摘要:

AbstractRabbit anti‐rat anti‐human thyrotropin anti‐idiotypic antibodies have been raised. These antibodies were active at the thyrotropin (TSH) receptor, in that they inhibited125I‐labeled bovine TSH binding to thyroid plasma membranes, stimulated adenylate cyclase activity through a guanyl nucleotide‐dependent mechanism, augmented radioiodide transport into isolated porcine thyroid follicular cells and induced such cultured cells to organize into follicles. Aside from substantiating the expectation that anti‐hormone anti‐idiotypic antibodies may possess properties of the original hormone, this work raised the possibility that thyroid‐stimulating antibodies which cause the hyperthyroidism of Graves' disease may be anti‐TSH anti‐i

ISSN:0014-2980    

DOI:10.1002/eji.1830130113

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY

摘要:

AbstractPurified OKT8+but not OKT4+T lymphocytes generated suppressor activity in autologous mixed lymphocyte reactions (AMLR) in the presence but not in the absence of interleukin 2 (IL 2) as determined in proliferative responses of peripheral blood mononuclear cells induced by Concanavalin A, the OKT3 monoclonal antibody and allogeneic cells (indicator systems for suppressor activity used in this study). Furthermore, treatment of AMLR‐activated T cells with the OKT8 antibody plus complement abolished suppressor cell activity whereas treatment of the cells with the OKT4 antibody plus complement did not.The three monoclonal anti‐HLA‐DR antibodies used in this study abrogated the induction, but not the effector phase, of suppressor cells in AMLR. The anti‐DR antibodies acted specifically on the stimulator non‐T cells and not on the responder T cells. The addition of IL2 to AMLR cultures performed in the presence of the anti‐DR antibodies did not restore or increase the suppressor activity whereas IL2 added to AMLR cultures exposed to control antibodies or medium alone increased the suppressor activity. Moreover, purified OKT8+T cells cocultured with autologous non‐T cells and IL2, in the presence of the anti‐DR antibodies, neither responded to IL2 by proliferating nor expressed suppressor function. In contrast, OKT8+T cells from similar cultures, but performed in the absence of the anti‐DR antibodies or exposed to control antibodies, proliferated to IL2 stimulation and exhibited suppressor activity. Unactivated OKT8+T cells were unresponsive to IL2 and unable to express suppressor function. Finally, the addition of the OKT8 antibody (in the absence of complement) to AMLR cultures had no effect on the generation of suppressor cells.From these results, we conclude the following: (a) OKT8+T lymphocytes become sensitive to IL2 by interacting with HLA‐DR antigens on the stimulator non‐T cells and, with the help of IL2, they express suppressor cell activity; (b) the OKT8 antigenic determinant on AMLR‐activated suppressor cells does not seem to participate in their process of activation; (c) results of previous studies showing that OKT4+T lymphocytes become sensitive to IL1 and are capable of synthesizing IL2 after interaction with HLA‐DR on the stimulator cells, and the findings presented here, lead us to suggest that both OKT4+and OKT8+T lymphocytes possess receptors for self HLA‐DR antigens and that neither the OKT8 nor the OKT4 antigenic determinants on these cells are involved in the recognition of HLA‐DR antigens. The suppressor activity generated in AMLR may be one mechanism whereby effector self‐tolerance is maintained in the fac

ISSN:0014-2980    

DOI:10.1002/eji.1830130114

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY

摘要:

