Thymic stromal lymphopoietin-dependent basophils promote Th2 cytokine responses following intestinal helminth infection.

Thymic stromal lymphopoietin-dependent basophils promote Th2 cytokine responses following intestinal helminth infection.
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DOI:
10.4049/jimmunol.1200691
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发表时间:
2012-11-01
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
通讯作者:
Artis D
Artis D
中科院分区:
其他
文献类型:
--
作者:
Giacomin PR;Siracusa MC;Walsh KP;Grencis RK;Kubo M;Comeau MR;Artis D

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CD4+ T helper type 2 (TH2) cytokine responses promote the development of allergic inflammation and are critical for immunity to parasitic helminth infection. Recent studies highlighted that basophils can promote TH2 cytokine-mediated inflammation and that phenotypic and functional heterogeneity exists between classical IL-3-elicited basophils versus TSLP-elicited basophils. However, whether distinct basophil populations develop following helminth infection, and their relative contributions to anti-helminth immune responses remain to be defined. Following Trichinella spiralis infection of mice, we show that basophil responses are rapidly induced in multiple tissue compartments, including intestinal-draining lymph nodes. Trichinella-induced basophil responses were IL-3-IL-3R-independent but critically dependent on TSLP-TSLPR interactions. Selective depletion of basophils following Trichinella infection impaired infection-induced CD4+ TH2 cytokine responses, suggesting that TSLP-dependent basophils augment TH2 cytokine responses following helminth infection. The identification and functional classification of TSLP-dependent basophils in a helminth infection model, coupled with their recently-described role in promoting atopic dermatitis, suggests these cells may be a critical population in promoting TH2 cytokine-associated inflammation in a variety of inflammatory or infectious settings. Collectively, these data suggest that the TSLP-basophil pathway may represent a new target in the design of therapeutic intervention strategies to promote or limit TH2 cytokine-dependent immunity and inflammation.
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