The release of TSLP and IL-33 affect the skin integrity, which unsettled transcription factor regulators. We investigate TSLP and IL-33 in Behçet disease (BD) and we prove the effect of the anti-inflammatory cytokine IL-37 in BD skin lesions on TSLP production. TSLP, IL-33 and GATA-3/T-bet, were measured using PCR in BD skin lesions. We tested the suppressive effect of IL-37 on skin samples stimulated with a cytokine mixture inducing TSLP expression. TSLP and IL-33 were increased in BD patients particularly in patients having skin manifestations and correlate with indexed skin lesions. TSLP expression in BD with skin lesions correlates significantly with the transcription factors GATA3/Tbet ratio. The anti-inflammatory mediator IL-37 acted as a suppressor of TSLP-skin synthesis. The microenvironment in cutaneous lesions of BD patients' skin lesions is dominated by the expression of IL-33 and TSLP along an inflammatory Th2-type current. IL-37 acts as a booster to restore homeostasis.

TSLP和IL-33的释放会影响皮肤完整性，这会影响转录因子调节剂的稳定性。我们调查了贝塞特病（BD）中的TSLP和IL-33，并证明了BD皮肤病变中抗炎细胞因子IL-37对TSLP产生的影响。在BD皮肤病变中使用PCR测量了TSLP，IL-33和GATA-3 / T-bet。我们测试了IL-37对细胞因子混合物诱导TSLP表达刺激的皮肤样品的抑制作用。BD患者中TSLP和IL-33升高，特别是在具有皮肤表现的患者中，并与索引的皮肤病变相关。患有皮肤病变的BD中的TSLP表达与转录因子GATA3 / Tbet比率显着相关。抗炎介质IL-37可以作为TSLP皮肤合成的抑制剂。BD患者皮肤病变的微环境 IL-33和TSLP沿炎性Th2型电流的表达占主导地位。IL-37充当恢复体内平衡的助推器。