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Modulation of CD1d Expression During MCMV Infection (134.11)

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Abstract CD1d is an MHC Class I-like antigen presenting molecule that is unique in that it presents lipids rather than peptides to a specific subset of T-cells called invariant Natural Killer T (iNKT) cells. Within hours of stimulation, activated iNKT cells release large quantities of cytokines, promoting cell-mediated immune responses. We examined the expression of CD1d on macrophages, dendritic cells, and B-cells from C57Bl/6 mice and on in vitro cultures both at steady state and during murine cytomegalovirus (MCMV) infection. We found an upregulation of CD1d mainly on macrophages that peaked at day 3 post-infection that was either minimal or not present in the other CD1d expressing cell types that we examined. The cause of this increased expression could potentially be direct (virus-mediated) and/or indirect (due to cytokines or other mediators). To test if CD1d upregulation was direct we used a GFP+ MCMV (clone RVG-102). To test for the roles of the main cytokines produced during MCMV infection we infected IFNαβ R and IL-12 deficient mice. We found that the modulated expression of CD1d on macrophages during MCMV infection is partially dependent of type 1 IFN and the infection itself. We are currently evaluating in more details the molecular mechanism and consequences of the MCMV induced CD1d upregulation. Supported by NIH grant 46709 and GAANN training grant.
Title: Modulation of CD1d Expression During MCMV Infection (134.11)
Description:
Abstract CD1d is an MHC Class I-like antigen presenting molecule that is unique in that it presents lipids rather than peptides to a specific subset of T-cells called invariant Natural Killer T (iNKT) cells.
Within hours of stimulation, activated iNKT cells release large quantities of cytokines, promoting cell-mediated immune responses.
We examined the expression of CD1d on macrophages, dendritic cells, and B-cells from C57Bl/6 mice and on in vitro cultures both at steady state and during murine cytomegalovirus (MCMV) infection.
We found an upregulation of CD1d mainly on macrophages that peaked at day 3 post-infection that was either minimal or not present in the other CD1d expressing cell types that we examined.
The cause of this increased expression could potentially be direct (virus-mediated) and/or indirect (due to cytokines or other mediators).
To test if CD1d upregulation was direct we used a GFP+ MCMV (clone RVG-102).
To test for the roles of the main cytokines produced during MCMV infection we infected IFNαβ R and IL-12 deficient mice.
We found that the modulated expression of CD1d on macrophages during MCMV infection is partially dependent of type 1 IFN and the infection itself.
We are currently evaluating in more details the molecular mechanism and consequences of the MCMV induced CD1d upregulation.
Supported by NIH grant 46709 and GAANN training grant.

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