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Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Immunology 2017 ; 151 (3): 280-90 Nephropedia Template TP
Mao L; Hou H; Wu S; Zhou Y; Wang J; Yu J; Wu X; Lu Y; Mao L; Bosco MJ; Wang F; Sun Z
Immunology 2017[Jul]; 151 (3): 280-90 PMID28108989show ga
B?lymphocyte hyperactivity in systemic lupus erythematosus (SLE) is T?cell?dependent, and CD4+ T?cell activation is essential to SLE pathogenesis. However, the mechanism of the deregulation of CD4+ T cells in SLE is largely unknown. T?cell immunoglobulin and ITIM domain (TIGIT) is a new inhibitory receptor preferentially expressed on activated CD4+ T cells. Here, we address the role of TIGIT in the pathogenesis of SLE. Our results showed that TIGIT expression on CD4+ T cells was significantly elevated in patients with SLE and highly correlated with the activity of the disease. TIGIT+CD4+ T cells from both healthy individuals and patients with SLE had a more activated phenotype than TIGIT?CD4+ T cells. In contrast, the activation, proliferation and cytokine production potential of TIGIT+CD4+ T cells were significantly lower than those of TIGIT?CD4+ T cells. Furthermore, activation of the TIGIT pathway by using CD155 could substantially down?regulate the activities of CD4+ T cells from SLE patients in vitro, and in vivo administration of CD155 resulted in a delayed development of SLE in MRL/lpr mice. TIGIT is a powerful negative regulator of CD4+ T cells in SLE, which suggests that the TIGIT signalling pathway may be used as a potential therapeutic target for treating this disease.