NDLI: B7-H3 augments the inflammatory response and is associated with human sepsis.

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B7-H3 augments the inflammatory response and is associated with human sepsis.

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B7-H3 augments the inflammatory response and is associated with human sepsis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Zhang, Guangbo Wang, Jian Zhang, Xueguang Kelly, Justin Redmond, H. Paul Gu, Guohao Hou, Jianquan Wang, Jiang Huai Zhou, Yinghui
Description	Author Affiliation: Zhang G ( Clinical Immunology Laboratory, First Affiliated Hospital, Soochow University, Suzhou, People's Republic of China.)
Abstract	B7-H3, a new member of the B7 superfamily, acts as both a T cell costimulator and coinhibitor, and thus plays a key role in the regulation of T cell-mediated immune responses. However, it is unclear whether B7-H3 is involved in the innate immune monocyte/macrophage-mediated inflammatory response. In this paper, we show that, although B7-H3 alone failed to stimulate proinflammatory cytokine release from murine macrophages, it strongly augmented both LPS- and bacterial lipoprotein-induced NF-kappaB activation and inflammatory response. This occurred in both a TLR4- and TLR2-dependent manner. Blockage of B7-H3 in vivo attenuated LPS-induced proinflammatory cytokine release and endotoxic shock-related lethality. Furthermore, we found that patients diagnosed with sepsis, in contrast to healthy individuals, exhibited significant levels of raised plasma soluble B7-H3 (sB7-H3) and that this level correlated with the clinical outcome and levels of plasma TNF-alpha and IL-6. In addition, a putative receptor for B7-H3 was detected on monocytes and peritoneal macrophages from septic patients but not on monocytes from healthy donors. Stimulation of human monocytes with LPS and inflammatory cytokines led to a substantial release of sB7-H3. Taken together, our data indicate that significantly elevated plasma sB7-H3 in septic patients may predict a poor outcome. Furthermore, we demonstrate that B7-H3 functions as a costimulator of innate immunity by augmenting proinflammatory cytokine release from bacterial cell wall product-stimulated monocytes/macrophages and may contribute positively to the development of sepsis.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	6
Volume Number	185
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2010-09-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Adjuvants, Immunologic Physiology Antigens, Cd Inflammation Mediators Receptors, Immunologic Sepsis Immunology Pathology Blood Toxicity Animals Antigens, Cd80 B7 Antigens Bacterial Outer Membrane Proteins Cell Line Cells, Cultured Immunity, Innate Interleukin-6 Lipopolysaccharides Macrophages Secretion Mice Mice, Inbred C3h Monocytes Microbiology Mortality Toll-like Receptor 2 Toll-like Receptor 4 Tumor Necrosis Factor-alpha Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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