Immunomodulation of the granulomatous response to schistosome eggs proceeds normally in ifn-γ and β-2 microglobuun-deficient mice

TY - JOUR

T1 - Immunomodulation of the granulomatous response to schistosome eggs proceeds normally in ifn-γ and β-2 microglobuun-deficient mice

AU - Yap, G.

PY - 1996

Y1 - 1996

N2 - The granulomatous response to parasite eggs is a major cause of pathology in schistosome infection. These CD4+T cell dependent-tissue reactions reach their maximum volume during acute infection and spontaneously decline during the chronic phase of the disease, a phenomenon which correlates with decreased lymphocyte proliferation as well as Th2 cytokine production. This down-modulation in host responsiveness to eggs has been attributed to CD8+ suppressor T cells. The latter regulatory cell population could exert its activity through the production of IFN-γ, a cytokine known to inhibit Th2 cell proliferation. This hypothesis was tested by infecting IFN-γ knockout (GKO) as well as CDS deficient β-2 microglobulin KO mice with Schistosoma mansoni and following development of egg-induced pathology and immune responses. Acute granuloma formation occurred normally in both KO strains as did the subsequent downmodulation of granuloma size. Moreover, adoptive transfer of chronic stage spleen cells from GKO mice suppressed granuloma size in WT recipients to the same extent as cells from WT donors. Furthermore, chronically infected KO mice of both strains displayed suppressed egg-induced Th2 responses indistinguishable from infected WT controls. These findings argue that neither IFN-γ nor MHC class-l restricted CD8+ T cells is essential for the development and immunomodulation of granulomatous responses to schistosome eggs.

AB - The granulomatous response to parasite eggs is a major cause of pathology in schistosome infection. These CD4+T cell dependent-tissue reactions reach their maximum volume during acute infection and spontaneously decline during the chronic phase of the disease, a phenomenon which correlates with decreased lymphocyte proliferation as well as Th2 cytokine production. This down-modulation in host responsiveness to eggs has been attributed to CD8+ suppressor T cells. The latter regulatory cell population could exert its activity through the production of IFN-γ, a cytokine known to inhibit Th2 cell proliferation. This hypothesis was tested by infecting IFN-γ knockout (GKO) as well as CDS deficient β-2 microglobulin KO mice with Schistosoma mansoni and following development of egg-induced pathology and immune responses. Acute granuloma formation occurred normally in both KO strains as did the subsequent downmodulation of granuloma size. Moreover, adoptive transfer of chronic stage spleen cells from GKO mice suppressed granuloma size in WT recipients to the same extent as cells from WT donors. Furthermore, chronically infected KO mice of both strains displayed suppressed egg-induced Th2 responses indistinguishable from infected WT controls. These findings argue that neither IFN-γ nor MHC class-l restricted CD8+ T cells is essential for the development and immunomodulation of granulomatous responses to schistosome eggs.

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M3 - Article

SN - 0892-6638

VL - 10

SP - A1434

JO - FASEB Journal

JF - FASEB Journal

IS - 6

ER -