Intraepithelial lymphocytes (IEL) provide a primary barrier against pathogen colonization in the intestinal mucosa. Prolonged or excessive IEL activation, however, can lead to tissue damage from inflammation.
Reporting recently in the journal Immunity, Inflammation and Disease, Danyvid Olivares-Villagomez, Ph.D., and colleagues propose a new mechanism for the regulation of inflammatory responses in the intestinal epithelium.
The researchers previously described a novel subset of IEL cells in the intestinal epithelium called innate iCD8alpha lymphocytes that do not express a T-cell receptor and are part of the innate immune system.
In this study, they demonstrate that the CD8alpha receptor associates with the thymus leukemia (TL) antigen to control inflammation. TL-deficient mice exhibit enhanced inflammation in response to colitis induced with anti-CD40 antibodies.
One way they may do this is by secreting granzymes, proteolytic enzymes that may promote recruitment of infiltrating cells into the epithelium. The researchers propose that dysregulation of iCD8alpha cells, for example due to TL deficiency, may enhance disease.
This research was supported by grants from the National Institutes of Health (DK058404, AI115419).
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