Zhou J, Matsuoka M, Cantor H, Homer R, Enelow RI.. Cutting Edge: Engagement of NKG2A on CD8+ Effector T Cells Limits Immunopathology in Influenza Pneumonia. J Immunol. 2008 Jan 1;180(1):25-9
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 immunopathology, 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 pathology upon CD8(+) T cell-mediated clearance in influenza pneumonia. Furthermore, blockade of NKG2A ligation resulted in the enhancement of lung injury induced by CD8(+) effector 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.
See Also:
- http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=18096998&dopt=AbstractPlus
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