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Titolo:
Host resistance and immune deviation in pigeon cytochrome c T-cell receptor transgenic mice infected with Toxoplasma gondii
Autore:
Collazo, CM; Miller, C; Yap, G; Hieny, S; Caspar, P; Schwartz, RH; Sher, A;
Indirizzi:
NIAID, Immunol Sect, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA NIAID Bethesda MD USA 20892 Parasit Dis Lab, NIH, Bethesda, MD 20892 USA NIAID, Cellular & Mol Immunol Lab, NIH, Bethesda, MD 20892 USA NIAID Bethesda MD USA 20892 Mol Immunol Lab, NIH, Bethesda, MD 20892 USA
Titolo Testata:
INFECTION AND IMMUNITY
fascicolo: 5, volume: 68, anno: 2000,
pagine: 2713 - 2719
SICI:
0019-9567(200005)68:5<2713:HRAIDI>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
IFN-GAMMA; MONOCLONAL-ANTIBODY; INTERLEUKIN-12; PARASITE; CYTOKINE; LYMPHOCYTES; INTERFERON; RESPONSES; CLONES; CD4(+);
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
26
Recensione:
Indirizzi per estratti:
Indirizzo: Collazo, CM NIAID, Immunol Sect, Parasit Dis Lab, NIH, Bldg 4,Room 126,4 Ctr Dr, Bethesda, MD 20892 USA NIAID Bldg 4,Room 126,4 Ctr Dr Bethesda MD USA 20892 20892 USA
Citazione:
C.M. Collazo et al., "Host resistance and immune deviation in pigeon cytochrome c T-cell receptor transgenic mice infected with Toxoplasma gondii", INFEC IMMUN, 68(5), 2000, pp. 2713-2719

Abstract

Resistance to Toxoplasma gondii has been shown to be mediated by gamma interferon (IFN-gamma) produced by NK, CD4(+), and CD8(+) T cells. While studies of SCID mice have implicated NK cells as the source of the cytokine in acute infection, several lines of evidence suggest that IFN-gamma productionby CD4(+) T lymphocytes also plays an important role in controlling early parasite growth. To evaluate whether this function is due to nonspecific asopposed to T-cell receptor (TCR)-dependent stimulation by the parasite, wehave examined the resistance to T. gondii infection of pigeon cytochrome ctransgenic (PCC-Tg) Rag-2(-/-) mice in which all CD4(+) T lymphocytes are unreactive with the protozoan. When inoculated with the ME49 strain, PCC-Tganimals exhibited only temporary control of acute infection and succumbed by day 17. Intracellular cytokine staining by flow cytometry revealed that,in contrast to infected nontransgenic controls, infected PCC-Tg animals failed to develop IFN-gamma-producing CD4(+) T cells. Moreover, the CD4(+) lymphocytes from these mice showed no evidence of activation as judged by lack of upregulated expression of CD44 or CD69, Nevertheless, when acutely infected transgenic mice were primed by PCC injection, the lymphokine responses measured after in vitro antigen restimulation displayed a strong Th1 biaswhich was shown to be dependent on endogenous interleukin 12 (IL-12), The above findings argue that, while T. gondii-induced IL-12 cannot trigger IFN-gamma production by CD4(+) T cells in the absence of TCR ligation, the pathogen is able to nonspecifically promote Th1 responses against nonparasite antigens, an effect that may explain the immunostimulatory properties of T.gondii infection.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/11/20 alle ore 04:07:49