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Biomedical subjects

C Jamin

Publications and source records attributed to C Jamin.

At least 19 recordsLinked to original sources
PubMed1998

The binding of some human antiendothelial cell antibodies induces endothelial cell apoptosis.

The pathogenic role of antiendothelial cell antibodies (AECA) remains unclear. They are frequently associated with antibodies to anionic phospholipids (PL), such as phosphatidylserine (PS), which is difficult to reconcile with the distribution of PL molecular species within the plasma membrane. Since it is already known that PS is transferred to the outer face of the membrane as a preclude to apoptosis, the possibility exists that apoptosis is initiated by AECA. AECA-positive/anti-PL antibody-negative sera from eight patients with systemic sclerosis (SS) and 21 control patients were evaluated. Endothelial cells (EC) were incubated with AECA and the exposure of PS was established through the binding of annexin V. Hypoploid cell enumeration, DNA fragmentation, and optical and ultrastructural analyses of EC were used to confirm apoptosis. Incubation of EC with AECA derived from six of eight patients with SS led to the expression of PS on the surface of the cells. This phenomenon was significantly more frequent in SS (P < 0.04) than in control diseases. The redistribution of plasma membrane PS preceded other events associated with apoptosis: hypoploidy, DNA fragmentation, and morphology characteristic for apoptosis. Apoptosis-inducing AECA did not recognize the Fas receptor. We conclude that AECA may be pathogenic by inducing apoptosis.

Annexin A5↗
PubMed1997

Modulation of CD72 by ligation of B cell receptor complex molecules on CD5+ B cells.

B cells expressing CD5 also carry its ligand, CD72. As an approach to understanding the role of CD5 and CD72 on B cells, we have examined the association of CD72 with CD5 and slgM by modulation/co-modulation and capping/co-capping following ligation of these surface molecules with specific antibodies. Modulation and co-modulation were measured after 24 h, whilst capping was measured after 1 h. CD5 and slgM co-modulated each other, CD72 co-modulated with slgM and CD5, but anti-CD72 did not affect either slgM or CD5. CD5 and slgM co-capped each other, whilst CD72 failed to co-cap with either slgM or CD5. The CD5-induced co-modulation of CD72 was partially blocked by specific protein tyrosine kinase inhibitor, but not the slgM-induced co-modulation, Protein kinase C (PKC) inhibitors abrogated the anti-mu- but not the anti-CD5-triggered modulation of CD72, whereas PKC activators prevented the CD5- but not the slgM-induced 24 h modulation of CD72. None of these drugs was able to modify the anti-CD72-induced modulation of CD72. Our data suggest that CD5 is physically associated with slgM in the B cell receptor complex but not with CD72. Furthermore, from the effect of drugs on modulation, there appears to be different associations of CD72 with slgM and CD5. These two pathways differed in some respects, consistent with a co-stimulatory function of CD72 and CD5 in B cell activation.

Antigenic Modulation↗
PubMed1997

[Estrogen replacement therapy: myth or reality?].

Before 50, women are protected against cardio-vascular diseases, and this protection disappears after this age. There are some strong epidemiologic arguments to attribute this loss of protection to the menopause. The ways of action of this hormonal shortage are still being discussed. Hypercholesterolemia seems to be a less important factor than with men, but signs of insulin resistance (hypertriglyceridemia, hypoHDLemia, androïd morphotype) play an important part. Estrogen HRT lowers coronarien risk, but published results are optimized by good health effect. Progestins do no affect results. The ways of action of estrogens are multiple. Some molecules and ways of administration have deleterious effects, the consequences of which are not known, in particular among patients with risk factors who would be the first to benefit from a preventive effect.

Coronary Disease↗
PubMed1996

Anti-CD5 extends the proliferative response of human CD5+ B cells activated with anti-IgM and interleukin-2.

