摘要:

AbstractThis report describes a surface molecule, Tp45, which appears to be involved in interleukin 2 production and Ca2+mobilization by Jurkat cells. The Tp45 molecule was identified by a monoclonal antibody, MX13, on the surface of either T3/TCR+or T3/TCR−human T cell lines. Biochemical data showed that mAb MX13 precipitated a single polypeptide chain of 45 kDa both under reduced and nonreduced conditions from lysates of125I‐surface‐labeled cells. Sequential immunodepletion experiments using lysates of125I‐labeled T3/TCR+cells showed that Tp45 was distinct from the α chain of the TCR complex. However, incubation of such cells with either anti‐T3 or anti‐TCR monoclonal antibody induced complete modulation of both the T3/TCR complex and Tp45. Conversely, complete modulation of both Tp45 and the T3/TCR complex was observed after incubation with anti‐Tp45 antibody. Functional studies showed that anti‐Tp45 antibody induced high levels of interleukin 2 production in Jurkat cells. In addition, incubation of these cells with the antibody resulted in Ca2+mobilization from internal stores.Anti‐Tp45 antibody reacted with 3–19% peripheral blood (E‐rosette‐positive) T cells in individual donors. The magnitude of the proliferative response elicited by anti‐Tp45 antibody for peripheral blood T cells was lower than that induced by an anti‐T3 antibody. This observation is compatible with the idea that only a subpopulation of T cells is reactive with anti‐Tp45. Multicolor flow cytometry analysis showed that the Tp45+cells belong p

ISSN:0014-2980    

DOI:10.1002/eji.1830171002

出版商:WILEY‐VCH Verlag GmbH    

年代:1987

数据来源: WILEY

摘要:

AbstractA potent immunosuppressive factor isolated from malignant ascites fluids showed serological cross‐reactivity with the E‐receptor of human peripheral blood T lymphocytes. Thus, this factor was named suppressive E‐receptor (SER) factor. In this study, we examined the effect of this immunosuppressor, SER, on lymphokine functions of human mononuclear cells participating in polyclonal T cell activation.SER is active at nanomolar concentrationsin vitroand the inhibitory effect of SER was most pronounced when added at the initiation of stimulation with phytohemag‐glutinin or anti‐T3 antibody. Concomitant with the inhibition on PHA‐induced DNA synthesis, lymphocytes that were treated with SER failed to progress beyond G1phase of cell cycle. These growth‐arrested cells did expire after 7 days of culturein vitro. This anti‐proliferative effect of SER was more easily demonstrated with normal lymphoid cells in culture than transformed cells or fibroblast cells. SER effectively interfered with the lympho‐proliferative properties of interleukin 2 (IL2) on human peripheral blood mononuclear cells and an IL2‐dependent murine cytotoxic T cell line. However, excess quantities of exogenous IL2, especially when added in conjunction with IL1, were able to partially overcome the ability of SER to inhibit T cell proliferation.In contrast to the inhibition on DNA synthesis of human lymphoblasts, expression of IL2 receptor was only minimally inhibited by SER during the first 24 h of culture (24% inhibition at 12 h and 34% inhibition at 24 h) but it was followed by full expression of IL2 receptor by 48 h. Thus, SER merely reduced the rate of expression of IL2 receptor and was not able to inhibit the transcription of new message from activated T lymphocytes. Taken together, these studies indicate that SER acts as a noncytolytic anti‐proliferative factor on immune responses that are mediated by T cells. SER appears to act on a relatively late event during T cell activation, perhaps on some portion of the DN

ISSN:0014-2980    

DOI:10.1002/eji.1830171003

出版商:WILEY‐VCH Verlag GmbH    

年代:1987

数据来源: WILEY

摘要:

AbstractHuman mononuclear leukocytes produce a growth factor (HGF) for hybridoma and plasmacytoma cells. HGF has recently been proven to be identical to IFN‐β2, 26‐kDa protein and BSF‐2. HGF can be quantitated in a proliferation assay with the HGF‐dependent hybridoma cell line B13.29. By selection of an extremely sensitive variant of this cell line, we were able to measure HGF production of single cells. Limiting dilution analysis of the producing cells in combination with size, density and adherence characteristics showed that HGF is produced by monocytes and not by lymphocytes. There was no need for the monocytes to be stimulated but the cells did require the presence of serum. This serum requirement could be met by purified bovine serum albumin, but not by other proteins like ovalbumin or human γ‐globulin. HGF productionin vitroby monocytes starts after 2 h of incubation and is completed

ISSN:0014-2980    

DOI:10.1002/eji.1830171004

出版商:WILEY‐VCH Verlag GmbH    

年代:1987

数据来源: WILEY

摘要:

AbstractExperimental infections withTrypanosoma bruceiAnTat 1.1. E not only account for a suppression of interleukin 2 (IL2) production, but also induce an impairment of IL2 receptor expression. Indeed, lymph node cells derived from infected mice failed to express IL2 receptors following mitogenic stimulation as compared to normal controls. This impairment was not attributed to a modulation of the number of T cells and was not caused by the presence of living parasites. Furthermore, the basal level of IL2 receptor expression could not be re‐established through the exogenous supply of recombinant IL2. This impairment of receptor expression was found to be mediated by suppressive cells that affect the relative number of receptor‐positive cells as well as the mean receptor density. On the other hand, the mitogen‐induced secretion of other T cell‐derived lymphokines was not inhibited during infection, indicating that the severe suppression of IL2 regulation was not attributed to a total paralysis of the T cell respons

ISSN:0014-2980    

DOI:10.1002/eji.1830171005

出版商:WILEY‐VCH Verlag GmbH    

年代:1987

数据来源: WILEY

摘要:

AbstractThe immunocytochemical characteristics of large granular lymphocytes (LGL), isolated from the liver sinusoids of euthymic and athymic (nude) rats, were investigated in electron microscopy by the immunoperoxidase technique. The LGL were found positive for MRCOX‐8 (natural killer cells and cytotoxic/suppressor T cells) and negative for MRCOX‐19 (pan‐T marker) in both rat strains. The LGL were heterogeneous in the expression of the natural killer cell marker asialo‐GM1 which was found on 56% of the LGL from euthymic and on 71% of the LGL from athymic rats. LGL were easily distinguished from the other cells in the preparations, “conventional” lymphocytes and monocytes, thanks to their highly characteristic ultrastruc‐tural features, in particular by the presence of specific electron‐dense cytoplasmic granules and rod‐cored vesicles. These features have been described formerly for the so‐called “pit cells” and are more reliable than the classical LGL characteristics at the light microscopic level,i.e.the presence of azurophilic granules. Our results give further support for the existence of an important population of natural killer cells

ISSN:0014-2980    

DOI:10.1002/eji.1830171006

出版商:WILEY‐VCH Verlag GmbH    

年代:1987

数据来源: WILEY

摘要:

AbstractThe involvement of Lyt‐2+T cells in the immunological control of cutaneous leishmaniasis was assessed by studying the course of the disease in mice in which the number of these cells was reduced by treatment with anti‐Lyt‐2 monoclonal antibody (mAb). Administration of anti‐Lyt‐2 mAb exacerbatedLeishmania major‐induced cutaneous lesions in both genetically resistant and susceptible mice. This effect correlated with a drastic reduction in the number of specific Lyt‐2+T cells generated during infection. These results, together with the observation that resistant mice possess higher numbers of specific Lyt‐2+T cells in lymph nodes draining their lesions than susceptible mice, 3 weeks after infection, indicate that Lyt‐2+T cells also play a role in the immunological control ofLeishmania majo

ISSN:0014-2980    

DOI:10.1002/eji.1830171007

出版商:WILEY‐VCH Verlag GmbH    

年代:1987

数据来源: WILEY

摘要:

AbstractThe human 26‐kDa glycoprotein (26K) is a cytokine produced by lymphoid as well as nonlymphoid cells. So far it is active as (a) a potent hybridoma and plasmacytoma growth factor on mouse cells, (b) a B cell differentiating factor on human cells, and (c) (for some authors) an interferon (IFN). Internally labeled recombinant human 26K, obtained by translation of mRNA inXenopusoocytes, was used to investigate the presence of specific receptors for this new cytokine and to analyze its binding to responsive cells. The results indicate that (a) the 26K‐responsive human lymphoblastoid CESS cells express about 1500 high‐affinity (Kd= 30 pM) binding sites for this cytokine, (b) this binding is not competed for by interleukin (IL)1, IL2, tumor necrosis factor (TNF), IFN‐α2, IFN‐β or IFN‐γ, and (c) these 26K‐binding sites are different from the classical type I (α‐β) IFN receptors by sodium dodecyl sulfate‐polyacrylami

ISSN:0014-2980    

DOI:10.1002/eji.1830171008

出版商:WILEY‐VCH Verlag GmbH    

年代:1987

数据来源: WILEY

摘要:

