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Suvas, S. et al.

Suvas, Azkur, Rouse,

Qa-1b and CD94-NKG2a interaction regulate cytolytic activity of herpes simplex virus-specific memory CD8+ T cells in the latently infected trigeminal ganglia.

After ocular infection, HSV-specific CD8+ T cells migrate to and are specifically retained in the ophthalmic branch of the trigeminal ganglia (TG) even at the time when replicating virus is no longer evident. Virus-specific CD8+ T cells maintain an activation phenotype and secrete IFN-gamma in the latent TG. In this report we demonstrated that activated virus-specific memory CD8+ T cells, although potentially cytolytic, also expressed the CD94-NK cell receptor subfamily G2a inhibitory molecule and were unable to exert cytotoxicity when engaged by Qa-1b expressing targets. Interestingly, many neurons in the latent TG expressed Qa-1b, and blocking of Qa-1b/CD94-NKG2a interaction in an ex vivo TG culture resulted in neuronal cell lysis. The expression of the inhibitory CD94-NKG2a molecule could be induced by TGF-beta1, which was shown to present as a bioactive molecule in the latent TG. Additionally, CD4+ forkhead/winged helix transcription factor 3+ T cells were also determined in the latent TG. Our results demonstrate the operation of a regulatory system in vivo that serves to protect irreplaceable neurons from destruction by the immune system.[1]

References

Qa-1b and CD94-NKG2a interaction regulate cytolytic activity of herpes simplex virus-specific memory CD8+ T cells in the latently infected trigeminal ganglia. Suvas, S., Azkur, A.K., Rouse, B.T. J. Immunol. (2006) [Pubmed]

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