AbstractMouse thymocytes, which are approximately 90% immature cortical cells, are low in surface sialic acid when compared with more mature cortisone‐resistant, presumably medullary, thymocytes and peripheral T lymphocytes. Thus, medullary thymocytes bind and are agglutinated by the N‐acetylneuraminic acid‐specific lectin, lobster agglutinin 1 (LAg1), whereas cortical thymocytes are not agglutinated by this lectin. It is demonstrated herein that mouse cortical thymocytes, purified using LAg1, do not respond to the mitogenic effects of concanavalin A (Con A). The lack of response to this lectin is not due to depletion of macrophages, since addition of macrophages does not restore the response. Populations of LAg1‐negative thymocytes can be made to respond weakly to Con A by the addition of interleukin 2, but this response appears to be due to the presence of a few contaminating LAg1‐binding thymocytes since it is abolished by treatment of the cells with rabbit anti‐LAg1 serum plus complement. Therefore highly purified cortical thymocytes not only cannot respond to Con A, but also they cannot be induced to respond by the addition of the T cell growth factor, interleukin 2. Thymocytes isolated by a single criterion, that is by virtue of their low amount of surface sialic acid, appear to be a truly immature population of

ISSN:0014-2980    

DOI:10.1002/eji.1830130115

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY

摘要:

AbstractThe nature of Ia antigens inducing lymphocyte proliferation and immune interferon (IFN‐γ) production in primary and secondary murine mixed lymphocyte cultures was studied by means of monoclonal anti‐Ia antibodies. In primary mixed lymphocyte cultures, both lymphocyte proliferation and IFN‐γ production were found to be controlled by Ia determinants coded for by the I‐A subregion. E alloantigen‐recognizing antibodies displayed consistent stimulation of both lymphocyte functions, instead of inhibition, suggesting a regulatory mechanism of the E molecule on lymphocyte activation. In secondary mixed lymphocyte cultures fewer Ia determinants seemed to be involved in lymphocyte proliferation, since only antibodies directed against specificities Ia.17 and Ia.19 were found capable of blocking lymphocyte proliferation. In contrast, IFN‐γ production, although significantly decreased by antibodies against specificities Ia.17 and Ia.19, was not completely abrogated, even by a mixture of all anti‐Ia antibodies.The data indicate that (a) in primary mixed lymphocyte reaction lymphocyte proliferation and IFN‐γ production are triggered by the same Ia specificities coded by the I‐A subregion and (b) in secondary mixed lymphocyte reaction, whereas lymphocyte proliferation is restricted to fewer determinants, IFN‐γ production shows a lower threshold of activation, being induced also by determinants ‘silent’ in prima

ISSN:0014-2980    

DOI:10.1002/eji.1830130116

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY

摘要:

AbstractNormal euthymic mice, injected i.v. with low doses of syngeneic monoclonal antibodies carrying “recurrent” idiotypes, develop a specific increase in numbers of splenic IgM plaque‐forming cells that are paratopically and idiotypically similar to the injected antibody. We have now studied the responsiveness to a C57BL/6 anti‐dextran α(1 → 6) and BALB/c anti‐TNP (trinitrophenyl) monoclonal antibodies in a variety of strains. It was found that such responses are controlled by two linkage groups, namely major histocompatibility complex (M

ISSN:0014-2980    

DOI:10.1002/eji.1830130117

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY

摘要:

AbstractPrevious work has shown that thymocytes of rats receiving two i.v. injections, 4 days apart, of large numbers of xenogeneic erythrocytes become tolerant of the injected cells whereas peripheral T cells in the same recipients make a vigorous response to the injected antigen. Results are herein presented of experiments on the effect of splenectomy on the induction of thymocyte tolerance produced in this way. Splenectomy performed either immediately before the first injection of erythrocytes, or between the two injections, completely prevented tolerance induction and tolerance was still incomplete when splenectomy was performed as late as a few hours after the second injection of tolerogen. Sham splenectomy had no effect on the erythrocyte‐induced thymocyte tolerance. The results demonstrate an essential role for the spleen in the tolerization of thymocytes in this system. Possible mechanisms and the implications for self tolerance are discusse

ISSN:0014-2980    

DOI:10.1002/eji.1830130118

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY

ISSN:0014-2980    

DOI:10.1002/eji.1830130119

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY

ISSN:0014-2980    

DOI:10.1002/eji.1830130102

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY