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Immunol Res. 2002;26(1-3):87-94.

Understanding immune-microbial homeostasis in intestine.

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  • 1Division of Gastroenterology and Hepatology, University of Alabama at Birmingham, 35294-0007, USA.


The mechanisms concerning how the immune system is able to deal with the massive antigen challenge represented by the commensal bacterial flora have been a mystery. Recently a number of animal models with impairment of these mechanisms have been identified. One of these is the C3H/HeJBir mouse, which, under certain environmental conditions, can spontaneously develop colitis, which later remits. These mice show increased B cell and T cell reactivity to antigens of the enteric bacterial flora. CD4+ T cells from this strain cause colitis, when activated by enteric bacterial antigens and transferred to histocompatible severe combined immunodeficiency recipients. This colitis is mediated by CD4+ Th1 cells and requires a sustained mucosal production of interleukin-12, which, in turn, is dependent on CD40L-CD40 interactions in the gut. Regulatory T cells that appear to limit the colitis have been identified and have the properties of the T-regulatory-1 subset. Functional Tr1 activity for bacterial antigens is present in the lamina propria CD4+ T cells. These Tr1 cells may exert their effects by inhibition of dendritic cell function in the mucosa, rather than by direct effects on Th 1 cells. Manyquestions remain to be answered, including, How do the enteric bacterial-host interactions shape the immune system for abnormal responses such as inflammatory bowel disease, autoimmunity, and allergy?

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