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

Studies were undertaken to determine a possible structural relationship between the secretory component (SC) and the receptor for IgA (Fc alpha R). An IgA-mediated rosetting technique was used to assess the presence of Fc alpha R+ cells in various lymphoid tissues from normal BALB/c mice and mice bearing an IgA plasmacytoma (MOPC 315). Tissues from the MOPC 315-bearing BALB/c mice were found to have a significantly higher percentage of Fc alpha R+ cells; thus, nonadherent spleen cells from MOPC 315-bearing mice were used as a source of Fc alpha R+ cells in these studies. The cells were preincubated with anti-SC and then assayed for the ability of IgA to bind to the Fc alpha R. Antisera to SC from various species inhibited the formation of IgA-mediated rosettes, although preincubation of the Fc alpha R+ cells with antisera directed against other cell surface molecules (e.g., Thy1.2, Lyt1, Lyt2, Fc gamma R, MHC class I and II) or preimmune sera had no significant effect on IgA-mediated rosette formation. Preabsorption of the anti-SC with secretory IgA or with free SC removed the inhibitory effect; preabsorption with myeloma IgA had no effect. These data suggest that SC and Fc alpha R are related serologically and may be structurally related, possible in the IgA-binding region.
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PMID:Antisera to the secretory component recognize the murine Fc receptor for IgA. 278 69

Detection of cell surface markers and cell surface receptors of resident peritoneal cells in MRL/Mp-1pr/1pr (MRL/1) and MRL/Mp-+/+ (MRL/n) mice was made by cytotoxic assay using anti-Thy1.2 and anti-IAk or anti-IE antibodies and rabbit anti-sheep red blood cell IgG coated sheep erythrocytes, respectively. MRL/1 mice showed a remarkable increase in the number of peritoneal cells, the main cells of which were not macrophages but T-cells. The cell surface Fc gamma-receptors on the peritoneal macrophages increased and their immune phagocytosis mediated by Fc gamma-receptors was enhanced. Ia expression of the macrophages showed a high value from in early life, but decreased at the end of life. On the contrary, MRL/n mice showed a low value in early life, which then increased after 15 weeks and continued at a high value until 25 weeks, the end of the experimental period. We described the characteristic increment of T-cells in the peritoneal cavity of MRL/1 mice and discussed the relationship between Ia expression and development of autoimmune symptoms in MRL/1 and MRL/n mice.
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PMID:Characterization of resident peritoneal cells in MRL mice. 326 May 71

The impairment of cellular immunity in mice infected with Mycobacterium lepraemurium was shown to correlate with the development of suppressor cells. We have previously reported that before suppressor activity is detectable in freshly harvested cell suspensions, suppressor cell precursors accumulate in the spleen of infected mice. Upon overnight culture in the presence of a regulatory cell subset, these precursor cells acquire the capacity to impair the concanavalin A (Con A)-induced proliferation of normal spleen cells. The purpose of this study was to determine the phenotype of the cells involved in this phenomenon. This was done by following the development of suppressor activity in spleen cell suspensions depleted of defined cell subsets of the adherent or the non-adherent cell fractions with selected MoAbs and immunomagnetic beads or by in vivo treatment. Our results indicate that the acquisition of suppressor activity requires the interaction of Ia+CD11b+Fc gamma R+IgG- asialo GM1- adherent cells with Thy1-CD4-CD8-IgG-Ia- asialo GM1-Fc gamma R+CD11b+ non-adherent cells. It is also shown that the development of suppressor activity is impaired by preventing cell-cell contact between these two cell subsets through coculture in 'Transwell chambers'. These observations support the conclusion that the in vitro acquisition of suppressor activity is a consequence of the maturation of suppressor cell precursors of the monocytic lineage induced by a receptor-ligand type interaction with a non-adherent cell subset that is clearly distinct from mature T, B and natural killer (NK) cells.
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PMID:Phenotypic characterization of two cell populations involved in the acquisition of suppressor activity by cultured spleen cells from Mycobacterium lepraemurium-infected mice. 853 66

Thymocytes of mice deficient in the recombinase-activating gene (RAG)-1 or RAG-2 cannot express and receive signals through the pre-TCR. As a result, thymocyte development in these mice terminates at the CD4/8 double negative (DN), IL-2R-alpha-positive stage. Nevertheless, RAG-deficient DN thymocytes express functional CD3 complexes and can therefore be induced by anti-CD3 epsilon mAb to mature to the CD4+8+ double positive stage. In the present paper we demonstrate that the peripheral lymphoid organs (lymph nodes, spleen) and peripheral blood of RAG-deficient mice harbor an immature T cell population which, similar to RAG-deficient DN thymocytes, contains high levels of cytoplasmic CD3 epsilon and responds to anti-CD3 epsilon mAb in vivo. With respect to surface phenotype (Thy1.2+, PgP-1+, HSA+, Fc gamma RII/III-, IL-2R-alpha-, c-kit-), these cells are similar to intermediate stage RAG-deficient DN thymocytes. Moreover, they express mRNA for pre-TCR-alpha and for the nondeleted RAG. Following injection of anti-CD3 epsilon mAb, these cells proliferate, down-regulate heat stable Ag and PgP-1, and partially differentiate to CD4+ and CD8+ double positive and single positive cells. The induced population displays a mixed phenotype, between that of immature thymocytes and lymph node T cells in normal mice. Induction is successful in thymectomized RAG-deficient mice, suggesting that it occurs in the periphery. However, after thymectomy, inducible cells disappear with an approximate half-life of 10 to 14 days. We suggest that DN thymocytes can emigrate and repopulate peripheral lymphoid organs of RAG-deficient mice. These cells respond to CD3 signaling by aberrant maturation, possibly due to the inappropriate microenvironment of peripheral lymphoid organs.
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PMID:Immature T cells in peripheral lymphoid organs of recombinase-activating gene-1/-2-deficient mice. Thymus dependence and responsiveness to anti-CD3 epsilon antibody. 856 35

We examined the effect of murine intestinal intraepithelial lymphocytes (IEL) on the proliferation of murine lymph node T cells (LN-T) in vitro. An IEL fraction prevented the proliferation of LN-T stimulated with antigen and X-irradiated spleen cells, or with anti-CD3 monoclonal antibodies (mAb). Concanavalin A-activated LN-T were less sensitive. Such an inhibitory activity was recovered from a CD8-depleted population by panning of bulk IEL using anti-CD8 alpha mAb. This population of BALB/c IEL showed less granzyme A activity, and its surface markers were positive for CD8 (4%), CD3 (80-90%), CD4 (2-6%), alpha-beta TcR (45-70%), and gamma-delta TcR (4-9%). Asialo-GM1 and Thy1.2 were variably expressed, but interleukin-2 (IL-2) receptor-alpha and Fc gamma receptor were not. By contrast, no cytotoxicity against YAC-1 was detected in a CD8-depleted IEL population by a 6-h 51Cr-release assay. Although IEL from severe-combined immunodeficient mice lacking CD4, CD8 and TcR, but expressing IL-2 receptor, showed cytotoxicity against YAC-1, their inhibitory activity against LN-T was almost the same as that by IEL from BALB/c mice. When LN-T blasts (greater than 75% CD4+) activated with anti-CD3 were treated with CD8-depleted IEL, intact cellular DNA of the T blasts disappeared within 1 h with increased amounts of small-sized DNA. These results suggest that CD8- IEL directly and nonspecifically kill lymph node CD4+ T blasts and possibly down-regulate TcR-mediated proliferation of peripheral T cells in the gut epithelium.
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PMID:Rapid killing of murine lymph node T blasts by intestinal intraepithelial lymphocytes in vitro. 860 34

A null cell line (SCM1) was established by a culture of spleen cells (SC) from normal adult C57B1/6 mice with complete medium alone for 10 days and followed by weekly cultures with a 25% WEHI-3 cell culture supernatant. Phenotype analysis showed that the SCM1 cells were negative for CD3, Thy1.2, B220, Mac-1, Gr-1, NK1.1 and MHC class II, but were positive for MHC class I, Fc gamma RII/ III, Fc epsilon RI, c-kit and the receptor against wheat germ agglutinin. These findings suggested that the SCM1 cells were mast cells. In an in vitro proliferation assay. SCM1 cells proliferated in the presence of either IL-3 or stem cell factor (SCF), but not in the presence of IL-4, whereas IL-4 showed an augmenting effect on their proliferation in the presence of either IL-3 or SCF. In analysing the mechanism by which such mast cells could be expanded from normal adult mouse SC, the addition of anti-IL-3 MoAb, but not anti-SCF MoAb, into the initial culture inhibited the subsequent expansion of either IL-3-or SCF-responding cells. The prior depletion of CD4+ T cells abrogated the capacity of the SC to enhance the expansion of SCF-responding cells, and this inability was restored by the addition of IL-3. Moreover, the culture supernatant of normal adult SC alone contained considerable levels of IL-3. Taken together, our findings suggest that, in an in vitro culture, CD4+ T cell-derived IL-3 therefore enhances the expansion of mast cells from the normal adult mouse spleen.
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PMID:IL-3 derived from CD4+ T cells is essential for the in vitro expansion of mast cells from the normal adult mouse spleen. 887 Jul 13