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© The Rockefeller University Press, 0022-1007/1997/11/1749/ $5.00
The Journal of Experimental Medicine, Volume 186, Number 10, November 17, 1997 1749-1756

Articles

Suppressive Role of B Cells in Chronic Colitis of T Cell Receptor {alpha} Mutant Mice

Atsushi Mizoguchi, Emiko Mizoguchi, R. Neal Smith, Frederic I. Preffer, and Atul K. Bhan

From the Immunopathology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114

The role of antibodies (Abs) in the development of chronic colitis in T cell receptor (TCR)-{alpha}–/– mice was explored by creating double mutant mice (TCR-{alpha}–/– x immunoglobulin (Ig)µ–/–), which lack B cells. TCR-{alpha}–/– x Igµ–/– mice spontaneously developed colitis at an earlier age, and the colitis was more severe than in TCR-{alpha}–/– mice. Colitis was induced in recombination-activating gene-1 (RAG-1–/–) mice by the transfer of mesenteric lymph node (MLN) cells from TCR-{alpha}–/– x Igµ–/– mice. When purified B cells from TCR-{alpha}–/– mice were mixed with MLN cells before cell transfer, colitis did not develop in RAG-1–/– mice. Administration of the purified Ig from TCR-{alpha}–/– mice and a mixture of monoclonal autoAbs reactive with colonic epithelial cells led to attenuation of colitis in TCR-{alpha}–/– x Igµ–/– mice. Apoptotic cells were increased in the colon, MLN, and spleen of TCR-{alpha}–/– x Igµ–/– mice as compared to Igµ–/– mice and TCR-{alpha}–/– mice. Administration of the purified Ig from TCR-{alpha}–/– mice into TCR-{alpha}–/– x 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.

Address correspondence to Dr. Atul K. Bhan, Immunopathology Unit-Cox5, Massachusetts General Hospital, 100 Blossom St., Boston, MA 02114. Phone: 617-726-2588; FAX: 617-726-2365; E-mail: bhan{at}helix.mgh.harvard.edu

1 Abbreviations used in this paper: BrdU, 5-bromo-2'-deoxyuridine; IBD, inflammatory bowel disease; MLN, mesenteric LN; RAG-1–/–, recombination-activating gene-1; Tdt, terminal deoxynucleotidyl transferase; TUNEL, terminal deoxynucleotidyltransferase–mediated d-UTP-biotin nick end labeling; UC, ulcerative colitis.


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