Journal
JOURNAL OF IMMUNOLOGY
Volume 165, Issue 5, Pages 2327-2330Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.165.5.2327
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Funding
- NATIONAL CANCER INSTITUTE [R01CA039621] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI025913] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R29NS037336] Funding Source: NIH RePORTER
- NCI NIH HHS [CA39621] Funding Source: Medline
- NIAID NIH HHS [AI25913] Funding Source: Medline
- NINDS NIH HHS [NS37336-01] Funding Source: Medline
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The contribution of the T cell chemoattractant chemokine IFN-inducible protein 10 (IP-10) in host defense following viral infection of the CNS was examined. IP-10 is expressed by astrocytes during acute encephalonyelitis in mouse hepatitis virus-infected mice, and the majority of T lymphocytes infiltrating into the CNS expressed the IP-10 receptor CXCR3. Treatment of mice with anti-IP-10 antisera led to increased mortality and delayed viral clearance from the CNS as compared with control mice. Further, administration of anti-IP-10 led to a >70% reduction (p less than or equal to 0.001) in CD4(+) and CD8(+) T lymphocyte infiltration into the CNS, which correlated with decreased (p less than or equal to 0.01) levels of IFN-gamma, These data indicate that IP-10 functions as a sentinel molecule in host defense and is essential in the development of a protective Th1 response against viral infection of the CNS.
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