Journal
BLOOD
Volume 124, Issue 24, Pages 3572-3576Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2014-07-587493
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Categories
Funding
- National Institutes of Health
- National Institute of Allergy and Infectious Diseases
- National Institute of Diabetes and Digestive and Kidney Diseases [AI026918, AI030663, AI078869, HL107202, AI046643, AI107328, K08DK101604, AI102011, DK63720]
- University of California
- San Francisco Diabetes Family Fund
- Department of Laboratory Medicine discretionary fund
- Sandler Asthma Basic Research Center at the University of California, San Francisco
- Howard Hughes Medical Institute
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Interleukin (IL)-2 promotes regulatory T-cell development and function, and treatment with IL-2 is being tested as therapy for some autoimmune diseases. However, patients receiving IL-2 treatment also experience eosinophilia due to an unknown mechanism. Here, we show that patients receiving low-dose IL-2 have elevated levels of serum IL-5, and this correlates with their degree of eosinophilia. In mice, low-dose IL-2-anti-IL-2 antibody complexes drove group 2 innate lymphoid cells (ILC2) to produce IL-5 and proliferate. Using genetic approaches in mice, we demonstrate that activation of ILC2 was responsible for the eosinophilia observed with IL-2 therapy. These observations reveal a novel cellular network that is activated during IL-2 treatment. A better understanding of the cross talk between these cell populations may lead to more effective targeting of IL-2 to treat autoimmune disease.
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