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)

The lpr autoimmune mice develop massive lymphadenopathy and autoimmune disease. Transfer of lpr autoimmune disease to normal mice by bone marrow transplantation did not succeed, but caused a severe wasting syndrome like graft-vs-host (GvH) disease (lpr-GvH). We previously demonstrated that the transfer of B6-lpr spleen cells to B6 mice ([B6-lpr----B6] chimera) caused acute GvH-like disease accompanied by remarkable CD8+ T cell expansion, and that chimera spleen cells had suppressive activity on mitogen responses of spleen cells from normal mice. In this paper, I studied strain difference of acute lpr-GvH disease and mechanism of suppressive activity further. [B6-lpr----B6] chimera spleen contained more than 70% of CD8+ cells. However, [MRL-lpr----MRL-(+)] chimera and [C3H-lpr----C3H] chimera contained less than 20% of CD8+ cells. Both B220+ DN T cells and CD 8+ T cells were requisite for expansion of CD8+ T cell in the chimera spleen. Mixed chimera experiments using CD8+ T cells from B6-lpr-Thy1.1 mice and B220+ DN T cells from B6-lpr mice showed that CD8+ but not B220+ DN T cells were direct precursors of expanding CD8+ T cells. The mechanism of suppressive activity on Con A responses was different from that on LPS responses. A cell-to-cell interaction was essential for suppression of Con A response without involvement of CD8- cells, while suppression of LPS responses was mainly exhibited by soluble factors. Suppression of LPS responses was abrogated by the presence of anti-IFN-gamma monoclonal antibody, suggesting that those factors contain IFN-gamma. These data suggest that CD8+ T cells from B6-lpr mice were activated by unidentified antigen(s) which were expressed by B6 but not B6-lpr cells, and that IFN-gamma and/or unknown inflammatory factors secreted by the CD8+ T cells induced pathological outcome indistinguishable from GvH reaction in B6 recipient mice.
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PMID:[Analysis of acute graft-vs-host like reaction in [B6-lpr----B6] spleen chimera mice]. 142 98

It was recently demonstrated that MRL-lpr lymphoid cells transferred into lethally irradiated MRL- +mice unexpectedly failed to induce the early onset of lupus syndrome and massive lymphadenopathy of the donor, instead they caused a severe wasting syndrome resembling graft-vs-host (GvH) disease. The present studies were carried out to characterize the cellular events involved in the severe GvH-like reaction developed in C57BL/6 (B6) recipients of B6-lpr spleen cells, designated as [B6-lpr----B6] chimeras. [B6-lpr----B6] chimeras showed at 2 weeks post transplantation marked splenomegaly consisting predominantly of Lyt2+ T cells (approximately 70%), and subsequently developed acute and severe depletion in spleen cells causing spleen atrophy and fibrosis. Spleen cells from chimeras at 2 weeks posttransfer were not cytotoxic to both recipient and donor ConA blast target cells. In contrast, those cells (irradiated to 3000 rad) considerably suppressed ConA-induced proliferative responses of B6 spleen cells. These nonspecific suppressor cells expressed Thy1 and Lyt2 antigens, but lacked L3T4 and B220 antigens. Furthermore, elimination of Thy1+ or B220+ but neither L3T4+ nor Lyt2+ cells from B6-lpr spleen cells before transfer retarded the generation of nonspecific suppressor cells but did not abrogate the GvH-like disease. These results suggest that the GvH-like disease and lymphoid atrophy in [B6-lpr----B6] chimeras were mediated by Lyt2+ suppressor T cells, and that B220+ T cells played a crucial role in the induction of these suppressor cells. The cell transfer model reported here may be very useful in understanding the immunological function of B220+ T cells in vivo.
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PMID:[Analysis of the mechanism of graft-vs-host like disease in [lpr/lpr----+/+] chimera]. 296 73