Journal
JOURNAL OF IMMUNOLOGY
Volume 189, Issue 9, Pages 4371-4378Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1200691
Keywords
-
Categories
Funding
- National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases P30 Center for Molecular Studies in Digestive and Liver Diseases [P30-DK050306]
- pilot grant program and scientific core facilities (Molecular Pathology and Imaging, Molecular Biology, Cell Culture and Mouse)
- Joint Children's Hospital of Philadelphia-Penn Center in Digestive, Liver and Pancreatic Medicine
- National Institutes of Health [AI061570, AI087990, AI074878, AI083480, AI095466, AI095608, AI097333]
- Burroughs Wellcome Fund Investigator in Pathogenesis of Infectious Disease Award
- National Institutes of Health Grant [F32-AI085828]
- National Health and Medical Research Council Overseas Biomedical Fellowship [613718]
- American Australian Association Education Fund
- National Cancer Institute Comprehensive Cancer Center [2-P30 CA016520]
- Wellcome Trust
- Abramson Cancer Center Flow Cytometry and Cell Sorting Resource Laboratory
- Amgen Inc.
Ask authors/readers for more resources
CD4(+) 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 and thymic stromal lymphopoietin (TSLP)-elicited basophils. However, whether distinct basophil populations develop after helminth infection and their relative contributions to anti-helminth immune responses remain to be defined. After 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 after Trichinella infection impaired infection-induced CD4(+) Th2 cytokine responses, suggesting that TSLP-dependent basophils augment Th2 cytokine responses after 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 that 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. The Journal of Immunology, 2012, 189: 4371-4378.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available