International Journal of Molecular and Cellular Medicine

en Evaluation of the Immune Checkpoints, TIM-3 and PD-1, as well as Anti-Inflammatory Cytokines IL-10, and TGF-β along with Diseases Activity in Chronic Spontaneous Urticaria Molecular & Cellular Immunology Molecular & Cellular Immunology Original Article Original Article <div style="text-align: justify;">Chronic spontaneous urticaria (CSU) is a skin disease caused by mast cells that produce inflammatory mediators. Immune checkpoint receptors such as program death-1 (PD-1) and T-cell immunoglobulin and mucin domain 3 (TIM-3) are essential for the pathophysiology of many autoimmune and allergic diseases. The aim of this study was to investigate the expression of PD-1 and TIM-3 in CSU patients and their relationship to the anti-inflammatory cytokines (TGF-β and IL-10). In the current study, peripheral blood mononuclear cells (PBMCs) from CSU patients and healthy individuals were used and the Urticaria Activity Score 7 (UAS7) was used to assess disease severity. TaqMan-based RT-PCR was used to assess the expression of TIM-3 and PD-1 as well as the anti-inflammatory cytokines transforming growth factor-β (TGF-β) and IL-10. The protein concentrations of TGF-β and IL-10 were also measured by ELISA. The relationship between the expression of TIM-3 and PD-1 as well as TGF- β and IL-10 and the severity of the disease was investigated. The results showed that PD-1 mRNA expression was significantly increased in CSU patients (P<0.0001), while TGF- β and IL-10 levels were higher in CSU patients, but this difference was not significant (p=0.638, p= 0.798). The increase in protein level of IL-10 was significant (P<0.0001).  There was also a positive correlation between the expression of PD-1 and TGF- β molecules and disease activity (P=0.0043, P=0.0018). In conclusion, the study found that the immune system expresses inhibitory molecules and anti-inflammatory cytokines to control disease severity. The higher expression of PD-1 molecules and IL-10 is associated with disease severity, suggesting that the immune system is trying to control inflammation and reduce disease severity.</div> <div style="text-align: justify;"> </div> TIM-3, PD-1, CSU, IL-10, TGF-β, UAS7 64 78 http://ijmcmed.org/browse.php?a_code=A-10-7958-1&slc_lang=en&sid=1 Hadi Sadeghi hadisadegi9494@gmail.com 100319475328460032796 100319475328460032796 No Department of Immunology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran. Javad Ghaffari javadneg@yahoo.com 100319475328460032797 100319475328460032797 No Pediatric Infectious Diseases Research Center, Mazandaran University of Medical Sciences, Sari, Iran. Javad Rajabi javadrajabi26@gmail.com 100319475328460032798 100319475328460032798 No Department of Immunology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran. Monireh Golpour 178greenbio@gmail.com 100319475328460032799 100319475328460032799 No Cancer Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran. Torsten Zuberbier torsten.zuberbier@charite.de 100319475328460032800 100319475328460032800 No Department of Dermatology and Allergy, Charité-Universitätsmedizin Berlin, a joint institution of Humboldt-Universität zu Berlin and Freie Universität Berlin, Berlin, Germany. Sadegh Fattahi fattahi_pgs@yahoo.com 100319475328460032801 100319475328460032801 No North Research Center of Pasteur Institute, Amol, Iran. Hossein Asgarian hasgarian@mazums.ac.ir 100319475328460032802 100319475328460032802 No Department of Immunology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran. Alireza Rafiei rafiei1710@gmail.com 100319475328460032803 100319475328460032803 Yes Department of Immunology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.