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Titolo:
Pathogenesis of herpes simplex virus-induced ocular immunoinflammatory lesions in B-cell-deficient mice
Autore:
Deshpande, SP; Zheng, M; Daheshia, M; Rouse, BT;
Indirizzi:
Univ Tennessee, Dept Microbiol, Knoxville, TN 37996 USA Univ Tennessee Knoxville TN USA 37996 Microbiol, Knoxville, TN 37996 USA
Titolo Testata:
JOURNAL OF VIROLOGY
fascicolo: 8, volume: 74, anno: 2000,
pagine: 3517 - 3524
SICI:
0022-538X(200004)74:8<3517:POHSVO>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
T-CELLS; STROMAL KERATITIS; PASSIVE-IMMUNIZATION; MONOCLONAL-ANTIBODY; NERVOUS-SYSTEM; DISEASE; LYMPHOCYTES; INDUCTION; INFECTION; MOUSE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
37
Recensione:
Indirizzi per estratti:
Indirizzo: Rouse, BT Univ Tennessee, Dept Microbiol, M409,Walters Life Sci Bldg, Knoxville, TN 37996 USA Univ Tennessee M409,Walters Life Sci Bldg Knoxville TN USA 37996
Citazione:
S.P. Deshpande et al., "Pathogenesis of herpes simplex virus-induced ocular immunoinflammatory lesions in B-cell-deficient mice", J VIROLOGY, 74(8), 2000, pp. 3517-3524

Abstract

The role of B cells and humoral immunity in herpes simplex virus (HSV) ocular infections was studied in immunoglobulin IJ. chain gene-targeted B-cell-deficient mice (mu K/O), At doses of virus well tolerated by immunocompetent mice, heightened susceptibility of mu K/O mice to herpetic encephalitis as well as to herpetic stromal keratitis (HSK) was observed. An explanationwas sought for the increased severity of HSK in the mu K/O mice. First, the lack of antibody responses in mu K/O mice resulted in longer viral persistence and dissemination to the corneal stroma, the site of inflammation. Prolonged virus expression in the corneal stroma was suggested to cause bystander activation of Th1-type CD4+ T cells, further contributing to the severity of HSK lesion expression in mu K/O mice, Second, mu K/O mice generated minimal Th2 cytokine responses compared to wild-type mice, Such responses might serve to downregulate the severity of Th1-mediated HSR lesions.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/04/20 alle ore 23:15:36