AbstractThe expression of major histocompatibility complex (MHC) class II antigens is down‐regulated when B cells differentiate into plasma cells. We have studied the mechanism of down‐regulation of MHC class II expression in a BALB/c strain‐derived murine plasmacytoma cell line, NS1. NS1 cells express MHC class I antigens but not MHC class II antigens. We tested 20 uncloned hybrid cell lines obtained from the fusion of NS1 cells with MHC class II‐expressing splenic B cells prepared from CBA, SJL or BALB/c mice. All the hybrid cell lines expressed MHC class I antigens of either or both parental haplotypes but did not express MHC class II. One NSI × splenic B cell hybrid clone, K3, was used to further validate these results; K3 cells expressed MHC class I but not MHC class II antigens. K3 was fused to the MHC class II‐expressing B lymphoma A20, and the seven resulting hybrid cell lines were again found to express MHC class I but not MHC class II antigens. Since NS1 is a subclone of the P3‐X63Ag8 murine plasmacytoma, we also tested one P3‐X63Ag8 × splenic B cell hybrid, Sp2/0, and two Sp2/0 × splenic B cell hybrids. All were found to express the appropriate MHC class I antigens but did not express MHC class II. Thus, our results suggest that the NS1 plasmacytoma suppresses MHC class II expression by a phenotypically dominant regulatory mechanism. We found that NS1 cells express correctly sized mRNA for the MHC class II genes Aα, Eα and the invariant chain. The co‐expression of MHC class I protein and I‐A and I‐E region gene transcripts provides strong evidence that the MHC gene cluster is structurally intact, and that lack of class II expression is due to a genetic regulatory mechanism. The amounts of class II mRNA expressed by NS1 cells were at least equivalent to those found in splenic lymphocytes. Therefore, this regulation must operat

ISSN:0014-2980    

DOI:10.1002/eji.1830171009

出版商:WILEY‐VCH Verlag GmbH    

年代:1987

数据来源: WILEY

摘要:

AbstractThe induction of T cell mitogenesis through CD3 is a complex process that requires at least two signals. The first one can be provided by Sepharose‐bound CD3. The second one is normally provided by monocytes. The signal provided by Sepharose‐bound CD3 is unable by itself to induce mitogenesis in monocyte highly depleted cells (MHDC).We describe here that the monoclonal antibody (mAb) 72‐5D3 belonging to CD45 (T200), which was not mitogenic by itself, could replace monocytes when MHDC were activated by Sepharose‐bound CD3. That is to say, in the absence of monocytes, mAb 72‐5D3 gave a second signal necessary for T cell proliferation. Using eleven anti‐CD45 mAb from other investigators we show that this effect is not a peculiar characteristic of 72‐5D3 mAb. The effect of the mAb 72‐5D3 was only effective in CD4‐positive cells and was not observed when MHDC were activated with either soluble CD3 or concanavalin A.As both phorbol myristate acetate and mAb 72‐5D3 can replace monocytes, a comparative study of their effects was undertaken. Phorbol myristate acetate but not mAb 72‐5D3 induced proliferation of MHDC when recombinant interleukin 2 (rIL2) was added. On the other hand mAb 72‐5D3 induced IL2 production in MHDC activated by Sepharose‐bound CD3 and increased the IL2 production in Sepharose‐bound CD3‐activated peripheral blood mononuclear cells.In conclusion, data presented in this report indicate that the T200 molecule could be involved in T cell proliferation by giving a signal that induces the production of IL 2 and bypass

ISSN:0014-2980    

DOI:10.1002/eji.1830171010

出版商:WILEY‐VCH Verlag GmbH    

年代:1987

数据来源: WILEY

摘要:

AbstractThe properties of the mononuclear phagocyte (Mph) high‐affinity Fc receptor, FcRI, were investigated using a novel monoclonal antibody (mAb) designated 10.1. This receptor was shown to be a protein of 71 kDa, presented chiefly on monocytes and the myeloid cell lines U937 and HL60. mAb 10.1 inhibited the binding to Mph of erythrocytes opsonized with rabbit IgG or human IgG3. It also blocked T cell proliferation induced by murine CD3 mAb of the IgG2abut not the IgG1subclass. These results suggest that rabbit IgG, human IgG3and murine IgG2aall bind to FcRI in a similar manner and that mAb 10.1 reacts with an epitope on FcRI near to the binding site for the Fc region of IgG. In addition, although it is well known that FcRI has a high affinity for both monomeric human IgG1and IgG3, we show in this study that while erythrocytes opsonized with human IgG3bind to Mph, equivalent cells opsonized with IgG1surprisingly do not. These results define further the nature of the constraints on the interaction between Mph FcRI and particular IgG

ISSN:0014-2980    

DOI:10.1002/eji.1830171011

出版商:WILEY‐VCH Verlag GmbH    

年代:1987

数据来源: WILEY