摘要:

AbstractThe AKR.H‐2bSL1 tumor cell line is susceptible to H‐2Kb‐restricted cytotoxic T lymphocytes (CTL) directed against the subclass of AKR endogenous leukemia virus‐induced tumors that express the Gross cell surface antigen (anti‐AKR/Gross virus CTL). A variant subclone (cl.18‐5) of AKR.H‐2bSL1 was isolated, whose susceptibility to lysis by conventional or cloned lines of anti‐AKR/Gross virus CTL was approximately 5% or less than that of the parental tumor. The cl.18‐5 variant was also ineffective when used as anin vivopriming cell or anin vitrostimulator cell in the generation of anti‐AKR/Gross virus CTL or as an unlabeled target cell in competitive inhibition assays. These results implied that the failure of cl.18‐5 to be lysed was due to a lack of recognition by the CTL.In contrast, cl.18‐5 was able to be lysed by and stimulate the generation of predominantly H‐2Db‐restricted CTL with apparent specificity for AKR minor histocompatibility antigens. The variant line was also about as susceptible as the parental AKR.H‐2bSL1 line to both allogeneic CTL and to H‐2Kb‐restricted, TNP‐specific CTL. Thus, the lack of recognition of cl.18‐5 by anti‐AKR/Gross virus CTL did not appear to be due to a failure to express functional H‐2 products or to a generalized insusceptibility to H‐2‐restricted CTL. Rather, cl.18‐5 appeared to be a selective variant and a useful probe for study

ISSN:0014-2980    

DOI:10.1002/eji.1830131102

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY

摘要:

AbstractDerived from the susceptible AKR.H‐2bSL1 tumor cell line, a variant tumor subclone, cl.18‐5, was selectively insusceptible to H‐2‐restricted anti‐AKR/Gross virus cytotoxic T lymphocytes (CTL) due to its failure to be recognized. In this study, the expression of virus‐related products by variant cl.18‐5 cells was compared to that of AKR.H‐2bSL1 cells and a susceptible clone, as an approach towards defining the virus‐associated antigens recognized by anti‐AKR/Gross virus CTL.Despite the type specificity of the CTL, cl.18‐5 displayed normal levels of the group‐specific antigen (gag) encoded proteins p30, p15, p12 and p10, and the gag‐associated Gross cell surface antigen. These results were confirmed by fluorescence‐activated cell sorter analysis employing monoclonal antibodies specific for either AKR p12 or the cell surface glycosylated form of AKR ecotropic gag product. In contrast, cl.18‐5 was variably less sensitive than AKR.H‐2bSL1 to the action of complement and xenogeneic antisera directed against the envelope (env) product gp70. In addition, a panel of five monoclonal antibodies to gp70, which detect distinct endogenous ecotropic viral determinants, lysed AKR.H‐2bSL1, but not cl.18‐5 cells. However, absorption experiments indicated that cl.18‐5 did express near normal levels of these specificities, suggesting an alteration in the orientation or topographical distribution of these determinants.Consistent with an inappropriate display of env products, cl.18‐5 was found to be deficient in the production of infectious ecotropic leukemia virus. The particulate fraction of the cell‐free supernatant of cl.18‐5 contained normal levels of reverse transcriptase activity, indicating that noninfectious viral particles were being produced. Collectively, these results point to an association between recognition by anti‐AKR/Gross virus CTL and the expression of eco

ISSN:0014-2980    

DOI:10.1002/eji.1830131103

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY

摘要:

AbstractWhen syngeneic lymphocytes and mitomycin C‐treated regenerating liver cells, prepared from partially hepatectomized mice, are cultured together, thein vitroDNA synthesis is activated (sMLHLR: syngeneic mixed hepatectomized‐liver cell‐lymphocyte culture). The Ia+Kupffer cells play an important role as stimulators in the response, since the stimulating activity of regenerating liver cells is lost either by the pretreatment with anti‐Ia monoclonal antibody plus complement or by the removing Kupffer cells from them. The lymphocytes are also activatedin vivoduring liver regeneration following partial hepatectomy. When lymphocytes, prepared from hepatectomized mice, are cultured with regenerating liver cells, the lymphocytes are stimulated to accelerate their DNA synthesis in a manner typical of the secondary immune responses (secondary sMLHLR). In primary sMLHLR, the responder cells are mainly Lyt‐1+, whereas, in secondary sMLHLR, they are mainly Lyt‐2+. The mechanism of changing the Lyt phenotype of major responder cells from Lyt‐1 to Lyt‐2 during sMLH

ISSN:0014-2980    

DOI:10.1002/eji.1830131104

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY

摘要:

