A viral CTL escape mutation leading to immunoglobulin-like transcript 4-mediated functional inhibition of myelomonocytic cells.

A viral CTL escape mutation leading to immunoglobulin-like transcript 4-mediated functional inhibition of myelomonocytic cells. Research Abstract Details 

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A viral CTL escape mutation leading to immunoglobulin-like transcript 4-mediated functional inhibition of myelomonocytic cells. Abstract Text:

Mathias Lichterfeld,Daniel G Kavanagh,Katie L Williams,Beenu Moza,Stanley K Mui,ToshiYuki Miura,Rohini Sivamurthy,Rachel Allgaier,Florencia Pereyra,Alicja Trocha,Margaret Feeney,Rajesh T Gandhi,Eric S Rosenberg,Marcus Altfeld,Todd M Allen,Rachel Allen,Bruce D Walker,Eric J Sundberg,Xu G Yu,Mathias Lichterfeld,Daniel G Kavanagh,Katie L Williams,Beenu Moza,Stanley K Mui,ToshiYuki Miura,Rohini Sivamurthy,Rachel Allgaier,Florencia Pereyra,Alicja Trocha,Margaret Feeney,Rajesh T Gandhi,Eric S Rosenberg,Marcus Altfeld,Todd M Allen,Rachel Allen,Bruce D Walker,Eric J Sundberg,Xu G Yu,

Viral mutational escape can reduce or abrogate recognition by the T cell receptor (TCR) of virus-specific CD8+ T cells. However, very little is known about the impact of cytotoxic T lymphocyte (CTL) epitope mutations on interactions between peptide-major histocompatibility complex (MHC) class I complexes and MHC class I receptors expressed on other cell types. Here, we analyzed a variant of the immunodominant human leukocyte antigen (HLA)-B2705-restricted HIV-1 Gag KK10 epitope (KRWIILGLNK) with an L to M amino acid substitution at position 6 (L6M), which arises as a CTL escape variant after primary infection but is sufficiently immunogenic to elicit a secondary, de novo HIV-1-specific CD8+ T cell response with an alternative TCR repertoire in chronic infection. In addition to altering recognition by HIV-1-specific CD8+ T cells, the HLA-B2705-KK10 L6M complex also exhibits substantially increased binding to the immunoglobulin-like transcript (ILT) receptor 4, an inhibitory MHC class I-specific receptor expressed on myelomonocytic cells. Binding of the B2705-KK10 L6M complex to ILT4 leads to a tolerogenic phenotype of myelomonocytic cells with lower surface expression of dendritic cell (DC) maturation markers and co-stimulatory molecules. These data suggest a link between CTL-driven mutational escape, altered recognition by innate MHC class I receptors on myelomonocytic cells, and functional impairment of DCs, and thus provide important new insight into biological consequences of viral sequence diversification.

A viral CTL escape mutation leading to immunoglobulin-like transcript 4-mediated functional inhibition of myelomonocytic cells. Publishing Authors By Initials

M Lichterfeld,DG Kavanagh,KL Williams,B Moza,SK Mui,T Miura,R Sivamurthy,R Allgaier,F Pereyra,A Trocha,M Feeney,RT Gandhi,ES Rosenberg,M Altfeld,TM Allen,R Allen,BD Walker,EJ Sundberg,XG Yu,M Lichterfeld,DG Kavanagh,KL Williams,B Moza,SK Mui,T Miura,R Sivamurthy,R Allgaier,F Pereyra,A Trocha,M Feeney,RT Gandhi,ES Rosenberg,M Altfeld,TM Allen,R Allen,BD Walker,EJ Sundberg,XG Yu,

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A viral CTL escape mutation leading to immunoglobulin-like transcript 4-mediated functional inhibition of myelomonocytic cells. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The Journal of experimental medicine

VOLUME: 204

Page Numbers: 2813-24

Journal Abbreviation: J. Exp. Med.

ISSN: 1540-9538

DAY: 19

MONTH: 11

YEAR: 2007

A viral CTL escape mutation leading to immunoglobulin-like transcript 4-mediated functional inhibition of myelomonocytic cells. Information

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LANGUAGE: eng

NlmUniqueID: 2985109

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Grant and Affiliation Information for A viral CTL escape mutation leading to immunoglobulin-like transcript 4-mediated functional inhibition of myelomonocytic cells.

AFFILIATION: Partners AIDS Research Center, Massachusetts General Hospital, and Harvard University Center for AIDS Research, Boston, MA 02129, USA.

Country: United States

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MEDLINETA: J Exp Med

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