The Journal of Experimental Medicine
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Published online 15 May 2006 doi:10.1084/jem.20052448
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 6, 1435-1446
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ARTICLE

 Type 2 immunity is controlled by IL-4/IL-13 expression in hematopoietic non-eosinophil cells of the innate immune system

David Voehringer, Tiffany A. Reese, Xiaozhu Huang, Kanade Shinkai, and Richard M. Locksley

Howard Hughes Medical Institute, Departments of Medicine and Microbiology/Immunology, University of California San Francisco, San Francisco, CA 94143

CORRESPONDENCE R.M. Locksley: locksley{at}medicine.ucsf.edu

Nippostrongylus brasiliensis infection and ovalbumin-induced allergic lung pathology are highly interleukin (IL)-4/IL-13 dependent, but the contributions of IL-4/IL-13 from adaptive (T helper [Th]2 cells) and innate (eosinophil, basophils, and mast cells) immune cells remain unknown. Although required for immunoglobulin (Ig)E induction, IL-4/IL-13 from Th2 cells was not required for worm expulsion, tissue inflammation, or airway hyperreactivity. In contrast, innate hematopoietic cell–derived IL-4/IL-13 was dispensable for Th2 cell differentiation in lymph nodes but required for effector cell recruitment and tissue responses. Eosinophils were not required for primary immune responses. Thus, components of type 2 immunity mediated by IL-4/IL-13 are partitioned between T cell–dependent IgE and an innate non-eosinophil tissue component, suggesting new strategies for interventions in allergic immunity.

Abbreviation used: tg, transgenic.


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