The Journal of Experimental Medicine
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Published online March 12, 2007
doi:10.1084/jem.20061791
The Journal of Experimental Medicine, Vol. 204, No. 3, 481-487
The Rockefeller University Press, 0022-1007 $30.00
© 2007 Perrigoue et al.
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BRIEF DEFINITIVE REPORT

 IL-31–IL-31R interactions negatively regulate type 2 inflammation in the lung

Jacqueline G. Perrigoue1, Ji Li2, Colby Zaph1, Michael Goldschmidt1, Phillip Scott1, Frederic J. de Sauvage2, Edward J. Pearce1, Nico Ghilardi2, and David Artis1

1 Department of Pathobiology, University of Pennsylvania, Philadelphia, PA 19104
2 Genentech, Inc., South San Francisco, CA 94080

CORRESPONDENCE David Artis: dartis{at}vet.upenn.edu OR Nico Ghilardi: ghilardi.nico{at}gene.com

Interleukin (IL) 31R{alpha} (glycoprotein 130–like monocyte receptor and glycoprotein 130–like receptor) heterodimerizes with oncostatin M receptor ß to bind IL-31, a cytokine expressed preferentially by CD4+ T helper type 2 (Th2) cells. However, the functions of IL-31–IL-31R signaling in immune regulation remain unknown. Here, we identify a novel role for IL-31R in limiting type 2 inflammation in the lung. After intravenous injection of Schistosoma mansoni eggs, IL-31R{alpha}–/– mice developed severe pulmonary inflammation, characterized by an increase in the area of granulomatous inflammation, increased numbers of resistin-like molecule {alpha}+ cells, and enhanced collagen deposition compared to WT counterparts. In vitro, macrophages generated from IL-31R{alpha}–/– mice promoted enhanced ovalbumin-specific CD4+ T cell proliferation and purified naive CD4+ T cells from IL-31R{alpha}–/– mice exhibited enhanced proliferation and expression of Th2 cytokines, identifying a T cell– and macrophage-intrinsic regulatory function for IL-31R signaling. In contrast, the generation of CD4+ T cell–mediated Th1 responses were normal in IL-31R{alpha}–/– mice, suggesting that the regulatory role of IL-31R signaling is limited to type 2 responses. Together, these data implicate IL-31R signaling as a novel negative regulatory pathway that specifically limits type 2 inflammation.

J.G. Perrigoue and J. Li contributed equally to this paper.


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