Mbinase (46), leading to the possibility that residual B10 cells may remain

Mbinase (46), leading to the possibility that residual B10 cells may remain that inhibit BRDU chemical information disease severity. Additionally, a congenital defect in B10 cell development may be compensated for by the increased availability of a separate IL-10-producing population. The same compensatory mechanisms are not evident in mice 11-Deoxojervine site depleted of mature B cells, as discussed above, which may provide a more comprehensive assessment of the role of B10 cell function during lupus. Inflammatory bowel disease Early studies of B cell immunoregulation relied on colitis as a model of autoimmune inflammation. A role for IL-10-mediated suppression of colitis was demonstrated by the generation of IL-10-/- mice, which develop spontaneous, chronic colitis by 7?1 weeks of age (47). Mizoguchi et al. (4, 48) demonstrated that B cells are capable of suppressing colitis in a separate model using TCR-/- mice in which mesenteric lymph node B cells upregulated CD1d and provided the IL-10 necessary for dampening disease. While studies by Mizoguchi and others have shown that B cells can mitigate gut-associated inflammation, a definitive role for B10 cell-mediated suppression by cells from both the spleen and the peritoneal cavity was demonstrated in three separate inflammatory bowel disease (IBD) models. Dextran sulfate sodium (DSS)-induced colitis, which is achieved by short-term administration of DSS in rodent drinking water and causes acute intestinal injury throughout the length of the colon, is significantly worse in B10 cell-deficient CD19-/- mice than in wildtype mice (49). The adoptive transfer of splenic CD1dhi CD5+ cells ameliorates disease by slowing weight loss and intestinal bleeding in an IL-10-dependent manner. Additional studies of DSS-induced colitis in IL-10 reporter Tiger mice have also shown that B10 cells in the spleen, mesenteric lymph nodes, and peritoneal cavity are capable of expressing IL-10 during the acute inflammation caused by DSS treatment (24). Thus, B10 cells play an active role in reducing gut-associated inflammation. B10 cells also suppress the spontaneous, chronic IBD modeled in IL-10-/- mice. Peritoneal cavity-derived B10 cells significantly delayed the onset of IBD in IL-10-/- recipients when transferred at 10?2 weeks of age and decreased the frequency of activated and cytokineproducing CD4+ T cells in the peritoneal cavity, mesenteric lymph nodes, and inguinalImmunol Rev. Author manuscript; available in PMC 2015 May 01.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptCandando et al.Pagelymph nodes of recipient mice. The anti-inflammatory effects of peritoneal cavity B10 cells were confirmed in a separate colitis model where the transfer of CD25- CD45RB hiCD4+ T cells into RAG2-/- mice causes an IBD-like disease (50). As in spontaneous IBD, the transfer of peritoneal cavity B10 cells suppressed T-cell-induced colitis in an IL-10dependent manner and decreased levels of IFN– and IL-17-producing T cells in the peritoneal cavity, mesenteric lymph nodes, and spleen (24). Therefore, B10 cells from the spleen and peritoneal cavity are capable of inhibiting gut-associated inflammation in both spontaneous and induced models of IBD. Collagen-induced arthritis Collagen-induced arthritis (CIA) serves as a model for human rheumatoid arthritis (RA) and is characterized by joint destruction and infiltration of antigen-specific T cells to sites of inflammation following collagen immunization in the DBA/1 strain of mice (51). B-cell.Mbinase (46), leading to the possibility that residual B10 cells may remain that inhibit disease severity. Additionally, a congenital defect in B10 cell development may be compensated for by the increased availability of a separate IL-10-producing population. The same compensatory mechanisms are not evident in mice depleted of mature B cells, as discussed above, which may provide a more comprehensive assessment of the role of B10 cell function during lupus. Inflammatory bowel disease Early studies of B cell immunoregulation relied on colitis as a model of autoimmune inflammation. A role for IL-10-mediated suppression of colitis was demonstrated by the generation of IL-10-/- mice, which develop spontaneous, chronic colitis by 7?1 weeks of age (47). Mizoguchi et al. (4, 48) demonstrated that B cells are capable of suppressing colitis in a separate model using TCR-/- mice in which mesenteric lymph node B cells upregulated CD1d and provided the IL-10 necessary for dampening disease. While studies by Mizoguchi and others have shown that B cells can mitigate gut-associated inflammation, a definitive role for B10 cell-mediated suppression by cells from both the spleen and the peritoneal cavity was demonstrated in three separate inflammatory bowel disease (IBD) models. Dextran sulfate sodium (DSS)-induced colitis, which is achieved by short-term administration of DSS in rodent drinking water and causes acute intestinal injury throughout the length of the colon, is significantly worse in B10 cell-deficient CD19-/- mice than in wildtype mice (49). The adoptive transfer of splenic CD1dhi CD5+ cells ameliorates disease by slowing weight loss and intestinal bleeding in an IL-10-dependent manner. Additional studies of DSS-induced colitis in IL-10 reporter Tiger mice have also shown that B10 cells in the spleen, mesenteric lymph nodes, and peritoneal cavity are capable of expressing IL-10 during the acute inflammation caused by DSS treatment (24). Thus, B10 cells play an active role in reducing gut-associated inflammation. B10 cells also suppress the spontaneous, chronic IBD modeled in IL-10-/- mice. Peritoneal cavity-derived B10 cells significantly delayed the onset of IBD in IL-10-/- recipients when transferred at 10?2 weeks of age and decreased the frequency of activated and cytokineproducing CD4+ T cells in the peritoneal cavity, mesenteric lymph nodes, and inguinalImmunol Rev. Author manuscript; available in PMC 2015 May 01.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptCandando et al.Pagelymph nodes of recipient mice. The anti-inflammatory effects of peritoneal cavity B10 cells were confirmed in a separate colitis model where the transfer of CD25- CD45RB hiCD4+ T cells into RAG2-/- mice causes an IBD-like disease (50). As in spontaneous IBD, the transfer of peritoneal cavity B10 cells suppressed T-cell-induced colitis in an IL-10dependent manner and decreased levels of IFN– and IL-17-producing T cells in the peritoneal cavity, mesenteric lymph nodes, and spleen (24). Therefore, B10 cells from the spleen and peritoneal cavity are capable of inhibiting gut-associated inflammation in both spontaneous and induced models of IBD. Collagen-induced arthritis Collagen-induced arthritis (CIA) serves as a model for human rheumatoid arthritis (RA) and is characterized by joint destruction and infiltration of antigen-specific T cells to sites of inflammation following collagen immunization in the DBA/1 strain of mice (51). B-cell.

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