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

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.