CD4+ T cells reactive to enteric bacterial antigens in spontaneously colitic C3H/HeJBir mice

Increased T helper cell type 1 response and ability to transfer disease

Yingzi Cong, Steven L. Brandwein, Robert P. McCabe, Audrey J Lazenby, Edward H. Birkenmeier, John P. Sundberg, Charles O. Elson

Research output: Contribution to journalArticle

302 Citations (Scopus)

Abstract

C3H/HeJBir mice are a new substrain that spontaneously develop colitis early in life. This study was done to determine the T cell reactivity of C3H/HeJBir mice to candidate antigens that might be involved in their disease. C3H/HeJBir CD4+ T cells were strongly reactive to antigens of the enteric bacterial flora, but not to epithelial or food antigens. The stimulatory material in the enteric bacteria was trypsin sensitive and restricted by class II major histocompatibility complex molecules, but did not have the properties of a superantigen. The precursor frequency of interleuken (IL)-2-producing, bacterial-reactive CD4+ T cells in colitic mice was 1 out of 2,000 compared to 1 out of 20,000-25,000 in noncolitic control mice. These T cells produced predominately IL-2 and interferon γ, consistent with a T helper type 1 cell response and were present at 3-4 wk, the age of onset of the colitis. Adoptive transfer of bacterial-antigen- activated CD4+ T cells from colitic C3H/HeJBir but not from control C3H/HeJ mice into C3H/HeSnJ scid/scid recipients induced colitis. These data represent a direct demonstration that T cells reactive with conventional antigens of the enteric bacterial flora can mediate chronic inflammatory bowel disease.

Original languageEnglish (US)
Pages (from-to)855-864
Number of pages10
JournalJournal of Experimental Medicine
Volume187
Issue number6
DOIs
StatePublished - Mar 16 1998

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Bacterial Antigens
Th1 Cells
Inbred C3H Mouse
T-Lymphocytes
Colitis
Antigens
Superantigens
Adoptive Transfer
Enterobacteriaceae
Major Histocompatibility Complex
Inflammatory Bowel Diseases
Age of Onset
Trypsin
Interferons
Food

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

CD4+ T cells reactive to enteric bacterial antigens in spontaneously colitic C3H/HeJBir mice : Increased T helper cell type 1 response and ability to transfer disease. / Cong, Yingzi; Brandwein, Steven L.; McCabe, Robert P.; Lazenby, Audrey J; Birkenmeier, Edward H.; Sundberg, John P.; Elson, Charles O.

In: Journal of Experimental Medicine, Vol. 187, No. 6, 16.03.1998, p. 855-864.

Research output: Contribution to journalArticle

Cong, Yingzi ; Brandwein, Steven L. ; McCabe, Robert P. ; Lazenby, Audrey J ; Birkenmeier, Edward H. ; Sundberg, John P. ; Elson, Charles O. / CD4+ T cells reactive to enteric bacterial antigens in spontaneously colitic C3H/HeJBir mice : Increased T helper cell type 1 response and ability to transfer disease. In: Journal of Experimental Medicine. 1998 ; Vol. 187, No. 6. pp. 855-864.
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abstract = "C3H/HeJBir mice are a new substrain that spontaneously develop colitis early in life. This study was done to determine the T cell reactivity of C3H/HeJBir mice to candidate antigens that might be involved in their disease. C3H/HeJBir CD4+ T cells were strongly reactive to antigens of the enteric bacterial flora, but not to epithelial or food antigens. The stimulatory material in the enteric bacteria was trypsin sensitive and restricted by class II major histocompatibility complex molecules, but did not have the properties of a superantigen. The precursor frequency of interleuken (IL)-2-producing, bacterial-reactive CD4+ T cells in colitic mice was 1 out of 2,000 compared to 1 out of 20,000-25,000 in noncolitic control mice. These T cells produced predominately IL-2 and interferon γ, consistent with a T helper type 1 cell response and were present at 3-4 wk, the age of onset of the colitis. Adoptive transfer of bacterial-antigen- activated CD4+ T cells from colitic C3H/HeJBir but not from control C3H/HeJ mice into C3H/HeSnJ scid/scid recipients induced colitis. These data represent a direct demonstration that T cells reactive with conventional antigens of the enteric bacterial flora can mediate chronic inflammatory bowel disease.",
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