摘要:

AbstractUsing a panel of monoclonal antibodies which detect framework determinants of human‐Ia à and β polypeptides and the DC‐specific monoclonal antibody Genox 353, thein vitroeffects of 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA) on the expression of Ia antigens by cells from chronic lymphocytic leukemia (CLL) patients have been studied. In all subjects studied a great increase in expression of framework Ia determinants was found following culture of CLL cells for 90 h with TPA at 10−7g/ml. TPA treatment of CLL cells also induced increased expression of Genox 353+antigens, in some cases where Genox 353 binding was either negligible or not detectable in cells cultured in the

ISSN:0014-2980    

DOI:10.1002/eji.1830130212

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY

摘要:

AbstractThe monoclonal antibody W6/32.1 recognizes a public determinant on the HLA‐A, B and C antigens of all tested human haplotypes. Though the antibody does not bind to normal mouse cells of any H‐2 haplotype, it does show an unexpected specificity for the T cell leukemia line MBL‐2 from a C57BL/6 mouse. It is shown that the murine antigen recognized by W6/32.1 is on an H‐2‐like molecule which also carries the determinant recognized by the monoclonal antibody B22‐249R1, specific for the H‐2Dbantigen. Unlike B22‐249R1, however, W6/32.1 does not bind to normal H‐2blymphocytes, nor to a variety of tumor cell lines of the H‐2bhaplotype. This crossreaction is specific to W6/32.1, and is not shared by other monoclonal antibodies of similar anti‐HLA specificities. Moreover, the affinity of W6/32.1 for its human antigen is substantially higher than for its mouse antigen. We conclude that W6/32.1 fortuitously recognizes a novel determinant on the H‐2Dbantigen of MBL‐2, rather than an extensive region of structural homology shared between HLA and H‐2. Thus for cells of the H‐2ballotype this determinant is detected only on MBL‐2, and by definition is thus an exampl

ISSN:0014-2980    

DOI:10.1002/eji.1830130213

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY

摘要:

AbstractMice injected from day of birth onwards with rabbit anti‐mouse IgM (anti‐μ) antibodies were found to be B cell‐deficient and defective for the induction of antigen‐reactive proliferating T cells (TPRLF). This defective induction was not due to the absence of circulating antigen‐specific antibodies since the daily injections of such antibodies during exposure to antigen did not restore the ability of anti‐IgM treated animals to generate TPRLF. Analyzing the cellular events implicated in the induction of virgin antigen‐reactive T cells, anti‐μ‐treated mice manifested impairment of the three interacting cell types involved in the induction of TPRLF. Thus, peritoneal and splenic antigen‐presenting cells from such animals were impaired in their capacity to signal a primary antigen‐specific T cell reaction. Their splenic lymphocytes could not function as initiator cells in transferring immunogenic signals to recruit TPRLFin normal recipients. Potent antigen‐specific splenic initiator cells failed to induce the recruitment of specific TPRLFin anti‐μ‐treated mice. The defective induction of TPRLFin anti‐μ‐treated mice may be due to a functional impairment of cells expressing membranebound IgM molecules which seemingly play a central role in the transfer of immunogenic signals for the recruitment of antigen‐specific circulating T cells. We suggest that splenic B cells function as initiators in the transfer of antigen‐induced signals from peritoneal antigen‐presenting cells to T cells. These seems to b

ISSN:0014-2980    

DOI:10.1002/eji.1830130214

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY

摘要:

AbstractLeukemic and normal hemopoietic cells were examined with the monoclonal antibodies DA2 and Genox 353 for the presence of HLA‐DR and DR‐linked (DC/MB) determinants, respectively. Although most non‐T acute leukemias and leukemic cell lines expressed the monomorphic DR determinant detected by DA2, fewer than expected expressed the DR‐linked polymorphic specificity detected by Genox 353. TdT+lymphoid precursors from normal bone marrow were also DA2+but Genox 353−. T cells and thymocytes which were DA2−, Genox 353−became DA2+, Genox 353+after activationin vitro.Immunoprecipitation using DA2 and Genox 353 gave bands on polyacrylamide gelelectrophoresis which were of different molecular weights. In addition, DA2 could absorb out Genox 353 determinants from a cell lysate whereas Genox 353 could not absorb out DA2 determinants. It is concluded that DA2 and Genox 353 detect HLA‐DR and DR‐linked (DC1/MB1) determinants, respectively, and that these are differentially expressed on hemopoietic cells durin

ISSN:0014-2980    

DOI:10.1002/eji.1830130215

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY

摘要:

AbstractK/D‐restricted male‐specific cytolytic T lymphocytes (CTL) have been cloned and assayed for male‐specific proliferation in the absence of exogenous interleukin 2 (T cell growth factor). The majority of freshly cloned CTL proliferate in response to cell‐bound antigen. The clones lose their proliferative potential after growing for three weeks in media contain

ISSN:0014-2980    

DOI:10.1002/eji.1830130216

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY

摘要:

AbstractThe immunologic effects initiated by injecting neonatal mice with phosphorylcholine (PC)‐protein conjugates were analyzed. Pretreated nude or thymus‐bearing mice produced greater proportions of low‐avidity, TEPC 15‐negative antibody than control animals when challenged as adults with thymus‐dependent (TD) or ‐independent (TI) PC‐conjugated antigen. Furthermore, pretreatment had a greater inhibitory effect on responses elicited by TD compared with TI antigen. These results demonstrate that exposure of neonatal mice to PC‐protein conjugates results in the selective inactivation of higher avidity, T15‐positive, PC‐reactive B cells; this process is independent of thymic function and the duration of hyporesponsiveness is linked to the relative T dependency of th

ISSN:0014-2980    

DOI:10.1002/eji.1830130217

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY

ISSN:0014-2980    

DOI:10.1002/eji.1830130218

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY

ISSN:0014-2980    

DOI:10.1002/eji.1830130201

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY