Suppressive role of B cells in chronic colitis of T cell receptor alpha mutant mice.
Suppressive role of B cells in chronic colitis of T cell receptor alpha mutant mice.
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DOI:
10.1084/jem.186.10.1749
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发表时间:
1997-11-17
期刊:
影响因子:
--
通讯作者:
Bhan AK
中科院分区:
文献类型:
--
作者:
Mizoguchi A;Mizoguchi E;Smith RN;Preffer FI;Bhan AK
The role of antibodies (Abs) in the development of chronic colitis in T cell receptor (TCR)-α−/− mice was explored by creating double mutant mice (TCR-α−/− × immunoglobulin (Ig)μ−/−), which lack B cells. TCR-α−/− × Igμ−/− mice spontaneously developed colitis at an earlier age, and the colitis was more severe than in TCR-α−/− mice. Colitis was induced in recombination-activating gene-1 (RAG-1−/−) mice by the transfer of mesenteric lymph node (MLN) cells from TCR-α−/− × Igμ−/− mice. When purified B cells from TCR-α−/− mice were mixed with MLN cells before cell transfer, colitis did not develop in RAG-1−/− mice. Administration of the purified Ig from TCR-α−/− mice and a mixture of monoclonal autoAbs reactive with colonic epithelial cells led to attenuation of colitis in TCR-α−/− × Igμ−/− mice. Apoptotic cells were increased in the colon, MLN, and spleen of TCR-α−/− × Igμ−/− mice as compared to Igμ−/− mice and TCR-α−/− mice. Administration of the purified Ig from TCR-α−/− mice into TCR-α−/− × Igμ−/− mice led to decrease in the number of apoptotic cells. These findings suggest that although B cells are not required for the initiation of colitis, B cells and Igs (autoAbs) can suppress colitis, presumably by affecting the clearance of apoptotic cells.
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影响因子:
15.3
作者:
Gilligan, H M;Bredy, B;Brady, H R;Hebert, M J;Slayter, H S;Xu, Y;Rauch, J;Shia, M A;Koh, J S;Levine, J S
通讯作者:
Levine, J S
DOI:
10.1084/jem.182.5.1567
发表时间:
1995-11-01
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Ma A;Datta M;Margosian E;Chen J;Horak I
通讯作者:
Horak I
影响因子:
5.4
作者:
BRUNO, L;ROCHA, B;RODEWALD, HR
通讯作者:
RODEWALD, HR
影响因子:
15.3
作者:
Mizoguchi, A;Mizoguchi, E;Bhan, AK
通讯作者:
Bhan, AK
影响因子:
64.8
作者:
MOMBAERTS, P;CLARKE, AR;TONEGAWA, S
通讯作者:
TONEGAWA, S