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J Vives

Publications and source records attributed to J Vives.

At least 73 records · Page 4Linked to original sources
PubMed1991

The protein kinase C-independent human B cell proliferation induced via surface immunoglobulins is unaffected by CD45 monoclonal antibodies.

In the present study the effect of 72-5D3 monoclonal antibody (CD45) on the proliferation induced by cross-linking of surface immunoglobulins on untreated and 4 beta-phorbol 12-myristate 13-acetate-treated human dense B cells was studied. The 72-5D3 mAb inhibited the proliferation induced via surface immunoglobulins alone or plus soluble T cell factors without affecting the release of inositol phosphate metabolites. However, after prolonged incubation (24 h) with high doses (100 ng/ml) of 4 beta-phorbol 12-myristate 13-acetate or mezerein, but not with 4 beta-phorbol, the same inhibitory effect did not take place. Therefore, our data support the hypothesis that protein kinase C is necessary for the antiproliferative effect of the 72-5D3 monoclonal antibodies.

Antigens, CD↗
PubMed1991

Serum levels of secretory IgA in ankylosing spondylitis.

An ELISA test was performed in order to measure the serum levels of secretory IgA (sIgA) in 51 patients with ankylosing spondylitis (AS) and 30 healthy controls. Raised values of sIgA were found in AS patients compared to controls. Patients with active disease, defined by clinical criteria, showed a significant elevation of serum sIgA compared to healthy controls (p = 0.03) or to patients with inactive disease (p = 0.02). A positive correlation between total serum IgA and sIgA was found (p = 0.001). Our findings further support the role of the mucosal stimulation in the pathogenesis of AS.

C-Reactive Protein↗
PubMed1990

Phosphorylation-mediated changes in the electrophoretic mobility of CD5 molecules.

This work shows that tumor promoter agents (TPA) induce the post-translational modification of the human lymphocyte surface CD5 antigen (Tp67) in several cellular types. Treatment of [32P]orthophosphate- and [35S]cysteine-labeled normal and lymphoblastoid T and B cells with active tumor promoters induced the rapid, transitory and dose-dependent appearance of hyperphosphorylated CD5 forms with higher apparent molecular masses. These changes in the electrophoretic mobility of CD5 molecules were independent of RNA and protein synthesis, as well as of differences in neuraminic acid content. The inhibition of the TPA-mediated changes by protein kinase C inhibitors (staurosporine and 1-(5-isoquinolylsulfonyl)-2-methylpiperazine) indicated its protein-kinase-C-mediated nature. Phosphatase digestion of CD5 immunoprecipitates reverted the TPA-mediated mobility changes showing its dependence on phosphorylation. Neuraminidase digestion of intact cells revealed that the target of the TPA effects are surface-expressed CD5 molecules. In conclusion, we suggest that the heterogeneity in the electrophoretic mobility induced by TPA could reflect some structural and/or functional differences within CD5 molecules.

Antigens, Differentiation↗
PubMed1990

CD27 induction on thymocytes.

CD27 mAb recognize a disulfide-linked homodimer of 55 kDa present in the majority of T cells and in a minor subpopulation of thymocytes. Although an increase of CD27 expression has been described in activated T cells, this Ag is poorly expressed in long term growing T cells. It has been also reported that CD27- becomes CD27+ upon activation. In the aim to better know the relationship between CD27 expression and the activation and maturation processes, the induction of this Ag in thymocytes was analyzed. The results obtained in this work show that: 1) CD27 is expressed only in thymocytes with high CD3 Ag density. 2) Its expression can be induced in low density CD3 CD4+ CD8+ cells by Con A and in low CD3 Ag density by PMA+ionomycin. 3) PMA alone or in combination with rIL-2 induces CD25 and CD71 expression but not CD27. 4) Unlike CD27, the Ag CD45RA, CD26, and CD76, which are present only in a minor thymocyte subpopulation, are not induced in double positive thymocytes. Because it has been reported that cyclosporin A interferes with thymocytes maturation and blocks the transition from double to single positive cells, its effect was measured on CD27 induction. Cyclosporin A did not inhibit CD25 expression induced by both Con A and PMA+ionomycin, but under these conditions it inhibited the induction of CD27. In this paper we discuss whether CD27 could be implicated in T cell maturation.

Antibodies, Monoclonal↗
PubMed1990

Differential effects of anti-CD45 monoclonal antibody on human B cell proliferation: a monoclonal antibody recognizing a neuraminidase-sensitive epitope of the T200 molecule enhances anti-immunoglobulin-induced proliferation.

