medical Sciences, Tehran, Iran Aliakbar Amirzargar Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran 2019 09 14 2020 04 02 Myocarditis is an inflammatory disease of the myocardium with lymphocyte infiltration and myocyte necrosis leading to a wide range of clinical presentations including heart failure, arrhythmia, and cardiogenic shock. Infectious and noninfectious agents may trigger the disease. The fact that immunosuppressive drugs are useful in several kinds of autoimmune myocarditis is proof of the autoimmune mechanisms involved in the development of myocarditis. Pathogenic mechanisms in myocardial inflammation are including inflammasome activation followed by myocyte destruction, myocarditis, and pericarditis. Intravenous immunoglobulin (IVIG) is a serum product made up of immunoglobulins, widely used in a variety of diseases. This product is effective in several immune-mediated pathologies. As well as the determined usage of IVIG in Kawasaki disease, IVIG may be useful in several kinds of heart failure including fulminant myocarditis, acute inflammatory cardiomyopathy, Giant Cell Myocarditis, and peripartum cardiomyopathy. Generally, IVIG is used in two different doses of low dose (200 to 400 mg/kg) and high dose (2 g/kg) regimen. The exact therapeutic effects of IVIG are not clear, however over the last decades, our knowledge about its mechanism of function has greatly enhanced. IVIG administration should be based on the accepted protocols of its transfusion. In this review article, we try to provide an overview of the different kinds of myocarditis, pathologic mechanisms and their common treatments and evaluation of the administration of IVIG in these diseases. Furthermore, we will review current protocols using IVIG in each disease individually. https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2520

Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 19 4 2020 08 25 348 361 EN Lamis El-Baz Department of Medicine, Section of Pulmonary and Critical Care Medicine, University of Chicago, Chicago, Illinois, USA AND Department of Zoology, Faculty of Science, Suez University, Suez, Egypt Nahla Shoukry Department of Zoology, Faculty of Science, Suez University, Suez, Egypt Hani Hafez Department of Zoology, Faculty of Science, Suez University, Suez, Egypt Robert Guzy Department of Medicine, Section of Pulmonary and Critical Care Medicine, University of Chicago, Chicago, Illinois, USA Mohamed Salem Department of Immunology and Biotechnology, Faculty of Science, Center of Excellence in Cancer Research, Tanta University, Tanta, Egypt 2020 02 15 2020 05 27 Impaired lung epithelial cell regeneration following injury may contribute to the development of pulmonary fibrosis. Epithelial-mesenchymal transition (EMT) is a critical event in embryonic development, wound healing following injury, and even cancer progression. Previous studies have shown that the combination of transforming growth factor beta-1 (TGFβ1) and fibroblast growth factor 2 (FGF2) induces EMT during cancer metastasis. However, this synergy remains to be elucidated in inducing EMT associated with wound healing after injury. We set out this study to determine the effect of fibroblast growth factor 2 (FGF2) on TGFβ1-induced EMT in the human lung epithelium. BEAS-2B and A549 cells were treated with TGFβ1, FGF2, or both. EMT phenotype was investigated morphologically and by measuring mRNA expression levels; using quantitative real-time PCR. E-cadherin expression was assayed by western blot and immunofluorescence staining. Cell migration was confirmed using a wound-healing assay. TGFβ1 induced a morphological change and a significant increase in cell migration of BEAS-2B cells. TGFβ1 significantly reduced E-cadherin (CDH1) mRNA expression and markedly induced expression of N-cadherin (CDH2), tenascin C (TNC), fibronectin (FN), actin alpha 2 (ACTA2), and collagen I (COL1A1). While FGF2 alone did not significantly alter EMT gene expression, it enhanced TGFβ1-induced suppression of CDH1 and upregulation of ACTA2, but not TNC, FN, and CDH2. FGF2 significantly inhibited TGFβ1-induced COL1A1 expression. Furthermore, FGF2 maintained TGFβ1-induced morphologic changes and increased the migration of TGFβ1-treated cells. This study suggests a synergistic effect between TGFβ1 and FGF2 in inducing EMT in lung epithelial cells, which may play an important role in wound healing and tissue repair after injury.  https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2712

Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 19 4 2020 08 25 447 451 Saba Arshi Department of Allergy and Clinical Immunology, Rasoul-E-Akram Hospital, Iran University of Medical Science, Tehran, Iran Narges Eslami Department of Allergy and Clinical Immunology, Mofid Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran Mohammad Nabavi Department of Allergy and Clinical Immunology, Rasoul-E-Akram Hospital, Iran University of Medical Science, Tehran, Iran Mohammad Bemanian Department of Allergy and Clinical Immunology, Rasoul-E-Akram Hospital, Iran University of Medical Science, Tehran, Iran Morteza Fallahpour Department of Allergy and Clinical Immunology, Rasoul-E-Akram Hospital, Iran University of Medical Science, Tehran, Iran Sima Shokri Department of Allergy and Clinical Immunology, Rasoul-E-Akram Hospital, Iran University of Medical Science, Tehran, Iran Javad Ahmadian Department of Pediatric, Emam Reza Hospital, Tabriz University of Medical Sciences, Tabriz, Iran Rasool Molatefi Department of Pediatrics, Bu Ali Hospital, Ardebil University of Medical Sciences, Ardebil, Iran Kyan Darabi Iran Allergy Clinics, Tehran, Iran Golam Reza Sedighi Department of Pediatric, Afzalipour Hospital, Kerman University of Medical Sciences, Kerman, Iran Zeinab Moinfar Department of Community Medicine, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran Sepideh Darougar Department of Pediatrics, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran 2020 03 10 2020 06 22 Asthma induced by ingestion of aspirin occurs when symptoms arise within 30 minutes to three hours after aspirin consumption. Previous data indicate that sensitivity to aspirin may be associated with poorly controlled asthma. This study aims to evaluate the frequency of aspirin sensitivity in patients with moderate to severe asthma receiving conventional asthma therapy. This clinical trial was conducted on 65 patients aged 18 to 65 years with moderate to severe asthma from February 2015 to February 2016 at the Allergy Department, Hazrat-e-Rasoul Hospital, Iran University of Medical Sciences, Tehran. To assess treatment responses in patients, forced expiratory volume in the first second (FEV1) and asthma control test (ACT) scores were measured at baseline and after 3 months. The results of the oral aspirin challenge revealed a prevalence of 35.38% for sensitivity to aspirin. Hypersensitivity reactions to aspirin were detected in 60.9% of the patients with moderate asthma and 39.1% of the patients with severe asthma. All patients with positive aspirin challenge tests suffered from rhinosinusitis and in 56.5% of cases, history of previous hypersensitivity reactions to non-steroidal anti-inflammatory drugs (NSAIDs) was detected. No meaningful differences were found between those patients with aspirin sensitivity and those with aspirin tolerance neither in mean pre-bronchodilator FEV1 nor in ACT scores pre- and post-treatment. To conclude, aspirin sensitivity was not found to have an association with an unfavorable response to conventional treatment in patients with uncontrolled asthma.  https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2741

Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 19 4 2020 08 25 362 372 Maral Ranjbar Department of Immunology, School of Medicine, Iran University of Medical Science, Tehran, Iran Mojdeh Matloubi Department of Immunology, School of Medicine, Iran University of Medical Science, Tehran, Iran Mohammad-Ali Assarehzadegan Department of Immunology, School of Medicine, Iran University of Medical Science, Tehran, Iran AND Immunology Research Center, Institute of Immunology and Infectious Diseases, Iran University of Medical Sciences, Tehran, Iran Morteza Fallahpour Department of Allergy, Rasool-e-Akram Hospital, Iran University of Medical Sciences, Tehran, Iran AND Firoozabadi Hospital, Iran University of Medical Sciences, Tehran, Iran Fatemeh Sadeghi Department of Immunology, School of Medicine, Iran University of Medical Science, Tehran, Iran Saeed Soleyman-Jahi Digestive Diseases Research Core Center, Division of Gastroenterology, School of Medicine, Washington University, St. Louis, USA Leila Janani Department of Biostatistics, School of Public Health, Iran University of Medical Science, Tehran, Iran 2019 12 05 2020 04 11 Thymic stromal lymphopoietin (TSLP) is a cytokine similar to IL-7, which is released by airway epithelial cells in response to injury and inflammation. Current literature is contradictory about the association between different single nucleotide polymorphisms (SNPs) of the TSLP gene and asthma development in different countries. We aimed to evaluate the association between two common TSLP SNPs (rs2289276 and rs2289278) and the risk of asthma in the Iranian population. Genotyping of the TSLP gene was performed in 126 adult asthmatic patients and 300 controls; using the TaqMan genotyping assay. Moreover, total serum IgE level and eosinophil count were assessed. The results indicated that the TT genotype of rs2289276 was inversely associated with the risk of asthma (p=0.002). A similar inverse association was detected in subgroups of atopic (p=0.001) and non-atopic (p=0.005) asthma. Moreover, the TT genotype of this SNP was more prevalent in severe and late-onset categories of asthma. In subgroup analysis, a significant sex-specific association between rs2290276 and asthma was observed in women (p=0.004). The prevalence of rs2289276 was extremely low, which made it infeasible to perform any further analysis. Overall, our findings indicated that rs2290276 SNP of the TSLP gene has a protective phenotype against asthma development in the Iranian population.  https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2624

Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 19 4 2020 08 25 337 347 Zohreh Jadali School of Public Health, Tehran University of Medical Sciences, Tehran, Iran 2019 07 29 2020 06 22 Recent literature has highlighted the importance of chronic inflammation in psoriasis pathogenesis. Non-resolving inflammation can trigger progressive tissue damage and inflammatory mediator release which in turn perpetuate the inflammatory cycle. Under normal conditions, inflammatory responses are tightly controlled through several mechanisms that restore normal tissue function and structure. Defects in regulatory mechanisms of the inflammatory response can result in persistent unresolved inflammation and further increases of inflammation. Therefore, this review focuses on defects in regulatory mechanisms of inflammatory responses that lead to uncontrolled chronic inflammation in psoriasis. Databases such as Pubmed Embase, ISI, and Iranian databases including Iranmedex, and SID were researched to identify relevant literature. The results of this review indicate that dysregulation of the inflammatory response may be a likely cause of various immune-mediated inflammatory disorders such as psoriasis. Based on current findings, advances in understanding the cellular and molecular mechanisms involved in inflammation resolution are not only improving our knowledge of the pathogenesis of chronic inflammatory diseases but also supporting the development of new therapeutic strategies. https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2473

Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 19 4 2020 08 25 373 385 Nosibah Abdul-Razek Department of Zoology, Immunity Division, Faculty of Science, Beni-Suef University, Beni-Suef, Egypt Al-Mahy M. El-Mallah Department of Zoology, Immunity Division, Faculty of Science, Beni-Suef University, Beni-Suef, Egypt Abdelaziz Abuelsaad Department of Zoology, Immunity Division, Faculty of Science, Beni-Suef University, Beni-Suef, Egypt Mahmoud Abdel-Latif Department of Zoology, Immunity Division, Faculty of Science, Beni-Suef University, Beni-Suef, Egypt 2019 12 26 2020 06 11 Diethylcarbamazine citrate (DEC) is known as an effective treatment for bronchial asthma because of its ability to reduce eosinophil trafficking to the lung tissue. The current study aimed to potentiate the anti-allergic effect of the drug by passive immunization of the asthmatic model with anti-DEC antibody or prior treatment with quercetin (Qur). Eight mice groups were categorized into control, the model of lung asthma, treated with DEC, passively immunized with anti(α)-bovine serum albumin Ab, anti-DEC Ab, prior exposure to 10, 20, or 40 mg Qur/Kg. b.wt. Both eosinophil peroxidase (EPO) and eotaxin2 in the lung tissues were performed. Serum levels of cytokines, bronchoalveolar lavage fluid  (BALF) IgE, rabbit anti-bovine serum albumin (anti-BSA), and DEC IgG in lung tissue homogenates were assayed by ELISA. Regarding the effect of anti-DEC Ab and Qur on DEC-induced recovery of histopathological alterations showed that the Ova group had peri-bronchial hyperplasia, mononuclear leukocyte infiltration, thickening in the wall of alveoli, and congested blood vessels. However, the reduction of inflammatory cells and thickened alveolar walls was dependent on the Qur dose. Qur40 enhanced the anti-allergic effect of DEC. Moreover, the present data revealed high levels of Th2 cytokines (IL-4 and IL-5) and IgE in the Ova group. An increased leukocyte infiltration/thickening of the alveolar wall and lung tissue EPO/eotaxin2 were also observed. Qur-40 could show an enhancement effect on DEC for the reduction of IL-4, IL-5, IgE, EPO, and eotaxin 2. Consequently, the IFN-γ/IL-4 ratio was increased. Qur at 40 mg/Kg could be recommended to enhance the DEC effect suggesting a novel approach for treatment. https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2654

Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 19 4 2020 08 25 386 396 Javad Boskabadi Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran AND Department of Clinical Pharmacy, School of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran Saeideh Saadat Department of Physiology, School of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran Mohammad Hosein Boskabady Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran AND Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran 2019 12 06 2020 03 14 This study was conducted to evaluate the possible mechanisms of the relaxant effects of hydroalcoholic extract of Plantago major (P. major) on tracheal smooth muscle (TSM) in rats. The effects of cumulative concentrations of P. major (5, 10, 20 and 40 mg/mL) and theophylline (0.2, 0.4, 0.6 and 0.8 mM) were evaluated on pre-contracted TSM with 10 μΜ methacholine or 60 mM KCl. To determine the possible mechanisms, the relaxant effect of the plant was also examined on incubated TSM with atropine, indomethacin, chlorpheniramine, glibenclamide, diltiazem, papaverine, and propranolol. The results indicated concentration-dependent relaxant effects for P. major in non-incubated TSM contracted by methacholine or KCl. There was no statistically significant difference in the relaxant effects of P. major between non-incubated and incubated tissues with indomethacin, papaverine, and propranolol. However, the relaxant effects of P. major in incubated tissues with atropine (p<0.01 to p<0.001), chlorpheniramine (p<0.05 to p<0.001), glibenclamide (p<0.05), or diltiazem (p<0.01) were significantly lower than non-incubated TSM. P. major indicated relatively potent relaxant effects which were lower than those of theophylline. Muscarinic and histamine (H1) receptors inhibition, as well as calcium channel blocking and potassium channel opening effects are suggested to contribute to the TSM relaxant effect of the plant.   https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2626

Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 19 4 2020 08 25 397 408 Wei Zhan Department of Colorectal Surgery, Affiliated Hospital of Guizhou Medical University, Guiyang, China Xin Liao Department of Imaging, Affiliated Hospital of Guizhou Medical University, Guiyang, China Zhongsheng Chen Guizhou Medical University, Guiyang, China Lianghe Li Guizhou Medical University, Guiyang, China Tian Tian Guizhou Medical University, Guiyang, China AND Department of Pathology, Guiyang Maternal and Child Health Hospital, Guiyang, China Rui Li Department of Traditional Chinese Medicine, Guizhou Provincial People’s Hospital, Guiyang, China 2019 06 24 2020 03 10 To detect the leucine-rich repeats and immunoglobulin 1 (LRIG1) ameliorated liver fibrosis and hepatic stellate cell (HSC) activation via inhibiting sphingosine kinase 1 (SphK1)/Sphingosine-1-Phosphate (S1P) pathway. C57BL/6 male mice (eight weeks old) were intraperitoneal injection with 10% carbon tetrachloride (CCl4) as an in vivo model. The LX-2 cells were induced as amodel for in vitro study by TGF-β (10 ng/mL). The Hematoxylin-eosin (HE) staining, Masson staining, and Sirius red staining results showed that CCl4 caused serious fibrosis and injury in liver tissue, high expression of type I collagen α1 chain (Col1α1) and α-smooth muscle actin (α-SMA) in liver tissue, while the LRIG1 expression level was significantly decreased in LX-2 cell lines. The LRIG1 ameliorated CCl4-induced liver fibrosis, indicated by the fibronectin, α-SMA, LRIG1, SphK1, Col1α1, fibrin Connexin 1 (Fn1), tissue inhibitor of metalloproteinase-1 (TIMP1), sphingosine-1-phosphate (S1P), transforming growth factor-beta 1 (TGF-β1) expression level changes. Similar results were observed in TGF-β1 treated of LX-2 cells. However, the effects were attenuated by treatment with LRIG1. Moreover, SphK1 inhibitors abrogated the effect of LRIG1 on fibrosis. These results demonstrated that LRIG1 improved liver fibrosis in vitro and in vivo via suppressing the SphK1/S1P pathway, indicating its potential use in the treatment of liver fibrosis. https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2443

Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 19 4 2020 08 25 409 415 Ahmad Talebian Department of Pediatric Neurology, Kashan University of Medical Sciences, Kashan, Iran Farzaneh Hassani Department of Pediatric Neurology, Kashan University of Medical Sciences, Kashan, Iran Hassan Nikoueinejad Nephrology and Urology Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran Hossein Akbari Department of Biostatistics and Public Health, Faculty of Health, Kashan University of Medical Sciences, Kashan, Iran 2020 03 02 2020 07 01 A febrile seizure is the most common type of seizure in young kids, which is not fully known. Inflammatory mediators can affect the pathogenesis of the disease. Considering the controversy about the impacts of interleukin 1 beta (IL-1β) and the lack of a study on interleukin 22 (IL-22), the purpose of the present study was to investigate the relationship between IL-22 and IL-1β serum levels with febrile seizure in young kids. Our case-control study has been conducted on 120 young kids aged 6-60 months with the sign of the fever. Rectal temperature was measured for allcases. Patients with febrile seizure (n=60) and patients with fever and without a seizure (n=60) were investigated as case and control groups, respectively. Serum levels of IL-22 and IL-1β were measured in all participants through the ELISA method. The serum level of IL-1β was significantly higher in the case group compared to the control group (p˂0.001), while there were no significant differences between the two groups in terms of IL-22 (p=0.92). Unlike IL-1β (p≤0.021), IL-22 showed no difference between two groups according to some demographic and clinical features like gender, age group, family history of febrile seizure, family history of epilepsy, and evolutionary status (p>0.22). Logistic multiple regression analysis showed that, unlike IL-1β (p˂0.001), IL-22 does not change the chance of febrile seizure in the study groups (p=0.737). The findings of this study indicated that, unlike IL-1β, IL-22 has not any changes/effects in the febrile seizure. https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2734

Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 19 4 2020 08 25 416 425 EN Leila Karimi Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran Nahid Eskandari Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran Vahid Shaygannejad Isfahan Neurosciences Research Center, Alzahra Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran Nasrin Zare Applied Physiology Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran Alireza Andalib Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran Hossein Khanahmad Department of Genetic and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran Omid Mirmosayyeb Isfahan Neurosciences Research Center, Alzahra Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran 2020 02 04 2020 08 25 T helper type 1 (Th1) and Th17 Cells with distinct cytokine profiles including interferon-gamma (IFN-γ) and interleukin 17 (IL-17) have a pivotal role in neuroinflammation and myelin destruction in the central nervous system (CNS) in MS. MicroRNA-29b (MiR-29b) and miR-326 contribute to regulating Th1 and Th17 differentiation and altered expression of the miRNAs could be associated with response to treatment in multiple sclerosis (MS). Therefore, our study aimed to evaluate the percentage of Th1 and Th17 and determining the expression levels of miR-29b-3p and miR-326 in these lymphocyte subpopulations between responsive and non-responsive to interferon beta (IFN-β) therapy in relapsing-remitting multiple sclerosis (RRMS) patients. The present study was performed on 40 RRMS patients following treatment with IFN-β. The percentage of Th1 cells and Th17 cells were determined by flow cytometry in responsive and non-responsive patients. The expression levels of miR-29b-3p and miR-326 were assessed in Th1 and Th17 cells by quantitative polymerase chain reaction (PCR). Enzyme-linked immunosorbent assay (ELISA) was applied to evaluate the plasma levels of IFN-γ and IL-17A. No significant difference was observed in the percentage of Th1 and Th17 cells as well as the expression levels of miR-29b-3p and miR-326 (in Th1 and Th17, respectively) in treated patients. Also, we did not find any significant difference in IFN-γ and IL-17A plasma concentration between responsive or non-responsive to IFN-β therapy in patients with RRMS. IFN-β may regulate other miRNAs in Th1 and Th17 cells than miR29b-3p and miR-326 in MS patients. https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2703

Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 19 4 2020 08 25 426 436 Negin Nokhandani Laboratory Sciences Research Center, Golestan University of Medical Sciences, Gorgan, Iran AND Department of Immunology, School of Medicine, Golestan University of Medical Sciences, Gorgan, Iran Mahdieh Naghavi Alhosseini Department of Immunology, School of Medicine, Golestan University of Medical Sciences, Gorgan, Iran Ali Memarian Department of Immunology, School of Medicine, Golestan University of Medical Sciences, Gorgan, Iran Homa Davoodi Cancer Research Center, Golestan University of Medical Sciences, Gorgan, Iran 2019 08 11 2020 02 15 Several studies have been conducted to find suitable combinations of drugs to increase the efficacy of chemotherapy and reduce the resistance of tumor cells to treatment. Lipopolysaccharide (LPS), as a ligand for Toll-like receptor 4 (TLR-4), can modify immune responses in different cancers. Although multiple studies have been performed in this area, the effect of LPS on tumor cells remains controversial. In the present study, the cytotoxic effects of 5-fluorouracil (5-FU), with or without LPS, were evaluated in human breast cancer cell line (MCF-7) on apoptosis and gene expression in downstream signaling pathways. MCF-7 was obtained from the Pasteur Institute of Iran. The effects of LPS and 5-FU on cytotoxicity, apoptosis, and gene expression in NF-κB, ERK, and AKT signaling pathways were evaluated by MTT assay, Annexin V/propidium iodide (PI) apoptosis assay, and qRT-PCR, respectively. Our findings showed that LPS alone did not significantly affect cytotoxicity or apoptosis, compared to the control cells (untreated cells), while combined with 5-FU, it caused a significant increase in the apoptosis of cancer cells and decreased cell viability. It was also concluded that LPS in combination with 5-FU increased TLR-4 expression and down-regulated gene expression in NF-κB, ERK, and AKT pathways (p=0.001). Although the role of LPS in tumor inhibition or progression remains controversial, our findings suggest that LPS can be considered a novel complementary approach intranslational oncology research of breast cancer therapy. https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2487

Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 19 4 2020 08 25 437 446 Shockrollah Farrokhi Department of Immunology, Faculty of Medicine, Boushehr University of Medical Sciences, Boushehr, Iran Faezeh Abbasi-rad Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran Nafiseh Esmaeil Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran Roya Sherkat Acquired Immunodeficiency Research Center, Isfahan University of Medical Sciences, Isfahan, Iran Reza Yazdani Research Center for Immunodeficiencies, Pediatrics Center of Excellence, Children's Medical Center Hospital, Tehran University of Medical Sciences, Tehran, Iran Sanaz Afshar-Ghasemlou Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran Saba Fekrvand Research Center for Immunodeficiencies, Pediatrics Center of Excellence, Children's Medical Center Hospital, Tehran University of Medical Sciences, Tehran, Iran Mazdak Ganjalikhani-Hakemi Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran AND Acquired Immunodeficiency Research Center, Isfahan University of Medical Sciences, Isfahan, Iran 2019 12 07 2020 06 11 Common variable immunodeficiency (CVID) is a primary immune deficiency disorder characterized by a failure in B cell differentiation, impaired immunoglobulin production,and defect in response to vaccines. As a result of defective B cell maturation and differentiation in CVID, the affected patients commonly present with reduced numbers of memory B cell and antibody-secreting plasma cells. B-cell lymphoma 6 protein (BCL6) and B lymphocyte induced maturation protein 1 (BLIMP1) molecules are two important transcription factors that have key roles in the maturation of B cells to plasma cells. Hence, in the current survey, we aimed to evaluate the mRNA and protein expression levels of BCL6 and BLIMP1 in B lymphocytes isolated from peripheral blood in CVID patients. We collected blood samples from 12 CVID patients and 12 healthy controls. We isolated peripheral blood mononuclear cells (PBMCs) using Ficoll density gradient separation. Then, CD19+ B cells were purified using MACS. The protein expression and transcriptional level of BCL6 and BLIMP1 were respectively measured using flow cytometry and real-time PCR. Our results showed that the BLIMP1 mRNA expression, as well as BLIMP1 protein expression, were significantly higher in CVID patients compared to control subjects (p=0.009 and p=0.007, respectively). However, we found no significant difference in mRNA and protein expression of BCL6 between patients and healthy controls. According to our findings, increased mRNA and protein expression levels of BLIMP1 could be involved in defective maturation of B cells in patients with CVID and elucidate mechanistic insights into the pathogenesis of this disorder. https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2631