Premium
Role for CTLA‐4 but not CD25 + T cells during Schistosoma mansoni infection of mice
Author(s) -
WALSH C. M.,
SMITH P.,
FALLON P. G.
Publication year - 2007
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/j.1365-3024.2007.00947.x
Subject(s) - immunology , il 2 receptor , biology , schistosoma mansoni , chronic infection , population , cytokine , immune system , schistosomiasis , t cell , medicine , helminths , environmental health
SUMMARY Schistosoma mansoni infection of mice increases the frequency of cells that are CD4 + CD25 + in the acute (4 and 8 weeks) and chronic (16 week) stages of infection. Depletion of > 85% of CD25 + cells in the acute or chronic stages of schistosome infection caused no overt changes in morbidity or immunological responses. The absence of effect in mice with CD25 + cells depleted may be due to the preferential expression of IL‐4 and IL‐10, two cytokines that are protective in schistosome infection, on CD25 − CD4 + cells. We also assessed infection‐induced changes of other regulatory markers, GITR, CD103 and CTLA‐4 on CD4 + cells. We identified a marked expansion of CTLA‐4 + population on CD25 − CD4 + cells in acute and chronic infection. Blocking of CTLA‐4 during acute, but not chronic infection, caused significant weight loss and altered the type 2 cytokine response of mice, with increased IL‐4 and IL‐5 production associated with significantly more Th2 cells and eosinophils in the liver granuloma. This study illustrates the complexity of regulation of T cells in schistosome infection and highlights a specific role for CTLA‐4 + , but not CD25 + cells, in the regulation of Th2 responses in helminth infection.