The CD5 T cell glycoprotein which is expressed by a subset of B cells has been shown to be involved in T cell activation and proliferation. No similar studies, to date, have addressed the role of CD5 on the B cell subset. CD5+ and CD5- B cells were sorted and stimulated with anti-CD5 monoclonal antibody (mAb) in vitro. The activation and proliferative responses of these two populations, as measured by analysis of proliferation marker, did not differ following anti-mu and interleukin (IL)-2 stimulation. The addition of anti-CD5 did not change the responsiveness of such activated CD5+ B cells but resulted in a decrease in CD25 expression. Pre-activation of B cells with phorbol 12-myristate 13-acetate, which increased CD5 expression, failed to alter the proliferative response of CD5+ B cells to anti-mu and IL-2 with or without addition of anti-CD5 mAb. Anti-mu and IL-2 treatment of CD5+ cells resulted in optimal proliferation measured at day 3 which decreased by day 6. However, addition of anti-CD5 mAb at day 3 prevented this decline in proliferative response. This dose-dependent effect was observed only when the anti-CD5 mAb was presented to the B cells in cross-linked form. Co-stimulation of CD5 did not lower the threshold of antigen to which the B cells responded. Taken together, these data support a functional role for CD5 on B cells acting as an accessory signal, following their primary activation through the B cell receptor complex and highlight differences in the role of CD5 associated with the T cell receptor complex.

Antibodies, Anti-Idiotypic↗
PubMed1996

CD5+B cells: differential capping and modulation of IgM and CD5.

CD5 is associated with the B-cell antigen receptor (BcR) complex. As an approach to understanding its role in B-cell function, the authors investigated the capping and modulation of CD5 and surface IgM (sIgM). Tonsillar B cells were treated with anti-IgM or anti-CD5 antibodies, capping examined after 1 h (by fluorescence microscopy) and modulation after 24 h (by flow cytometry). CD5 co-capped and co-modulated with sIgM. Of various drugs tested, only the protein tyrosine kinase inhibitor (genistein) had any effect on capping and co-capping. Capping of sIgM (and co-capping of CD5) but not capping of CD5 (or co-capping of sIgM) was inhibited by genistein. None of the other drugs affecting PKC or cytoskeletal structures (colchicine and cytochalasin D) had any effect. However, the PKC inhibitors, staurosporine and H-7, inhibited the modulation of sIgM by anti-IgM but not CD5 by anti-CD5. In contrast, PKC activators, PMA and mezerein, inhibited modulation of CD5 by anti-CD5 but not sIgM by anti-IgM. This suggests that direct ligation of CD5 utilizes different signalling pathways compared with sIgM. It seems likely that in CD5+ cells, interaction of CD5 with its ligand CD72 modulates signals transmitted through the BcR.

Antibodies, Monoclonal↗
PubMed1996

Novel enzyme-linked immunosorbent assays for the detection of anti-Fc gamma receptor autoantibodies.

There is a substantial interest in the role of antineutrophil antibodies since Fc gamma receptors (Fc gamma Rs) have been identified as the target for the majority of such autoantibodies. Antineutrophil antibodies have long been detected by an indirect immunofluorescence technique. Following optimization of the flow cytometric method of detection, we developed three enzyme-linked immunosorbent assays (ELISAs), each specific for autoantibodies against one of the three classes of human Fc gamma R. Fc gamma RI and Fc gamma RII were purified from cultured cells, and Fc gamma RIII was produced as a recombinant molecule. These were then used as capture agents in the respective ELISAs. When applied in parallel to a sizeable group of patients with primary Sjögren's syndrome, both methods established that anti-Fc gamma R autoantibodies were heterogeneous. This finding indicates that different populations of partly cross-reactive antibodies are detectable by these two methods.

Autoantibodies↗
PubMed1996

Establishment and characterization of permanent human endothelial cell clones.

Though vasculitic diseases have been claimed to be associated with anti-endothelial cells antibodies (AECA), there is a widespread awareness of the limitations of the tests currently in use. Our objective was therefore to establish clones, in the hope that some of them would express disease-specific membrane autoantigens. Two EC lines and 7 clones were established by fusing human umbilical vein EC with epithelial A549/8 cells, and cloning by limiting dilution. An additional clone was derived from the EA.hy 926 cell line. All clones carried EC markers, such as thrombomoduline (TM) and platelet-EC adhesion molecule 1 but differed from each other, depending on whether they expressed HLA class II antigen, LFA-1, thrombospondin receptor or von Willebrand factor (vWf) antigen. Clones were also characterized by their ability to release tissue plasminogen activator, interleukin 6, TM and vWf. This panel is meant to distinguish reactivities of AECA.

Antibodies, Monoclonal↗
PubMed1996

[Hormonal replacement treatment: therapeutic protocols].

