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Biomedical subjects

C Jamin

Publications and source records attributed to C Jamin.

At least 37 records · Page 2Linked to original sources
PubMed2001

Soluble Fcgamma receptor IIIb alters the function of polymorphonuclear neutrophils but extends their survival.

We have established that polymorphonuclear neutrophil (PMN)-binding anti-Fcgamma receptor IIIb (FcgammaRIIIb) autoantibodies (autoAb) inhibit the function of these cells but extend their survival. Here, we show that recombinant FcgammaRIIIb (rFcgammaRIIIb), as well as purified FcgammaRIIIb (pFcgammaRIIIb), deteriorated the PMN adherence and respiratory burst in a dose-dependent manner. Furthermore, rFcgammaRIIIb and pFcgammaRIIIb reduced the level of annexin V-binding PMN from 23.6 +/- 1.6 % to 6.3 +/- 1.0 and 11.0 +/- 1.0 %, respectively, while human serum albumin exerted no effects. Incubation of rFcgammaRIIIb with those autoAb binding to soluble FcgammaRIIIb resulted in the attachment of such immune complexes (IC) to the cells, thereby also delaying apoptosis (44.9 +/- 5.9 versus 18.0 +/- 2.0 % annexin V-binding PMN after 16 hours). Soluble FcgammaRIIIb, in concert with FcgammaRIIIb / anti-FcgammaRIIIb IC, produced similar effects in that the percentage of annexin V-binding PMN declined to 16.0 +/-1.9 %. It was thus suggested that FcgammaRIIIb / anti-FcgammaRIIIb IC inserted the Fc region of their IgG into the membrane FcgammaRIIIb. Such an interpretation is consistent with our finding that, whereas aggregated IgG and anti-FcgammaRIIIb monoclonal Ab prevented membrane FcgammaRIIIb / IC interaction, neither soluble FcgammaRIIIb, nor anti-cgammaRII did so. We conclude that the function and the life span of PMN are influenced synergistically by soluble FcgammaRIIIb and anti-FcgammaRIIIb autoAb.

Antigen-Antibody Complex↗
PubMed2001

[Evaluation of weight and morphotype of French women in gynecological consultation].

Weight and morphology change with age in proportions which depend on numerous environmental factors. This French study on 3,000 women age between 40 and 70, seeing their gynecologist, has shown that the average body mass index of this population is 23.97 kg/m2, and that the waist hip ratio is 0.81. Those two parameters increase with age and are reduced when women have a physical activity for more than 2 hours a week and are on oral contraception or hormone replacement therapy. Women on percutaneous hormone replacement therapy have a lower body mass index and a lower waist hip ratio. Cigarette smoking goes with a lower body mass index. When it dates back to more than 5 years, menopause is associated with a body mass index increase. In this population, the proportion of women under hormone replacement therapy is 69%, mostly percutaneous estrogenotherapy on a discontinuous sequential rhythm.

Administration, Cutaneous↗
PubMed2001

Functional heterogeneity of anti-endothelial cell antibodies.

While it has been claimed that some anti-endothelial cell antibodies (AECA) activate EC, there is also evidence that others trigger apoptosis. To address the issue of whether activation is a prerequisite for AECA-mediated apoptosis of EC, 23 AECA-positive sera were evaluated for their ability to induce activation and/or apoptosis. Activation was defined as an over-expression of E-selectin and intercellular adhesion molecule 1. Optical microscopy, annexin V binding, hypoploid cell enumeration, and determination of poly (ADP-ribose) polymerase cleavage-related products were used to assess apoptosis. Four functional profiles were defined: 10 sera promoted activation and apoptosis (act+/apo+), one was act+/apo-, six act-/apo+, and the remaining six act-/apo-. The reduced membrane expression of thrombomodulin was associated with apoptosis, rather than activation. Caspase-3 was implicated in the two models of apoptosis, the ratios of several survival proteins to Bax decreased, regardless of the ability of apo+ AECA to activate the cells, while radical oxygen species did not appear to be involved. Furthermore, it occurred that macrophages engulfed EC treated with apoptosis-promoting AECA, but not those incubated with AECA that did not induce apoptosis. Hence, AECA represent an extremely heterogeneous family of autoantibodies, not only because of the variety of their target antigens, but also the subsequent diversity of their effects.

