Cross-reactivity of TNP immune effector T cells that mediate contact hypersensitivity and inflammatory bowel disease in the mouse

Background: Experiments were aimed to test the crossreactivity of immune Th 1 cells that mediate contact hypersensitivity (CHS) or inflammatory bowel d isease (IBD) to TNP in the mouse. Methods: CBA/J mice were immunized either epicutaneously or intrarectally with TNP and after appropriate time interv als were challenged with antigen in a crossed manner. The CHS reaction was measured by the ear swelling test. IBD was quantified by increase of colon weight and myeloperoxidase level. Both reactions were confirmed histologica lly. In passive-transfer experiments, mesenteric lymph node cells of animal s sensitized intrarectally and peripheral lymph node and spleen cells of mi ce immunized epicutaneously were used. In some experiments, before being im munized mice were made either unresponsive to the TNP hapten by induction o f suppressor T cells, or resistant to suppression after induction of upregu latory T cells. Results: Irrespective of the mode of sensitization upon app ropriate challenge with antigen all mice developed a good CHS reaction as w ell as significant IBD. This cross-reactivity could be passively transferre d by immune cells. In mice in which antigen-specific down- or upregulatory cells were induced before sensitization both CHS and IBD to TNP were modula ted accordingly. Conclusion: TNP hapten deposited on skin or on mucosal sur faces induces effector cells that recognize antigen independent of its tiss ue localization, and produce a local inflammatory reaction. TNP-specific up - and downregulatory cells, shown before to regulate the CHS reaction, simi larly modulate the generation and development of hapten-induced IBD, Copyri ght (C) 2000 S. Karger AG, Basel.