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Apoptotic Cells Activate NKT Cells through T Cell Ig-Like Mucin-Like–1 Resulting in Airway Hyperreactivity

Content Provider	Scilit
Author	Lee, Hyun-Hee Meyer, Everett H. Goya, Sho Pichavant, Muriel Kim, Hye Young Bu, Xia Umetsu, Sarah E. Jones, Jennifer C. Savage, Paul B. Iwakura, Yoichiro Casasnovas, Jose M. Kaplan, Gerardo Freeman, Gordon J. DeKruyff, Rosemarie H. Umetsu, Dale T.
Copyright Year	2010
Description	T cell Ig-like mucin-like–1 (TIM-1) is an important asthma susceptibility gene, but the immunological mechanisms by which TIM-1 functions remain uncertain. TIM-1 is also a receptor for phosphatidylserine (PtdSer), an important marker of cells undergoing programmed cell death, or apoptosis. We now demonstrate that NKT cells constitutively express TIM-1 and become activated by apoptotic cells expressing PtdSer. TIM-1 recognition of PtdSer induced NKT cell activation, proliferation, and cytokine production. Moreover, the induction of apoptosis in airway epithelial cells activated pulmonary NKT cells and unexpectedly resulted in airway hyperreactivity, a cardinal feature of asthma, in an NKT cell-dependent and TIM-1–dependent fashion. These results suggest that TIM-1 serves as a pattern recognition receptor on NKT cells that senses PtdSer on apoptotic cells as a damage-associated molecular pattern. Furthermore, these results provide evidence for a novel innate pathway that results in airway hyperreactivity and may help to explain how TIM-1 and NKT cells regulate asthma.
Ending Page	5235
Page Count	11
Starting Page	5225
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1001116
Alternate Webpage(s)	http://www.jimmunol.org/content/185/9/5225.full.pdf
Journal	The Journal of Immunology
Issue Number	9
Volume Number	185
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2010-11-01
Access Restriction	Open
Subject Keyword	Cell Death Nkt Cells Like Mucin
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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