Journal
JOURNAL OF IMMUNOLOGY
Volume 180, Issue 1, Pages 25-29Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.180.1.25
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Funding
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI069360] Funding Source: NIH RePORTER
- NIAID NIH HHS [AI069360] Funding Source: Medline
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Influenza pneumonia results in considerable lung injury, a significant component of which is mediated by CD8(+) T cell Ag recognition in the distal airways and alveoli. TNF-alpha produced by Ag-specific CD8(+) T cells appears primarily responsible for this immunopatbologv, and we have examined the negative regulation of CD8(+) TNF production by CD94/NKG2A engagement with its receptor, Qa-1b. TNF production by antiviral CD8(+) T cells was significantly enhanced by NKG2A blockade in vitro, and mice deficient in the NKG2A ligand, Qa-1b, manifested significantly greater pulmonary pathologv upon CD8(+) T cell-mediated clearance in influenza pneumonia. Furthermore, blockade of NKG2A ligation resulted in the enhancement of lung injuiy induced by CD8(+) effect or cell recognition of alveolar Ag in vivo in the absence of infectious virus. These data demonstrate that CD94/NKG2A transduces a biologically important signal in vivo to activated CD8(+) T cells that limits immunopathology in severe influenza infection.
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