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)

Inflammatory cells were isolated from West Nile virus (WNV)-infected CBA/H (H-2k) mouse brains, and their function and cell surface markers were studied. Two populations of cytolytic lymphocytes were detected. One population, which lysed WNV-infected and uninfected L929 (H-2k), YAC-1 (H-2a), P815 (H-2d), OH (H-2KdDk) and 2R (H-2KkDb) target cells, had a phenotype of L3T4- Lyt2- Thy1 +/- asialo GM1+ and hence were natural killer (NK) cells. The other, which lysed WNV-infected cells to a greater extent than uninfected L929 cells, had a phenotype of L3T4- Lyt2+ Thy1+ asialo GM1- and were cytotoxic T cells. In addition, the presence of the latter population was demonstrated by the specific lysis of syngeneic WNV-infected astrocytes, a cell type which is resistant to NK cell lysis. The cell surface markers of isolated inflammatory cells were determined by two colour flow cytometry. This showed that 15 to 40% of the cells were Thy1+, among which about 3% were Lyt2+. No L3T4+ cells were detected.
J Gen Virol 1989 Mar
PMID:Identification of cytolytic lymphocytes in West Nile virus-infected murine central nervous system. 254 51

In confirmation of previous reports, we observed lysis of mouse hepatitis virus (MHV)-infected target cells in the presence of spleen and lymph node cells from nonimmunized mice possessing a B cell surface phenotype (IgM+, IgG+, J11d+, Ia+, Fc+, Thy1-, MAC-1- and asialo-GM1-). Lysis was inhibited by MHV-specific antisera. The presence of immunoglobulin at the surface of B cells is not required for cytolysis since MHV-infected target cells are lysed in the presence of the B cell hybridoma Sp2/0, which fails to synthesize immunoglobulin. Using 51Cr-labelled Sp2/0 cells, both target and effector cells were shown to undergo cytolysis. Direct observation of target and effector cells co-incubated after labelling with different fluorescent dyes demonstrated that lysis correlates with the fusion of B cells and MHV-infected cells. These findings are consistent with the idea that the E2 protein of MHV, which is expressed on the infected cell surface and has receptor and membrane-fusion activities at neutral pH, selectively mediates fusion with cells of B lymphocyte lineage. This may represent a general mechanism by which enveloped viruses with fusion proteins that function at neutral pH can interfere with the function of subsets of immune cells.
J Gen Virol 1989 Jun
PMID:Target and effector cell fusion accounts for B lymphocyte-mediated lysis of mouse hepatitis virus-infected cells. 254 86

Murine cytomegalovirus (MCMV)-immune lymph node (LN) cells were generated following 4 days culture of draining popliteal LN cells removed after bilateral hind footpad inoculation of mice with 4 X 10(2) p.f.u. MCMV. This cell population expressed both cytotoxic activity against MCMV-infected mouse embryo fibroblasts (MEF) and the capacity to release lymphokine upon stimulation with MCMV-infected MEF. Cytotoxicity and lymphokine release were Class I, H-2-restricted, virus-specific and dependent upon Thy1. 2+, Lyt2+ cells. Mixing of 5 X 10(5) MCMV-immune T cells with an excess of syngeneic MCMV-infected MEF stimulators produced detectable levels of the lymphokine interleukin-3 by 1 h, with a maximum rate of its release between 1 and 6 h and plateau levels by 14 h. The capacity to stimulate virus-specific MCMV-immune T cells was acquired by MEF at 1 h after MCMV infection with maximum stimulator ability attained by 8 h. In the presence of a fixed number of MCMV-immune T cells, and titration to excess of syngeneic 3 h or 18 h MCMV-infected MEF, lower interleukin-3 plateau levels were obtained with 3 h than with 18 h MCMV-infected stimulators. This suggested that fewer T cells responded to 3 h than to 18 h MCMV-infected MEF.
J Gen Virol 1985 Dec
PMID:The cytotoxic response to murine cytomegalovirus. III. Lymphokine release and cytotoxicity are dependent upon phenotypically similar immune cell populations. 286 28

A strong delayed-type hypersensitivity (DTH) response to lactate dehydrogenase-elevating virus (LDV) in mice was induced by immunization with u.v.- or heat-inactivated virus by the intravenous, intraperitoneal and especially the subcutaneous route. The peak DTH response was seen 7 days after immunization. Live virus, in contrast, did not induce a DTH response in young (1- to 3-month-old) mice irrespective of inoculation route, except after pretreatment with cyclophosphamide (CY), when the response peaked at 14 days. Live virus, however, induced a significant DTH response in old mice (greater than 8 months) without CY. The DTH response to inactivated virus was reduced when live virus was given intraperitoneally at the same time, but was partially restored when Ia-positive peritoneal cells were also given intravenously. The DTH response induced in infected mice pretreated with CY was suppressed by injection of spleen cells from infected or from normal 1- to 3-month-old mice. Suppression by normal spleen cells was abolished by treatment with anti-Thy1.2, anti-Lyt1 and anti-Lyt2 plus complement, whereas suppression by spleen cells from infected mice was prevented by anti-Thy1.2 and anti-Lyt2 plus complement. It is concluded that suppression of the DTH response was associated with induction of suppressor T cells and that severe depletion of Ia-positive cells may also have played a part.
J Gen Virol 1986 Oct
PMID:Live lactate dehydrogenase-elevating virus (LDV) induces suppressor T cells that inhibit the development of delayed hypersensitivity to LDV. 294 91

A cytotoxic response to murine cytomegalovirus (MCMV) was obtained by the culture of lymph node cells from mice inoculated with MCMV into both hind footpads 7 days previously. The cytotoxicity was mediated by Thy1.2+, Lyt2+, H-2-restricted effector cells and was virus-specific. Investigation of the in vitro conditions established that T cell proliferation was necessary for optimal generation of cytotoxicity, that proliferation was dependent upon Thy1.2+, Lyt2+ cell populations and that supernatants from concanavalin A-activated spleen cells enhanced the levels of cytotoxicity obtained.
J Gen Virol 1985 Apr
PMID:The cytotoxic response to murine cytomegalovirus. II. In vitro requirements for generation of cytotoxic T cells. 298 18

Sin Nombre virus (SNV) causes hantavirus pulmonary syndrome (HPS), with a high rate of mortality in humans who are infected by the transmission of virus from the natural rodent host. In humans, cytotoxic T lymphocytes (CTL) specific for SNV appear to play an important role in the pathogenicity of HPS. There is a correlation between the frequencies of SNV-specific CTLs and the severity of HPS disease. In order to create a mouse model to study the role of SNV-specific T cells in vivo, T cell responses to SNV nucleocapsid (N) protein in B6.PL Thy1(a)/Cy mice (H-2(b)) immunized with plasmid DNA or recombinant vaccinia virus expressing SNV N protein were examined. Four peptides, NC94-101, NC175-189, NC217-231 and NC331-345, were recognized by CD8(+) T cells in CTL and ELISPOT assays in SNV N-immunized mice. Interestingly, two of these epitopes are located in the central region of the SNV N protein, where several human CD8(+) T-cell epitopes have been defined in Puumala virus and SNV. CTL lines specific for these four epitopes were cross-reactive to corresponding Puumala virus peptides, but only one of them was cross-reactive to Hantaan virus peptides. These results will enable the analysis of the roles of CTL in immunopathology of HPS in experimental mouse models of HPS.
J Gen Virol 2004 Jul
PMID:Identification and analysis for cross-reactivity among hantaviruses of H-2b-restricted cytotoxic T-lymphocyte epitopes in Sin Nombre virus nucleocapsid protein. 1521 76