Journal
JOURNAL OF IMMUNOLOGY
Volume 193, Issue 7, Pages 3717-3725Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1401307
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Funding
- National Institutes of Health (NIH) [AI061570, AI087990, AI074878, AI106697, AI095466, AI095608, AI102942, AI097333, T32-AR007465-28, 5-P30-AR-057217, KL2-RR024132, K08-AR065577-01, AI085828, K22-AI110573, T-32A106516, F30-AI112023, T32-AI007532, F32-AI098365, KL2TR000139]
- Mary Connolly Braun
- Arguild Foundation
- Laffey-McHugh Foundation
- Benjamin Franklin Society research grant
- Cancer Research Institute Student Training and Research in Tumor Immunology grant
- Swiss National Science Foundation [PA00P3-136468]
- Burroughs Wellcome Fund
- National Center for Research Resources
- National Center for Advancing Translational Sciences
- Skin Disease Research Center through NIH Grant [SDRC 5-P30-AR-057217]
- Swiss National Science Foundation (SNF) [PA00P3_136468] Funding Source: Swiss National Science Foundation (SNF)
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Type 2 inflammation underlies allergic diseases such as atopic dermatitis, which is characterized by the accumulation of basophils and group 2 innate lymphoid cells (ILC2s) in inflamed skin lesions. Although murine studies have demonstrated that cutaneous basophil and ILC2 responses are dependent on thymic stromal lymphopoietin, whether these cell populations interact to regulate the development of cutaneous type 2 inflammation is poorly defined. In this study, we identify that basophils and ILC2s significantly accumulate in inflamed human and murine skin and form clusters not observed in control skin. We demonstrate that murine basophil responses precede ILC2 responses and that basophils are the dominant IL-4-enhanced GFP-expressing cell type in inflamed skin. Furthermore, basophils and IL-4 were necessary for the optimal accumulation of ILC2s and induction of atopic dermatitis-like disease. We show that ILC2s express IL-4R alpha and proliferate in an IL-4-dependent manner. Additionally, basophil-derived IL-4 was required for cutaneous ILC2 responses in vivo and directly regulated ILC2 proliferation ex vivo. Collectively, these data reveal a previously unrecognized role for basophil-derived IL-4 in promoting ILC2 responses during cutaneous inflammation.
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