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)

Highly susceptible naive BALB/c mice or mice that had previously been immunized i.v. with solubilized homologous antigen (partially resistant) were infected with Leishmania amazonensis. Histologically, the main differences between the two groups were lymphocytic infiltration and macrophage activation. Assays of T-cell function at 3 and 10 weeks after infection revealed that purified T-cells did not proliferate following treatment with leishmania antigen. A mitogenic anti-CD3 monoclonal antibody (mAb) failed to activate T-cells after 3 weeks of infection as judged by proliferation and IL-2 secretion assays. After 10 weeks of infection, anti-CD3 mAb fully activated T-cells to proliferation and IL-2 secretion. On the other hand, T-cells released IL-3 in response to leishmania antigen, anti-CD3 mAb and anti-Thy1 mAb at 3 and 10 weeks post-infection. Surprisingly, a mitogenic anti-Thy 1 mAb (G7) fully activated T-cells even at 3 weeks of infection as judged by proliferative and IL-2 secretion assays. No significant differences were found in the proliferative or interleukin secretory responses of T-cells from animals that had been infected in either the presence or the absence of prior immunization. Since the Thy1 triggering pathway has different accessory cell and cytokine requirements than does the CD3: TCR lymphocyte activation pathway, it is possible that immunization was more effective in changing the cellular interactions of the T-lymphocyte than in altering its intrinsic capabilities.
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PMID:T-lymphocytes in experimental Leishmania amazonensis infection: comparison between immunized and naive BALB/c mice. 158 41

Binding of cognate Radiation leukemia virus (RadLV) by the C6VL/1 thymoma involves a subset of TCR molecules in association with CD4 molecules expressed by that cell line. A CD4- variant of C6VL/1 has now been isolated which also has RadLV binding capacity. Stable expression of the TCR, class I, and CD5 molecules but not Thy1.2 and CD4 molecules has been demonstrated, and the C6VL/1 origin of this cell has been confirmed by Southern blot analysis using probes specific for the TCR beta chain gene. This cell line has maintained binding capacity for RadLV/C6VL prepared as an immunoabsorbent matrix, but unlike the parent C6VL/1 cell line, binds significantly less well to the related RadLV/VL3 isolate. Binding of the variant cell line to RadLV/C6VL can be completely inhibited by anti-clonotypic antibody to the TCR but only weakly by anti-H-2Kb antibody used at the same concentration. These data suggest that the TCR on C6VL/1 can interact with RadLV in the absence of any co-receptor function of CD4 and implicates the TCR as a sufficient receptor for retrovirus.
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PMID:Unique role for the T cell receptor in retrovirus binding by the C6VL thymoma. 217 45

Radiation leukemia virus (RadLV)-induced thymomas and malignant thymocytes from AKR mice have been shown to bind specifically retrovirus produced by these cell lines. Each lymphoma has been shown to have greatest specificity for cognate virus suggestive of an immune-specific receptor. The question of receptor identity has been addressed here using the RadLV-induced murine T cell lymphoma, C6VL/1, and antibodies specific for known cell surface determinants present on these cells. This lymphoma has been shown to bind both homologous and heterologous RadLV isolates, but to have greatest specificity for homologous retrovirus since homologous free virions can best block the interaction between cells and virus adhered to the wells of a microtitre plate. A clonotypic anti-TCR antibody has been shown to completely inhibit C6VL/1 binding to the homologous virus, RadLV/C6VL, but not to the heterologous virus, RadLV/VL3. Anti-CD4, anti-Thy1.2 as well as anti-H-2Kb and not anti-H-2Db antibodies were found to partially inhibit the interaction with both RadLV/C6VL and RadLV/VL3, yet neither of these virus preparations appears to be contaminated with Class I molecules as measured by radioimmunoassay. The binding interaction between C6VL/1 and RadLV/C6VL appears specifically to involve the TCR since antibody against the clonotypic site on the TCR heterodimer uniquely inhibits this interaction, while the binding of C6VL/1 to RadLV/VL3 appears to involve the H-2Kb molecule. When free virus particles were absorbed to receptors on C6VL/1, both RadLV/VL3 and RadLV/C6VL inhibited the binding of antibody to the TCR and CD4 molecules, while the binding of several anti-H-2Kb antibodies was specifically inhibited by RadLV/VL3. There are at least two known T cell surface structures involved in the interaction of the T cell lymphoma, C6VL/1, with RadLV. These are the TCR complex (comprising the TCR heterodimer and CD4), and the Class I H-2Kb molecule. Since the TCR molecule has been shown to comodulate with H-2Kb molecules when cells were cultured in the presence of anti-H-2Kb antibodies, and the CD4 and H-2Kb molecules have been shown to comodulate with the TCR on only a subpopulation of C6VL/1 cells treated with anti-TCR antibody, this suggests that the H-2Kb molecule may also be part of the larger molecular complex including CD4/8 which can form around the TCR heterodimer.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Binding of radiation leukemia viruses to a thymic lymphoma involves some class I molecules on the T cell as well as the T cell receptor complex. 255 69

