CD4 T Cells in IBD: Crossing the Line?

Excerpt

Several lines of evidence have suggested a major contribution of CD4+ T cells toward the pathogenesis of inflammatory bowel disease (IBD). A growing body of genetic associations in Crohn’s disease (CD) and ulcerative colitis (UC) have identified polymorphisms in or near genes central to CD4+ T cell function, such as the receptor for interleukin (IL)-23 [1], a cytokine essential for the survival of the Th17 subset of CD4+ T cells, which is implicated in the pathogenesis of several animal models of autoimmunity [2]. Similarly, clinical efficacy has been conclusively demonstrated in large clinical trials of drugs targeting proteins important for CD4+ T cells. Finally, IBD patients infected with human immunodeficiency virus (HIV) have a milder course with fewer disease flares likely as a consequence of CD4+ T cell depletion [3]. Yet, the mechanism by which CD4+ T cells contribute to IBD pathogenesis has remained elusive. …