NDLI: Soluble, but not transmembrane, TNF- is required during influenza infection to limit the magnitude of immune responses and the extent of immunopathology.

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Soluble, but not transmembrane, TNF- is required during influenza infection to limit the magnitude of immune responses and the extent of immunopathology.

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Soluble, but not transmembrane, TNF- is required during influenza infection to limit the magnitude of immune responses and the extent of immunopathology.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Ely, Kenneth H. Enelow, Richard I. DeBerge, Matthew P.
Description	Author Affiliation: DeBerge MP ( Department of Medicine, Geisel School of Medicine at Dartmouth College, Lebanon, NH 03756); Ely KH ( Department of Medicine, Geisel School of Medicine at Dartmouth College, Lebanon, NH 03756); Enelow RI ( Department of Medicine, Geisel School of Medicine at Dartmouth College, Lebanon, NH 03756)
Abstract	TNF- is a pleotropic cytokine that has both proinflammatory and anti-inflammatory functions during influenza infection. TNF- is first expressed as a transmembrane protein that is proteolytically processed to release a soluble form. Transmembrane TNF- (memTNF- ) and soluble TNF- (solTNF- ) have been shown to exert distinct tissue-protective or tissue-pathologic effects in several disease models. However, the relative contributions of memTNF- or solTNF- in regulating pulmonary immunopathology following influenza infection are unclear. Therefore, we performed intranasal influenza infection in mice exclusively expressing noncleavable memTNF- or lacking TNF- entirely and examined the outcomes. We found that solTNF- , but not memTNF- , was required to limit the size of the immune response and the extent of injury. In the absence of solTNF- , there was a significant increase in the CD8(+) T cell response, including virus-specific CD8(+) T cells, which was due in part to an increased resistance to activation-induced cell death. We found that solTNF- mediates these immunoregulatory effects primarily through TNFR1, because mice deficient in TNFR1, but not TNFR2, exhibited dysregulated immune responses and exacerbated injury similar to that observed in mice lacking solTNF- . We also found that solTNF- expression was required early during infection to regulate the magnitude of the CD8(+) T cell response, indicating that early inflammatory events are critical for the regulation of the effector phase. Taken together, these findings suggest that processing of memTNF- to release solTNF- is a critical event regulating the immune response during influenza infection.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1302729
Journal	The Journal of Immunology
Issue Number	12
Volume Number	192
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-06-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cd8-positive T-lymphocytes Immunology Cell Membrane Influenza A Virus, H1n1 Subtype Orthomyxoviridae Infections Receptors, Tumor Necrosis Factor, Type I Tumor Necrosis Factor-alpha Animals Pathology Cell Death Genetics Mice Mice, Knockout Receptors, Tumor Necrosis Factor, Type Ii Solubility Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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