We have generated seven monoclonal antibodies (mAb) that recognize the T200 molecule. These mAb have been classified by competitive binding assay in flow cytometry into three groups each reacting with a different epitope of the T200 molecule: (a) 136-4B5, that shows a sialic acid nature, (b) 135-4H9, 135-4C5, 144-2, 155-2 and (c) 72-5D3, 124-2H12b. A heterogeneous effect was observed when they were tested on an anti-immunoglobulin-induced B cell proliferation. Whereas 72-5D3 and 135-4H9 mAb inhibited the proliferative response of B cells, 136-4B5 mAb greatly enhanced it, both effects being dose dependent. We can conclude that anti-CD45 mAb have a different and contrary functional behavior on anti-Ig-induced B cell proliferation, depending on the epitope recognized. The basis for such a difference could reside in the glucidic nature of the epitope recognized by the 136-4B5 mAb.

Antibodies, Anti-Idiotypic↗
PubMed1990

Inhibitory effect of IL-4 on the sepharose-CD3-induced proliferation of the CD4CD45RO human T cell subset.

CD45R monoclonal antibodies are able to distinguish two different subsets of the CD4 human T cells. This phenotypic split is accompanied by functional diversity. In this report we have analyzed the capabilities of CD45R subsets of CD4 human T cells to use interleukin 2 (IL-2) and IL-4 as growth factors. We have found that both cell subsets are able to proliferate after stimulation with Sepharose-CD3 in the presence of externally added IL-2 or IL-4. However, the response to IL-4 of CD4CD45RO cells was comparatively lower than the response of CD4CD45RA cells. Both cell subsets showed a good response to Sepharose-CD3 plus adherent cells (AC), but when IL-4 was present in the culture only the CD4CD45RA cells showed an enhancement in the Sepharose-CD3-induced proliferation, while proliferation of the CD4CD45RO T cell subset was inhibited. Similar effects were seen, however, in the response to CD4CD45RA or CD4CD45RO cells to Sepharose-CD3 plus IL-2. Although the precise mechanism of the inhibitory effect of IL-4 is not known, the results obtained suggest that IL-4 could interfere in some way with the signalling of IL-2 to the proliferation of the CD4CD45RO T cell subset.

Antigens, Differentiation↗
PubMed1990

Involvement of the CDw50 molecule in allorecognition.

The CDw50 differentiation antigen is defined by 101-1D2 and 140-11 monoclonal antibodies (mAb), both produced and characterized in our laboratory. This molecule is broadly expressed on hematopoetic cells but not on other cells. In this report we show that these 2 mAb recognize different epitopes of the same molecule, which are resistant to neuraminidase and proteases. We also demonstrate that the CDw50 antigen is expressed on thymocytes and T lymphocytes as an N-glycosylated glycoprotein monomer with a relative molecular weight (Mr) of 130,000 daltons with intrachain disulfide bonds, and that this molecule is resistant to treatment with phosphatidylinositol (PI) phospholipase C and therefore probably not PI-anchored to the membrane. CDw50 is a poorly or non-constitutively phosphorylated molecule that becomes phosphorylated by treatment with phorbol 12-myristate 13-acetate (PMA) of peripheral blood mononuclear cells (PBMC). The addition of affinity-purified CDw50 mAb inhibits primary mixed lymphocyte culture (MLC) but not secondary MLC, cytotoxicity or proliferation induced by mitogens. The inhibition of alloreactivity is mediated at the level of both responding and stimulator cells.

Antibodies, Monoclonal↗
PubMed1990

Protein kinase C-dependent up-regulation of CD5 surface expression on normal and lymphoblastoid T cells.

As an approach to study the mechanisms regulating the surface expression of CD5 antigen on T cells, the effects of agents that activate different lymphocyte functions were examined. Active tumour promoter agents (TPA), such as phorbol ester analogues [phorbol 12-myristate 13-acetate (PMA), phorbol 12, 13-dibutyrate (PBu2)] and mezerein, were able to increase the expression of CD5 on the cell surface of all T-cell lines), as deduced from immunofluorescence and immunoprecipitation analysis. The TPA-induced CD5 up-regulation occurred in a dose-and time-dependent manner and was dependent on protein and RNA synthesis. From the other stimuli tested, the T-cell mitogens [phytohaemagglutinin (PHA) and concanavalin A (Con A)], as well as monoclonal antibodies (mAb) against the CD3 complex, also increased CD5 expression, although to a lesser degree. In all cases the increments were shown to be dependent on protein kinase C (PKC), as evidenced by their inhibition with staurosporine, a potent inhibitor of PKC activation. These data suggest that CD5 up-regulation on T cells can be a physiological event that depends on PKC activation.

Antigens, Differentiation↗
PubMed1989

Heterogeneity in the electrophoretic mobility of CD5 molecules after phorbol ester stimulation.