Hormonal replacement therapy concerns an increasing number of women: therefore it would be beneficial to vary its doses and administration modes in order to ensure the treatment's efficiency and innocuity. Furthermore, this treatment has to take into account the fact that women often wish not to have withdraw bleedings. It also has to adapt to various clinical situations like fibroids, adenomyosis, endometriosis, hysterectomy and old age. The general situation and particular cases are discussed in this text.

Age Factors↗
PubMed1996

Do some antiphospholipid antibodies target endothelial cells?

Anti-endothelial cell activity is partly due to antiphospholipid antibodies (aPLA) because: a) the two types of antibodies are present in patients with connective tissue diseases and cardiolipin-binding monoclonal antibodies recognize endothelial cells (EC); b) anionic phospholipids are detectable on the outer face of the EC membrane lipid bilayer and an anti-beta 2-glycoprotein I (beta 2-GPI) monoclonal antibody binds to EC; c) the binding of aPLA to EC and the functional affinity of this binding are dependent on the presence of beta 2-GPI; d) anti-EC antibodies trigger the expression of anionic phospholipids on the outer leaflet of the EC membrane.

Antibodies, Antiphospholipid↗
PubMed1995

Anti CD5 sustains the proliferative response of IgM-activated human CD5+ B cells.

The CD5 molecule is expressed by most T cells but it is present on a minor B cell subset. Whilst several studies have provided information on the physiological role of T cell CD5, the functional role of CD5 on B lymphocytes remains unclear. To address this question, tonsillar CD5+ B cells were sorted by dual-colour fluorescence and FACS. Sorted cells were stimulated with polyclonal anti-IgM antibodies (Ab), and monoclonal (MoAb) F(ab')2 fragments of anti-CD5. Proliferative responses were evaluated by enumeration of Ki-67 positive cells using quantitative flow cytometry. Co-stimulation with anti-CD5 MoAb for 3 days did not affect the anti-IgM and IL2-induced proliferation of CD5+ B cells. This was seen under conditions where the anti-CD5 was soluble, adsorbed to the microwells or cross-linked by anti-mouse antibodies. Fewer CD25+ cells were detected, however, in the presence of anti-CD5. In contrast, the proliferative response of CD5+ B cells prestimulated for 3 days with IL-2 and anti-IgM, was sustained in a further 3-day culture period when anti-CD5 was added. It is concluded that CD5 occupancy might provide an additional signal to activated CD5+ B cells favouring their proliferation and differentiation into autoantibody secreting cells.

Antibodies↗
PubMed1995

[Biological surveillance of hormone substitution: relying on the plasma levels of estradiol or the products used?].

The success of hormone substitution in menopaused women is widely recognized. Generally an oestrogen or a progesterone is used. The aim of this work was to determine whether the oestrogen treatment can be monitored on the basis of the induced plasma levels of oestradiol and whether there is any difference between specific products available. A review of the literature and personal observations concerning the pharmacokinetics of different oestrogen therapies has shown that the single assay of oestradiol is insufficient to adapt dosages and that different products are dosed differently giving variable reproductibility between the different formulations available.

Adult↗
PubMed1995

[Pregnancy after diagnosis of menopause].

Menopause is a probability diagnosis. Menopause does not mean permanent infertility, particularly in the case of premature menopause. We have realised a national enquiry in order to precise the pregnancy phenomenon after diagnosis of menopause. We found 116 pregnancy cases, which occurred 2.4 years (average) after menopause diagnosis. Pregnancies occur more often in the case of premature menopause and seem to be favoured by hormonal replacement therapy.

Adult↗
PubMed1993

CD5+ B cells and the immune system.

The CD5+ B-cell population is prominent in early life and may play a key role in the ontogeny of the immune system. Transplantation studies in mice are in support of CD5+ B cells as a separate lineage from CD5- B cells. In both mice and men there is evidence in favour of CD5 being an activation antigen rather than a lineage marker, but the jury is still out! The frequency of CD5+ B cells appears to be under genetic influence. CD5+ B cells are receptive to many cytokines including IL-2 and IL-5 and themselves produce a number of cytokines especially IL-10. The function of the CD5 molecule on B cells is presently unknown but it might be involved in interaction with CD72 on other B cells. CD5+ B cells generally utilise minimally mutated germ-line genes and produce low avidity auto- and polyreactive antibodies (natural antibodies) generally of the IgM class.

Animals↗