It doesn't take much to set off certain Th17 cells lurking in the intestines of patients with Crohn's disease. And on page 525, Kleinschek et al. find a marker that pinpoints those easy-to-incite cells.
Historically, T helper (Th)-1 cells were blamed for causing inflammation in Crohn's disease, psoriasis, and various autoimmune disorders. Interleukin (IL)-17–producing Th17 cells are also found in many of these diseases, although their role in disease pathology is poorly understood. To better characterize these newcomers, Kleinschek et al. examined tissue biopsies and blood samples from people with severe Crohn's disease.
In the inflamed intestinal tissue, the authors found an abundance of Th17 cells expressing the surface receptor CD161, which was recently shown to predict a Th17 fate for naive T cells in the thymus and umbilical cord. Here, the authors found that CD161 was present on differentiated cells that produced IL-17 and other Th17-type cytokines such as IL-17F and IL-22.
CD161+ T cells from the blood of Crohn's patients expressed more IL-17 and IL-23R, and could be quickly stimulated to produce inflammatory cytokines with IL-23 alone. Th17 cells from healthy participants required an additional cytokine, IL-1β, for activation.
The abundant expression of gut homing integrins on circulating CD161+ Th17 cells suggests that these cells migrate to sites of intestinal inflammation.
Whether or not CD161 is mechanistically involved with the proliferation or differentiation of Th17 cells remains unknown. For now, the authors say that CD161 could provide a marker for clinicians to identify pathogenic T cells, thereby identifying patients who could be at risk of severe inflammatory bowel disorders.
