Journal
JOURNAL OF IMMUNOLOGY
Volume 173, Issue 10, Pages 5929-5933Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.173.10.5929
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Funding
- NCI NIH HHS [CA 100191, CA 90337] Funding Source: Medline
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The ability for the professional APC to cross-present Ag to MHC class I from parenchymal cells is essential for priming as well as tolerance of CD8(+) T cells against intracellular Ags. Since cross-presentations of non-cell-associated free Ags are inefficient, the roles of molecular chaperones or beat shock proteins (HSPs) in chaperoning Ags to APCs have been postulated. We herein genetically addressed this hypothesis using mice that were defective of heat shock factor 1 (Hsf1), a major transcription factor fir HSPs. Hsf1(-/-) mice have a decreased expression of several HSPs including HSP90 and HSP70. Using multiple Ag systems, we demonstrated that cross-priming of Ag-specific CD8+ T cells was inefficient when Ag expression was restricted to Hsf1(-/-) non-APCs. Our study provides the first genetic evidence for the roles of Hsf1 in regulating cross-presentation of MHC class I-associated Ags.
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