As judged by Western blot analysis, phorbol 12-myristate 13-acetate (PMA) and phorbol 12,13-dibutyrate (PDBU) induce the rapid and dose-dependent appearance of slower mobility CD5 molecular forms from peripheral blood mononuclear cell (PBMC) and thymus cell lysates. This phenomenon was inhibited by staurosporine, suggesting that it can be mediated by PKC activation. Furthermore, under our experimental conditions, neither Concanavalin A, nor Phytohaemagglutinin P or the calcium ionophore A23187 were able to reproduce the phorbol ester-induced changes in the CD5 electrophoretic mobility. When immunoprecipitated from phorbol ester-stimulated P32 labelled PBMC lysates, the slower mobility of CD5 molecules was associated to important phosphorylation. This special electrophoretic behaviour after phorbol ester-stimulation makes CD5 different from other lymphocyte surface glycoproteins and may have important implications in the elucidation of the biological role of this molecule as discussed below.

Alkaloids↗
PubMed1989

Responsiveness of systemic lupus erythematosus T cells to signals provided through LCA T200 (CD45) and T1 (CD5) antigens.

It is currently unclear whether the T cell defective capacity to proliferate and to secrete interleukin-2 (IL-2) observed in systemic lupus erythematosus (SLE) reflects an intrinsic disorder of the T cell or defects secondary to a monocyte dysfunction. In order to clarify whether the disorder is intrinsic to the T cell, we have studied the proliferative capacity of cells highly depleted of monocytes, activated by Seph-CD3, as 'first signal,' and by monoclonal antibodies (MoAbs) CD45 and CD5 as 'second signal,' in 14 SLE patients. There were no significant differences between SLE patients and healthy volunteers in the response of the monocyte-depleted cells to Seph-CD3+CD45; Seph-CD3+CD5; Seph-CD3+IL-2; and Seph-CD3+phorbol myristate acetate (PMA). However, active SLE compared with non-active SLE had an impaired response of peripheral blood mononuclear cells (PBMC) to Seph-CD3 and to Seph-CD3+IL-2. The good responses obtained to second signals provided through CD45 and CD5 indicate that at least these mechanisms are not intrinsically impaired in SLE T cells. These findings, together with the abnormal response of PBMC suggest that a monocyte dysfunction plays an important role in SLE T cells hyporesponsiveness.

Adolescent↗
PubMed1988

Changes in idiotypic predominance in the anti-arsonate response by priming with anti-idiotypic antibodies.

The predominant selection of CRI-A-bearing antibodies during the anti-arsonate (ARS) response of A/J mice has been used as a model to analyse the mechanism involved in the process of clonal selection and establishment of predominance. In order to assess the importance of the affinity and adaptability of CRI-A clones in this process, we tested the capability of a minor recurrent idiotype (id-1A3), present in a CRI-Aanti-ARS monoclonal antibody (65-1A3), to develop a normal anti-ARS response. Our results show that the id-1A3 predominance, established by anti-id-1A3 administration was stable during the primary and secondary anti-ARS response and that this predominance occurred concomitantly with low levels of CRI-A. Thus, a change in the idiotype predominance was achieved. In spite of the high levels of id-1A3, the anti-ARS antibody concentration, the affinity values, and the kinetics of the immune response were similar to those of the control group. All these results show that CRI-A clones are not essential in the normal development of the anti-ARS antibody response of A/J mice, and suggest that factors other than affinity could be involved in the establishment of the CRI-A predominance.

Animals↗
PubMed1987

A second signal for T cell mitogenesis provided by monoclonal antibodies CD45 (T200).

The 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 IL2 and bypasses the necessity of monocytes.

Animals↗
PubMed1987

CD43 monoclonal antibodies recognize the large sialoglycoprotein of human leukocytes.

In this study data are presented indicating that the molecule identified by the recently described CD43 cluster of monoclonal antibodies (mAb; Oxford, 1986) is the human analogue to the one originally described in rat as leukocyte sialoglycoprotein (LSGP). This conclusion is based on several criteria. Both molecular mass (105 kDa) and cellular distribution are similar to the antigens previously described in the rat with the mAb W3/13 and subsequently in humans with L10 mAb. Sialidase treatment of the molecule immunoprecipitated by 84-3C1 mAb (CD43) resulted in a decreased electrophoretic mobility on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. L10 mAb inhibited the binding of 84-3C1 mAb to the cell membrane suggesting that both mAb recognized the same molecule. Moreover, the presence in the CD3-4-8- thymic populations of the sialidase-sensitive epitope recognized by mAb 84-3C1 suggests that there is no simple correlation between the thymic maturation and the degree of sialylation.

Amino Acids↗