期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 107, 期 2, 页码 R15-R22出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI11540
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资金
- NCI NIH HHS [CA74730, CA43143, CA52004, R01 CA043143, R01 CA058524, CA58524, R01 CA074730, R01 CA052004] Funding Source: Medline
- NHLBI NIH HHS [R01 HL060090] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA052004, R01CA074730, R01CA058524, R01CA043143, R55CA074730] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL060090] Funding Source: NIH RePORTER
Infection of medial smooth muscle cells with gamma -herpesvirus 68 (gamma HV68) causes severe chronic vasculitis that is restricted to the great elastic arteries. We show here that persistence of disease in the great elastic arteries is (a) due to inefficient clearance of viral infection from this site compared with other organs or other vascular sites, and (b) associated with failure of T cells and macrophages to enter the virus-infected elastic media. These findings demonstrate immunoprivilege of the media of the great elastic arteries. We found that IFN-gamma acted on somatic cells during acute infection to prevent the establishment of medial infection and on hematopoietic cells to determine the severity of disease in this sire. The immunoprivileged elastic media may provide a site for persistence of pathogens or self antigens leading to chronic vascular disease, a process regulated by IFN-gamma actions on both somatic and hematopoietic cells. These concepts have significant implications for understanding immune responses contributing to or controlling chronic inflammatory diseases of the great vessels.
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