Journal
JOURNAL OF IMMUNOLOGY
Volume 185, Issue 3, Pages 1920-1926Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0902217
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Funding
- Ministry of Health, Labor and Welfare of Japan
- Ministry of Education, Culture, Sports, Science and Technology of Japan
- National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD
- Grants-in-Aid for Scientific Research [21390303, 21390295] Funding Source: KAKEN
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We previously showed that transplantation with IL-21R gene-deficient splenocytes resulted in less severe graft-versus-host disease (GVHD) than was observed with wild type splenocytes. In this study, we sought to find mechanism(s) explaining this observation. Recipients of donor CD4(+) T cells lacking IL-21R exhibited diminished GVHD symptoms, with reduced inflammatory cell infiltration into the liver and intestine, leading to prolonged survival. After transplantation, CD4(+) T cell numbers in the spleen were reduced, and MLR and cytokine production by CD4(+) T cells were impaired. These results suggest that IL-21 might promote GVHD through enhanced production of effector CD4(+) T cells. Moreover, we found that CD25 depletion altered neither the impaired MLR in vitro nor the ameliorated GVHD symptoms in vivo. Thus, the attenuated GVHD might be caused by an impairment of effector T cell differentiation itself, rather than by an increase in regulatory T cells and suppression of effector T cells. The Journal of Immunology, 2010, 185: 1920-1926.
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