AbstractThe lymph node cells (LNC) activatedin vivoby liver regeneration following partial hepatectomy of mice (primed lymph node cells) respond to regenerating liver cellsin vitrowith typical secondary immune response characteristics (Miyahara, S. et al.,Eur. J. Immunol.1983.13: 878). These LNC activatedin vivosuppress the proliferation of responder lymphocytes cultured with mitomycin C‐treated regenerating syngeneic liver cells (sMLHLR). The suppressive activity was already present in LNC 4 days after partial hepatectomy and remained unchanged for at least 16 days. These primed LNC were effective not only on sMLHLR but also on syngeneic mixed lymphocyte culture (sMLR) and allogeneic mixed lymphocyte culture, of which responder cells share the I‐A (I‐B) subregions of the major histocompatibility complex (MHC) with primed LNC. At least one cell in the suppressor circuit is a T cell. The primed LNC restimulatesin vitrowith regenerating liver cells (in vitroreactivated primed LNC) suppressed the proliferation of syngeneic responder cells in sMLR, but not of cells from congeneic mice differing from thein vitroreactivated primed LNC at a cluster of genes linked to the Ig locus. Thus the suppressive activity of primed LNC is controlled by the I‐A (I‐B) subregions of the MHC and that ofin vitroreactivated primed LNC by genes in the Ig region. The role of these suppressive cells in liver regeneration is

ISSN:0014-2980    

DOI:10.1002/eji.1830131105

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY

摘要:

AbstractThe involvement of rheumatoid factor (RF)‐secreting cells in normal immune responses was examined by screening hybridomas derived from 129/Sv mice during primary and secondary immune responses against foreign proteins. No RF‐secreting cells were detected during primary responses, but up to 10% of the total number of clones obtained during secondary responses produced IgM with anti‐IgG activity. Like typical mouse RF, these anti‐IgG autoantibodies had a strict isotypic specificity, mostly for IgG1, and a much stronger avidity for immune complexes than for native IgG. The selective activation of IgG1‐specific RF during these secondary immune reactions was not due to fortuitous antigenic similarities between mouse IgG1and the antigens used for immunization, nor did it result from the use of adjuvants for priming, or from contamination of antigen preparations with lipopolysaccharide. It is therefore concluded that, in the 129/Sv mouse, RF production during secondary immune responses is a physiological p

ISSN:0014-2980    

DOI:10.1002/eji.1830131106

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY

摘要:

AbstractProduction of IgM rheumatoid factor (RF) during secondary immune responses was studied in normal mouse strains by measuring RF synthesis in spleen cell cultures. A considerable, although transient, RF response was observed in BALB/c and C57BL/6 mice immunized and i. v. boosted with various protein antigens and with sheep erythrocytes. With most antigens, RF production equalled or exceeded that of antigen‐specific IgM, but it peaked and subsided earlier. No RF production was detected when either priming or boosting was omitted. The isotypic specificity of RF depended upon the antigens used for immunization: all proteins tested stimulated the synthesis of RF specific for IgG1, whereas sheep erythrocytes induced both IgG1‐ and IgG2a‐specific RF. Reconstitution experiments of irradiated naïve C57BL/6 mice with various combinations of syngeneic antibody against human transferrin and primed or unprimed spleen cells indicated that important RF responses could be induced only when antigen was injected into mice that had received both antibody and immune spleen

ISSN:0014-2980    

DOI:10.1002/eji.1830131107

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY

摘要:

AbstractIt has recently been demonstrated that the injection of adult mice with an affinitypurified goat antibody to mouse IgD (GaMδ) stimulates activation of the humoral immune system that resembles, on a polyclonal level, specific B cell activation by a T cell‐dependent antigen. One to 2 days after adult BALB/c mice are injected with 200 μg of GaMδ, their splenic B lymphocytes undergo a series of T‐independent activation steps that include increases in surface (s) Ia expression, cell size and DNA synthesis. Seven days after GaMδ injection, these cells undergo T‐dependent activation steps, that include further proliferation as well as differentiation into IgG1‐secreting cells. We have now studied the ontogeny of the T‐independent (day 2) and T‐dependent (day 7) activation steps by injecting 100–200 μg of GaMδ into 3‐day‐ to 10‐week‐old BALB/c mice. GaMδ failed to induce increases in B cell sIa expression or size 2 days after injection of mice 2 weeks old or younger and failed to stimulate increased DNA synthesis 2 days after injection of 4‐week‐old mice. In contrast, increases in spleen cell sIa expression, size and DNA synthesis were seen 7days after injection of 6‐ to 8‐day‐old mice. Furthermore, increases in the numbers of spleen cells with large amounts of intracytoplasmic IgG1were seen at the same time, although these increases were much less than were seen in GaMδ‐treated adult mice. Thus, the ability of GaMδ to induce T help and to act in concert with such help to stimulate B cell proliferation and differentiation precedes in ontogeny the ability of GaMδ to directly induce B cell proliferation and early differentiative events. In addition, the early activating events that we have studied are not required for T‐dependent B cell proliferation and antibody production to occur, althougt they appear to contribute to the magnitud

