Common immunologic mechanisms in inflammatory bowel disease and spondylarthropathies

Abstract

Spondyloarthropathies (SpA) are commonly observed extra-intestinal manifestations of both Crohn's disease (CD) and ulcerative colitis (UC), the two major forms of inflammatory bowel diseases (IBD). However, the immunological link between these two clinical entities is still poorly understood. Several lines of evidence indicate that SpA may originate from the relocation to the joints of the immune process primarily induced in the gut. The transfer of the intestinal inflammatory process into the joints implicates that immune cells activated in the gut-draining lymph nodes can localize, at a certain point of the intestinal disease, either into the gut or into the joints. This is indicated by the overlapping expression of adhesion molecules observed on the surface of intestinal and synovial endothelial cells during inflammation. Moreover bacterial antigens and HLA-B27 expression may be implicated in the reactivation of T cells at the articular level. Finally, accumulating evidence indicates that a T helper 17 cell-mediated immune response may contribute to IBD and IBD-related SpA with a crucial role played by tumor necrosis factor-alpha in CD and to a lesser extent in UC.

Figure 1

The heterogeneous expression of adhesion molecules allows T cells activated in the gut to home into the joints. CCR9: Chemokine receptor-9; CCL-25: Chemokine ligand-25; MadCAM1: Mucosal addressin cell-adhesion molecule-1; VCAM1: Vascular cell adhesion molecule-1; ICAM :Intracellular adhesion molecule; VLA-4: Very late antigen-4; LFA-1: Lymphocyte function associated antigen-1; VAP-1: Vascular adhesion protein-1.