Journal
INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 6, Issue 6, Pages 1020-1028Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.intimp.2006.01.013
Keywords
Toll-like receptor; innate immunity; SB431542; cytokines
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Funding
- NIAID NIH HHS [AI 51877] Funding Source: Medline
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NK cells are an important component of innate immunity, and they can promote CTL and Th1 cell development and macrophage activation via cytokines. TGF-beta is believed to be an important inummoregulatory molecule, and for this reason several TGF-beta inhibitors are currently in clinical development. However, the modulation of specific innate immune responses by endogenous human TGF-beta remains unclear. In this study, we demonstrate that blocking the action of endogenous TGF-beta resulted in an increase in both the percentage of responding NK cells and the amount of IFN-gamma produced by human NK cells when stimulated by monokines and TLR agonists. Blocking endogenous TGF-beta resulted in significant NK cell IFN-gamma production under suboptimal stimulation conditions. Our findings also suggest that TGF-beta associated with other blood cells may be involved in limiting NK cell activation. Thus, inhibiting endogenous TGF-beta provides a means to shift NK cell activation and promote cellular immunity. (c) 2006 Elsevier B.V All rights reserved.
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