ISSN:0014-2980    

DOI:10.1002/eji.1830131108

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY

摘要:

AbstractT cell clones were selected which were cytotoxic for human class I major histocompatibility target antigens. Specificity was based on target cell panel studies and inhibition by monoclonal antibodies to class I determinants. Eight clones were Leu 2+3−. The cytotoxicity of these clones was inhibited by antibody to the Leu 2 antigen. Two clones expressed the Leu 2−3+phenotype and were not inhibited by anti‐Leu 2a or anti‐Leu 3a antibodies. These studies indicate that class I‐specific cytotoxic T cells are distributed in both T cell subsets, though predominantly in the Leu 2+3−group. In addition, these studies suggest that the Leu 3 molecule may not function in identical fashion in Leu 3+cytotoxic T cells, which recognize class I target antigens, as in those which recognize class

ISSN:0014-2980    

DOI:10.1002/eji.1830131109

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY

摘要:

AbstractThe present findings demonstrate that a total i. v. transfer of 100 × 106C57BL/6 (B6) parental spleen cells into untreated (C57BL/6 × DBA/2)F1hybrids (B6D2F1) resulted in acute runting, which was associated with a significantly elevated graft‐vs.‐host (GVH) index over a one‐month period following GVH induction. Furthermore, this B6‐induced acute GVH disease was associated with a marked depression of natural killer (NK) cell activity (spleen and peripheral blood) (with or without addition of mouse fibroblast interferon), which correlated with lymphoid cell hypocellularity, prominent splenic extramedullary hematopoiesis (EMH), and parallel depressions of both concanavalin A‐ and lipopolysaccharide‐induced mitogenesis. Significantly increased killing by antibody‐dependent cellular cytotoxicity of antibody‐coated chicken red blood cells, as well as increased T cell killing of the NK‐insensitive cell line P815 (as compared to the significantly decreased killing of the NK‐sensitive cell line YAC‐1) was also observed in the spleens of this 100 × 106B6‐injected F1group.In marked contrast to this 100 × 106B6‐injected acute GVH group, untreated mice injected i. v. with the same or greater numbers of parental DBA/2 spleen cells (100 × 106‐150 × 106DBA/2 spleen cells) exhibited a milder and more chronic form of GVH disease, which was not associated with a significant decrease of NK activity. It was of considerable interest that a total i. v. transfer of 50 × 106B6 spleen cells (i.e.one‐half of that required to produce acute GVH, markedly depressed NK, and prominent splenic EMH) into B6D2F1hybrids also resulted in a more chronic form of GVH disease, but was associated with significantly increased levels of NK acti

ISSN:0014-2980    

DOI:10.1002/eji.1830131110

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY

摘要:

AbstractSeveral monoclonal antibodies (mAb) against rabbit leukocytes were characterized in binding and functional studies. mAb 1.24 stains thymocytes, bone marrow cells, peripheral T and B cells and blood monocytes. T cells express more 1.24 antigen than B cells. In the absence of added complement (C), mAb 1.24 inhibits alloantigen‐, concanavalin A (Con A)‐, and phytohemagglutinin (PHA)‐, but not pokeweed mitogen (PWM)‐ or anti‐immunoglobulin (Ig)‐induced cell proliferation. It also strongly blocks anti‐sheep erythrocyte plaque‐forming cell responses. A second mAb, designated 4.B9, binds to 20% of thymocytes and to most, if not all, peripheral T cells andin vitro‐activated T cell blasts. A third one, 10.B3, is reactive with the nearly entire thymocyte and a major peripheral T cell population. Two‐color membrane immunofluorescence reveals the presence of a small population of peripheral blood leukocytes which bear surface Ig and are weakly stained by mAb 4.B9 and 10.B3. Without C, both 4.B9 and 10.B3 inhibit Con A‐ and PHA‐induced mitogenesis, but have no effect on PWM‐, antigen‐, or alloantigen‐induced cell proliferation. Depletion of 4.B9+cells by panning or complement lysis completely abrogates proliferative responsiveness to antigen and alloantigen, significantly reduces responsiveness to the T cell mitogens Con A and PHA, but enhances that to the B cell mitogen anti‐Ig. A fourth mAb, 12.C7, binds to 60% of thymocytes and to 10–30% of peripheral T lymphocytes at high‐level fluorescence. T cell blasts obtained in mixed leukocyte reactions are partially stained by mAb 12.C7, while those obtained after Con A or PHA activation are not. In addition, mAb 12.C7 is completely unreactive with B cells or monocytes. Without complement, it does not seem to interfere with any of thein vitrofunctions tested. All antigens studied here do not appear to be expressed in nonleukon tissues, as they do not bind to erythrocytes and are absent from brain, heart, liver and kidney as shown

ISSN:0014-2980    

DOI:10.1002/eji.1830131111

出版商:WILEY‐VCH Verlag GmbH    

年代:1983

数据来源: WILEY