Journal
JOURNAL OF IMMUNOLOGY
Volume 180, Issue 7, Pages 4885-4891Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.180.7.4885
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Funding
- NHLBI NIH HHS [P01 HL036110, P01 HL036110-20A10017, HL 036110] Funding Source: Medline
- NIAID NIH HHS [R01 AI059746, R01 AI052353, AI 059746-01, U19 AI031599, AI 031599, P01 AI031599-090012, AI 05447, R01 AI059746-01, P01 AI031599] Funding Source: Medline
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Although the innate immune function of mast cells in the acute phase of parasitic and bacterial infections is well established, their participation in chronic immune responses to indolent infection remains incompletely understood. In parasitic infection with Trichinella spiralis, the immune response incorporates both lymphocyte and mast cell-dependent effector functions for pathogen eradication. Among the mechanistic insights still unresolved in the reaction to T. spiralis are the means by which mast cells respond to parasites and the mast cell effector functions that contribute to the immunologic response to this pathogen. We hypothesized that mast cell elaboration of tryptase may comprise an important effector component in this response. Indeed, we find that mice deficient in the tryptase mouse mast cell protease-6 (mMCP-6) display a significant difference in their response to T. spiralis larvae in chronically infected skeletal muscle tissue. Mechanistically, this is associated with a profound inability to recruit eosinophils to larvae in mMCP-6-deficient mice. Analysis of IgE-deficient mice demonstrates an identical defect in eosinophil recruitment. These findings establish that mast cell secretion of the tryptase mMCP-6, a function directed by the activity of the adaptive immune system, contributes to eosinophil recruitment to the site of larval infection, thereby comprising an integral link in the chronic immune response to parasitic infection.
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