CD137 functions mainly as a costimulatory molecule for T cell activation. However, its functions have been found in a variety of other immune and nonimmune cells. Transfer of BM2 CD4⁺ T cells into unirradiated, MHC II-mismatched C57BL/6 mice induces lupus-like chronic GVHD, which occurs because donor CD4⁺ T cells break host B cell tolerance with help from host CD4⁺ T cells. We found that chronic GVHD was inhibited when CD137^-/- mice were used as the host in this chronic GVHD model. Instead, they exhibited evident loss of body weight, indicating that they had acute GVHD. Indeed, their splenocytes were markedly depleted and they had severe intestinal and liver GVHD. Consistent with these phenotype changes, there were increased numbers of Th1 and Th17 cells but decreased numbers of Treg cells in the spleen of CD137^-/- recipient mice 10 days after disease induction. Our results indicate that host CD137 signaling is a key factor to determine the fate of donor CD4⁺ T cells during GVHD course.

CITATION INFORMATION: Cho H, Lee J, Kim J, Moon U, Kwon B, Park S, Park K. Absence of Host CD137 Signaling Converts Chronic GVHD Toward Acute GVHD. Am J Transplant. 2016;16 (suppl 3).

« Back to 2016 American Transplant Congress