期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 46, 期 1, 页码 114-121出版社
WILEY-BLACKWELL
DOI: 10.1002/eji.201545613
关键词
Cpa3(Cre); Kit(W)/Kit(Wv); Leishmaniasis; Mast cell; Th1/Th2
类别
资金
- Behring/Rontgen-Stiftung
- Deutsches Zentrum fur Infektionsforschung
- Deutsche Forschungsgemeinschaft [SFB Transregio 156]
- ERC [233074]
- European Research Council (ERC) [233074] Funding Source: European Research Council (ERC)
The genus leishmania comprises different protozoan parasites which are causative agents of muco-cutaneous and systemic, potentially lethal diseases. After infection with the species Leishmania major, resistant mice expand Th1 cells which stimulate macrophages for Leishmania destruction. In contrast, susceptible mice generate Th2 cells which deactivate macrophages, leading to systemic spread of the pathogens. Th-cell differentiation is determined within the first days, and Th2 cell differentiation requires IL-4, whereby the initial IL-4 source is often unknown. Mast cells are potential sources of IL-4, and hence their role in murine leishmaniasis has previously been studied in mast cell-deficient Kit mutant mice, although these mice display immunological phenotypes beyond mast cell deficiency. We therefore readdressed this question by infecting Kit-independent mast cell-deficient mice that are Th1 (C57BL/6 Cpa(Cre)) or Th2 (BALB/c Cpa(Cre)) prone with L. major. Using different parasite doses and intra-or subcutaneous infection routes, the results demonstrate no role of mast cells on lesion size development, parasite load, immune cell phenotypes expanding in draining lymph nodes, and cytokine production during murine cutaneous leishmaniasis. Thus, other cell types such as ILCs or T cells have to be considered as primary source of Th2-driving IL-4.
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