Immune proteins called HLA molecules help to activate killer T cell responses against pathogens. But according to a study that will be published online on December 14th in the Journal of Experimental Medicine (www.jem.org), one particular group of HLA molecules cripples this activation, perhaps explaining why HIV-infected individuals who express these HLAs progress to AIDS more rapidly than others.
AIDS develops more rapidly in individuals who express HLA B*35-Px than in those who express the highly related HLA B*35PY proteins. The new study, lead by Xu Yu at Massachusetts General Hospital, shows that B*35-Px molecules bind to and activate an inhibitory receptor on dendritic cells — cells that are needed to activate protective T cells. These findings suggest that inhibitory dendritic cell receptors should be taken into consideration during future efforts to design HIV-1 vaccines and therapies.
About The Journal of Experimental Medicine
The Journal of Experimental Medicine (JEM) is published by the Rockefeller University Press. All editorial decisions on manuscripts submitted are made by active scientists in conjunction with our in-house scientific editors. JEM content is posted to PubMed Central, where it is available to the public for free six months after publication. Authors retain copyright of their published works and third parties may reuse the content for non-commercial purposes under a creative commons license. For more information, please visit www.jem.org.
Huang, J., et al. 2009. J. Exp. Med. doi:10.1084/jem.20091386
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