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

Pulmonary intraparenchymal leukocytes were purified from normal mice. By flow cytometry, 20-30% of the lymphocytes were positive for the expression of Mac1, a cell-surface antigen largely restricted to macrophages, neutrophils and natural killer (NK) cells. Sorted Mac1+ lung lymphocytes were large and had abundant cytoplasm with few azurophilic granules. Because Mac1+ lymphocytes did not contain any asiallo GM1+ cells, they are not likely to be NK cells. By a two-color flow cytometric analysis, Mac1+ lymphocytes were demonstrated to be TCR-alpha beta intermediate+, TCR-gamma delta-, CD3intermediate+, CD4-, CD8-, Thy1-, CD5-, and B220-. These Mac1+ alpha beta T cells were not found in other organs such as spleen, thymus, liver, bone marrow and intestine of mice uninfected and infected with Mycobacterium bovis BCG. There was a considerable population of this unusual subset of alpha beta T cells in the lungs of congenitally athymic nude mice. In the Mac1+ alpha beta T-cell population, the proportions of V beta 8+ T cells and of forbidden T-cell clones expressing V beta 6 TCR were not much different from that in the conventional T-cell population. These results indicated that extrathymically developed alpha beta T cells reside in considerable proportions in the lung and that Mac1 clearly discriminates these cells from conventional ones. Interestingly, the proportion of these cells increased in the lungs of mice infected with M. bovis BCG, which raises a possibility that these cells may play some role in the host defense against mycobacterial infection.
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PMID:Mac1 discriminates unusual CD4-CD8- double-negative T cells bearing alpha beta antigen receptor from conventional ones with either CD4 or CD8 in murine lung. 759 Sep 10

We have previously established conditions under which murine yolk sac cells can be maintained in vitro in the absence of thymus, and we reported that a spontaneously transformed Thy1.2+ yolk sac cell line was obtained after long term culture in vitro. We now provide further phenotypic characterization of a clone, YSA1, of this Thy1.2+ cell line showing that it expresses Thy1.2, CD3/TCR V beta 8, IL-2 receptor (IL2R), and heat stable antigen (HSAg), but does not express CD4/CD8 or TCR gamma delta. The YSA1 clone is an immature cell as indicated by the expression of IL2R and HSAg and by nonproduction of IL-2 upon stimulation by anti-CD3 antibody. The data show that yolk sac stem cells can differentiate into CD3/TCR expressing cells in the absence of thymus, but do not progress in vitro paralleling observations made on freshly-isolated yolk sac stem cells.
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PMID:A cloned lymphoid Thy1+ tumor line derived from murine yolk sac cells maintained in long-term cell culture in the absence of a thymic microenvironment expresses an unusual cell surface phenotype. 790 86

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

Recent evidence has indicated that the intestinal epithelium may be a major extrathymic site of T cell production. However, which of the multiple intestinal intraepithelial lymphocyte (IEL) subsets are extrathymic in origin has been controversial. We now report that the thymus is an integral component of IEL maturation and is required for a novel two-stage process of T cell production. Thus, in neonatally thymectomized mice TCR-gamma delta IELs were depleted and some TCR-alpha beta IELs were of an immature phenotype. Thymus grafting experiments revealed that all TCR-gamma delta and TCR-alpha beta IEL subsets could be thymus-derived, including TCR-alpha beta cells lacking Thy1 and CD8 beta. In utero anti-TCR-gamma delta mAb treatments resulted in depletion of gamma delta IEL without subsequent re-emergence of this subset in adulthood, whereas anti-TCR-alpha beta mAb treatment only marginally reduced the alpha beta IEL subset. These findings suggest that TCR-alpha beta and TCR-gamma delta IELs arose at distinct developmental stages. Overall, the results indicate that some IEL precursors are thymus-derived but require further thymic influence to mature in the periphery.
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PMID:A novel pathway of thymus-directed T lymphocyte maturation. 802 68

