On the other hand, downregulation of IRF4 might dampen exaggerated responses during autoimmunity. Future studies further investigating
the molecular actions of IRF4 may facilitate the development of such strategies and their employment in therapeutic settings. This work was supported by Deutsche Forschungsgemeinschaft, grants HU 1824/2-1 and SFB/TR22 to M.L. The authors declare no financial or commercial conflict of interest. “
“Ly49G2 (G2+) NK cells mediate murine (M)CMV resistance in MHC Dk-expressing mice. Bone marrow transplantation (BMT) studies revealed that G2+ NK cell-mediated MCMV resistance requires Dk in both hematopoietic and nonhematopoietic cells. As a Ly49G2 ligand, Dk in both cell lineages may contribute to lysis of virus-infected cells. Alternatively, Maraviroc datasheet cellular differences in self-MHC Dk may have affected NK-cell education, and consequently NK cell-mediated viral clearance. We investigated the Dk-licensing effect on BM-derived NK cells in BMT recipients by analyzing cytokines, cytotoxicity and MCMV resistance.
In BMT recipients with lineage-restricted Dk, G2+ NK-cell reactivity and cytotoxicity was diminished in comparison to BMT recipients with self-MHC in all cells. Reduced G2+ NK-mediated MCMV resistance in BMT recipients with lineage-restricted self-MHC indicates that licensing of G2+ NK cells is related to NK-cell reactivity selleck products and viral control. Titrating donor BM with self-MHC-bearing hematopoietic cells, as well as adoptive transfer of mature G2+ NK cells into BMT recipients with self-MHC
in non-hematopoietic cells only, enhanced NK-cell licensing and rescued MCMV resistance. This disparate self-MHC NK-cell education model would suggest that inadequately licensed NK cells corresponded to inefficient viral sensing and clearance. “
“Colitis is still before a significant disease challenge in humans, but its underlying mechanism remains to be fully elucidated. The transient receptor potential vanilloid (TRPV) ion channel plays an important pathological role in host immunity, as deficiency of TRPV compromises host defence in vivo and in vitro. Using a DSS-induced colitis mouse model, the function of TRPV2 in the development of colitis was investigated, utilizing TRPV2−/− and Wt mice. Less severe colitis was observed in TRPV2−/−, compared to that of Wt mice, at the clinical, histopathological and immunohistochemical levels. Compared to Wt mice, reduced severity of colitis in TRPV2−/− mice may be due to less intestinal inflammation via reduced recruitment of macrophages. The TRPV2 pathway contributes to the development of colitis. These data provide useful information for potential therapeutic intervention in colitis patients. “
“Bcl11b is a transcription factor that, within the hematopoietic system, is expressed specifically in T cells.