Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.1.1.148 (Thy1)
 1,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During a secondary immune response to Listeria monocytogenes (LM), the production of IFN-gamma was still required for resistance, but it was considerably less dependent on IL-12 production. When IL-12 was neutralized in vivo using specific hamster antimurine IL-12 mAbs, there was a dramatically increased susceptibility to infection during primary listeriosis but much less during a secondary infection. However, neutralization of IFN-gamma in vivo resulted in a similar increased susceptibility during both primary and secondary listeriosis. In culture, splenocytes isolated from unimmunized mice produced IFN-gamma in response to heat-killed L. monocytogenes (hk-LM) that was absolutely dependent upon IL-12 production. However, directly stimulating the TCR with anti-CD3-epsilon mAbs resulted in IFN-gamma production that was unaffected by neutralizing IL-12 in vitro. In contrast, splenocytes isolated from LM-immune mice produced IFN-gamma in response to hk-LM, part of which was independent on IL-12 production. However, anti-CD3-epsilon Ab-stimulated IFN-gamma production remained independent of IL-12 production. The source of hk-LM-induced, IL-12-independent IFN-gamma production was the T cell because anti-Thy1.2 Ab plus complement treatment in vitro completely abolished it. Together, these data support a model of memory T cells being produced during the primary infection with LM that can be stimulated to produce IFN-gamma during the secondary response to LM, partially independent of macrophage IL-12 production.
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PMID:Secondary response to Listeria infection requires IFN-gamma but is partially independent of IL-12. 756 Oct 37

It is well known that IFN-gamma is crucial in the host defense against an intravenous infection with Listeria monocytogenes in mice. Recent studies have shown that listeriosis is caused by a food-born infection. Therefore, the production and role of IFN-gamma in the small intestines of intragastric infected-mice were investigated. On day 1 of infection, the number of bacteria cells in the feces peaked and endogenous IFN-gamma was detected in the small intestines by the immunohistochemical method, suggesting that host responses involving IFN-gamma production might occur in the early phase of infection in the small intestines. By FACS analysis, intraepithelial lymphocytes (IEL) were mainly CD3+CD8+ T cells and TCR-gamma delta+ cells were observed frequently in IEL. IFN-gamma producing cells could be detected in intestinal IEL of mice by ELISPOT assay. The analysis by reverse transcription-polymerase chain reaction analysis showed that IFN-gamma mRNA was detected in IEL of the infected mice, whereas the expression of IFN-gamma mRNA was suppressed in IEL of the mice treated with anti-CD8 mAb or anti-Thy1.2 mAb. These results suggested that Thy-1+CD+TCR-gamma delta+ T cells might be the principal source of IFN-gamma production in IEL of the infected mice. Administration of anti-IFN-gamma mAb resulted in suppression of anti-listerial resistance in the intestines. Furthermore, administration of anti-CD 8 mAb resulted in suppression of the local anti-listerial resistance on day 1 of infection. These results suggest that IFN-gamma is produced in IEL and might play a protective role in Listeria monocytogenes in the small intestines.
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PMID:[Host defense and endogenous interferon-gamma in the intestines during an oral infection with Listeria monocytogenes]. 795 93