Since the modulation of the immune system at birth may influence the course of insulin-dependent (type 1) diabetes, we investigated whether neonatal injections of cyclosporin (CsA) to newborn non-obese diabetic (NOD) mice influence diabetes during later life. Two groups of 90 mice (45 female, 45 male) were injected intraperitoneally for the first 6 days of life with CsA (10 mg/kg per day) or with vehicle. In female NOD mice, the onset of diabetes was earlier and cumulative incidence was higher after neonatal treatment with CsA (P < 0.01). The incidence of diabetes was also dramatically enhanced in male NOD mice (P < 0.01), which normally display a very low disease incidence. Concomitantly, the severity of lymphocytic infiltration of the pancreatic islets was higher in female NOD mice neonatally treated by CsA (P < 0.02), and to a lesser extent in males, than in control mice. After administration of CsA to newborn NOD mice, there was a reduction (P < 0.01) of both CD4+CD8- and CD4-CD8+ thymocytes, whereas the number of double positive CD4+CD8+ thymocytes was increased. Concomitantly, Thy1-2+ cells in spleen were decreased (P < 0.01), and spleen cells expressing either CD3 molecule or alpha beta TCR complex were diminished (P < 0.01). Both CD4+ and CD8+ spleen T cells were depleted. By contrast, the low percentage of gamma delta TCR-expressing splenocytes was not modified. Numbers of MHC class 1+ or MHC class 2+ spleen cells were also depressed (P < 0.01). After neonatal injections of CsA, spleen cells showed a reduced response to concanavalin A (Con A) (P < 0.01). On the contrary, stimulation indices of splenocytes incubated with xenogeneic insulin-producing cell extracts were enhanced (P < 0.03). Proliferation indices of splenocytes to self class 2 antigens, generating suppressor cell activity, during syngeneic mixed lymphocyte reaction (SMLR) were significantly reduced (P < 0.01). Irradiated NOD mice were used as recipients for spleen cells from CsA-neonatally treated NOD mice. They displayed enhanced insulitis 2 weeks after transfer, and diabetes was successfully produced by 1 month after transfer in 50% of the recipients. By contrast, NOD mice which received control syngeneic spleen cells remained normoglycaemic, with only moderate islet infiltration which would be expected of NOD mice of this age. Thus, neonatal injections of CsA markedly enhance diabetes in both female and male NOD mice.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neonatal injections of cyclosporin enhance autoimmune diabetes in non-obese diabetic mice. 803 11

Up to 90% of CD8+ intraepithelial lymphocytes (IEL) of the murine large intestine (LI) belong to the alpha/beta T cell lineage and consist of two subsets. One subset expresses both alpha and beta subunits of the CD8 coreceptor, and is uniformly Thy1+, CD5+, B220-, CD2+, CD28+. The CD8 alpha+beta+ LI-IEL exclude self-reacting V beta structures, and readily proliferate in vivo in response to T cell receptor-mediated stimuli. The CD8 alpha+beta- subset of TCR-alpha/beta+ LI-IEL is Thy1-/+, CD5-, B220+, CD2+/-, and CD28-. It contains cells with potentially self-reacting V beta s and is responsive in vivo to high doses of anti-TCR-alpha/beta monoclonal antibody (mAb), but not to bacterial superantigens. Both subsets are abundant in LI-IEL of old nude mice, and CD8 alpha+beta+ LI-IEL in nude mice undergo the same V beta deletions as in euthymic mice of the same background. Both subsets express the intestinal T cell-specific integrin alpha M290 beta 7, known to be a homing receptor for IEL. Unusually high proportions of CD69+ cells within both subsets indicate chronic activation. The proportions of CD69+ and alpha M290 beta 7+ cells within the CD8 alpha+beta+ subset increase with age, probably due to constant antigenic challenge. We propose that CD8 alpha+beta+ and CD8 alpha+beta- subsets of LI-IEL permanently reside in LI and represent a lineage different from spleen and lymph node CD8+ T cells. The CD8 alpha+beta+ undergoes negative selection, and is responsive to TCR-mediated stimuli. The CD8 alpha+beta- subset of LI-IEL is a subject of distinct selection mechanisms, and has low responsiveness to TCR-mediated stimuli.
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PMID:Heterogeneity and biased T cell receptor alpha/beta repertoire of mucosal CD8+ cells from murine large intestine: implications for functional state. 804 26


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