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Neither interleukin‐4 receptor α expression on CD4 + T cells, or macrophages and neutrophils is required for protective immunity to Trichinella spiralis
Author(s) -
Michels Chesney E.,
Scales Hannah E.,
Saunders Karin A.,
McGowan S.,
Brombracher Frank,
Alexander James,
Lawrence Catherine E.
Publication year - 2009
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2008.02987.x
Subject(s) - trichinella spiralis , biology , immunology , immune system , immunoglobulin e , immunity , antibody , cytokine , bone marrow , antigen
Summary The T helper type 2 (Th2) mediated expulsion of the gastrointestinal nematode Trichinella spiralis requires interleukin‐4 receptor α (IL‐4Rα) expression on both bone‐marrow‐derived and non‐bone‐marrow‐derived cells. To more definitively investigate the role of IL‐4/IL‐13 responsiveness in the development of protective immunity to T. spiralis , cell‐specific IL‐4Rα signalling on CD4 + T cells (Lck cre IL‐4Rα −/flox ) and macrophages/neutrophils (LysM cre IL‐4Rα −/flox ) was analysed on the BALB/c background. Infection of wild‐type and control IL‐4Rα −/flox mice induced a Th2‐type immune response with elevated IL‐4 cytokine production, parasite‐specific immunoglobulin G1 (IgG1), total IgE, intestinal mastocytosis and enteropathy. In contrast, global IL‐4Rα‐deficient BALB/c mice showed reduced worm expulsion, antibody production, intestinal mastocytosis and gut pathology. BALB/c mice generated with cell‐specific deletion of IL‐4Rα on CD4 + T lymphocytes or macrophages/neutrophils, controlled gastrointestinal helminth infection by eliciting a protective immune response comparable to that observed with wild‐type and IL‐4Rα −/flox controls. Together, this shows that the development of host protective Th2 responses accompanied by parasite loss is independent of IL‐4Rα expression on CD4 + T cells and macrophages/neutrophils.