@article{oai:soar-ir.repo.nii.ac.jp:00020842, author = {Sanjo, Hideki and Tokumaru, Shigeo and Akira, Shizuo and Taki, Shinsuke}, issue = {7}, journal = {PLOS ONE}, month = {Jul}, note = {The kinase TAK is required for the development of conventional and regulatory T cells. We previously reported that mice with conditional deletion of TAK1 in T cells (Lck-cre: TAK1(fl/fl) mice) exhibited severe T lymphopenia, and were nevertheless predisposed to spontaneous colitis with unknown etiology. Here we focused on the immunopathological mechanism in colitic Lck-cre: TAK1(fl/fl) mice. We found that 'leaky' CD4(+) T cells retaining TAK1 acquired inflammatory phenotypes that contribute to disease onset in Lck-cre: TAK1(fl/fl) mice. Furthermore, the gut microbiota-triggered signaling was also a key event leading to the pathogenesis. We discovered that Lck-cre: TAK1(fl/fl) mice were almost completely devoid of TCR alpha beta(+) CD8 alpha(+) intestinal intraepithelial lymphocytes (IELs) and this was largely due to the developmental defect of the thymic precursors by TAK1 deficiency. Remarkably, transfer of TCR alpha beta(+) CD8 alpha(+) IELs from wild-type mice ameliorated colitis in Lck-cre: TAK1(fl/fl) mice. Taken together, our current study highlighted the emerging role of TAK1 in configuring the gut-specialized T cell subset, which regulates mucosal homeostasis under lymphopenic conditions., Article, PLOS ONE.10(7):e0128761(2015)}, title = {Conditional Deletion of TAK1 in T Cells Reveals a Pivotal Role of TCR alpha beta(+) Intraepithelial Lymphocytes in Preventing Lymphopenia-Associated Colitis}, volume = {10}, year = {2015} }