Abstract
Soltys, J., Goyal, P. K., and Wakelin, D. 1999. Cellular immune responses in mice infected with the intestinal nematodeTrichuris muris.Experimental Parasitology92,40–47. CBA and B10.BR mice show variation in immune response to the intestinal nematodeTrichuris muris. CBA mice develop strong resistance, eliminating worms from the intestine; B10BR mice are permissive and develop chronic infec tions. It is already known that resistance and permissiveness reflect differential T helper responses. The data reported here show that resis tant CBA mice express good antigen-specific lymphocyte proliferative responses to infection, whereas cells from B10.BR mice are relatively anergic, although still responsive to Concanavalin A (ConA). The possibility that the altered proliferative responsiveness seen in infected B10.BR mice reflected quantitative or qualitative changes in T helper cells was examined by comparing cytokine production and expression of cell surface markers (CD4, CD8, and CD28) in mesenteric lymph node cells and spleen cells from both strains and comparing these with the characteristics of cells from resistant CBA mice and from CBA mice that had been rendered permissive to infection by a combination of irradiation and corticosteroid treatment. As expected, cells from B10.BR mice produced high levels of interferon-γ (IFN-γ), whereas those from CBA mice released high levels of IL-5, whether stimulated with adult worm somatic antigens, excretory/secretory antigens, or ConA. Immunosuppressed CBA mice produced high levels of both IFN-γ and IL-5 throughout the experiment. FACS analysis revealed a decrease of CD4+ and an initial increase in CD8+ cells in all infected mice. No major changes occurred in the relative proportion of CD28+cells. Further evaluation of the CD28 costimulatory molecule, measured as mean fluorescence intensity, displayed down-regulation in permis sive and immunosuppressed mice. The data obtained suggest that lym phocyte unresponsiveness and permissiveness toT. murisinfection may be associated with a down-regulation or an initially reduced ex pression of costimulatory CD28 molecules.
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