Letter abstract
Nature Medicine 13, 1248 - 1252 (2007)
Published online: 23 September 2007 | doi:10.1038/nm1633
Adaptive immune cells temper initial innate responses
Kwang Dong Kim1,2,3, Jie Zhao1,3, Sogyong Auh2, Xuanming Yang1, Peishuang Du1, Hong Tang1 & Yang-Xin Fu1,2
Toll-like receptors (TLRs) recognize conserved microbial structures called pathogen-associated molecular patterns. Signaling from TLRs leads to upregulation of co-stimulatory molecules for better priming of T cells and secretion of inflammatory cytokines by innate immune cells1, 2, 3, 4. Lymphocyte-deficient hosts often die of acute infection, presumably owing to their lack of an adaptive immune response to effectively clear pathogens. However, we show here that an unleashed innate immune response due to the absence of residential T cells can also be a direct cause of death. Viral infection or administration of poly(I:C), a ligand for TLR3, led to cytokine storm in T-cell- or lymphocyte-deficient mice in a fashion dependent on NK cells and tumor necrosis factor. We have further shown, through the depletion of CD4+ and CD8+ cells in wild-type mice and the transfer of T lymphocytes into Rag-1–deficient mice, respectively, that T cells are both necessary and sufficient to temper the early innate response. In addition to the effects of natural regulatory T cells, close contact of resting CD4+CD25-Foxp3- or CD8+ T cells with innate cells could also suppress the cytokine surge by various innate cells in an antigen-independent fashion. Therefore, adaptive immune cells have an unexpected role in tempering initial innate responses.
- Center for Infection and Immunity and National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, 15 Da Tun Road, Chaoyang District, Beijing 100101, China.
- Department of Pathology, University of Chicago, Chicago, Illinois 60637, USA,
- These authors contributed equally to this work.
Correspondence to: Hong Tang1 e-mail: tanghong@moon.ibp.ac.cn
Correspondence to: Yang-Xin Fu1,2 e-mail: yfu@uchicago.edu
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