Antibody Diversity↗
PubMed2001

APC resistance and third-generation oral contraceptives: Acquired resistance to activated protein C, oral contraceptives and the risk of thromboembolic disease.

Using a newly-developed technique, a severe acquired plasma resistance to activated protein C has been described in women using third-generation (rather than second-generation) oral contraceptives. The following items are discussed: (i) the technical parameters used to appreciate the effect of activated protein C induce a bias of interpretation, the mean intrinsic effect of activated protein C, in plasmas from women on second or third-generation oral contraceptives being strictly identical; (ii) there are no data available to show that this assay can indicate a thromboembolic risk in asymptomatic women on oral contraceptives; and (iii) this assay is a global and non-specific test, basically sensitive to the plasma concentrations of many coagulation factors which are increased or decreased by oestrogens and progestogens. For instance protein S, in which oral contraceptive-induced modifications account for the differential effect of oral contraceptives on Rosing's assay, but which modifications are not related to the thromboembolic risk of oral contraceptives. The androgenic potential of the progestogen may counteract the effect of oestrogens in the test. More generally, in such a complex situation in which there is a 'modification of the modification', there is no haemostasis-related test which provides a risk indicator for thrombosis. Based on testing of the plasma response to activated protein C, it is impossible to state that third-generation oral contraceptives induce a more important thromboembolic risk than oral contraceptives containing a more androgenic progestogen.

Activated Protein C Resistance↗
PubMed2001

Differential effects of anti-Fc gamma RIIIb autoantibodies on polymorphonuclear neutrophil apoptosis and function.

Anti-Fc gamma receptor IIIb (Fc gammaRIIIb) human autoantibodies (Ab) have been classified previously into three groups, based on the results of an indirect immunofluorescence (IIF) test and an enzyme-linked immunosorbent assay (ELISA): IIF+/ELISA+ (group A), IIF+/ELISA- (group B), and IIF-/ELISA+ (group C) sera. In this study, differential effects between IIF+ autoAb, recognizing cell-bound Fc gammaR, and those ELISA+, recognizing only cell-free Fc gammaR, were studied on polymorphonuclear neutrophils (PMN). Neither group A nor B autoAb was cytotoxic, although both prolonged the survival of PMN by delaying spontaneous apoptosis. By the same extent, the PMN-binding antisera stimulated the appearance of a CD11b(dim) population, following a 12-h incubation. This event was associated with a lowered expression of beta2 integrin molecules, resulting in altered PMN function. Treatment with groups A and B autoAb reduced adhesiveness and respiratory burst. This impairment of the responses was more pronounced when the cells originated from donors NA1+ NA1+ rather than donors NA2+ NA2+. From our observations, the influences of anti-Fc gammaRIIIb autoAb on PMN survival, as well as function and subsequent dysregulation of the inflammatory response, have proven somewhat dependent on their target antigens, as determined by IIF coupled with ELISA and Fc gammaRIIIb polymorphism.

Antibody-Dependent Cell Cytotoxicity↗
PubMed2000

Increased N-linked glycosylation leading to oversialylation of monomeric immunoglobulin A1 from patients with Sjögren's syndrome.

Increased serum immunoglobulin A (IgA) level is a common finding in primary Sjögren's syndrome (pSS). IgA might not be properly eliminated because of an abnormal glycosylation. We reported previously that IgA1 from patients with pSS was oversialylated. We extend this finding by showing that monomeric IgA1 contains more sialic acid (SA) in patients than in controls, as determined by enzyme-linked immunosorbent assay (ELISA) and Western blot with Sambucus nigra agglutinin (SNA), a lectin specific for SA. To localize this excess of SA on the N- and/or O-linked oligosaccharides, we analysed them separately, using N- and O-linked oligosaccharide profiling kits based on fluorophore-assisted carbohydrate electrophoresis. N-linked, but not O-linked, oligosaccharides of patients' IgA1 were oversialylated, and this seemed to be linked to an excess of SA on the same number of polysaccharides as normal IgA1. To localize the abnormality to the Fab and/or Fc fragments, monomeric IgA1 was digested with protease, separated and transferred to nitrocellulose, where SA was identified by SNA. Both Fab and Fc fragments appeared to be oversialylated. Oversialylation of N-linked oligosaccharides of IgA1 from patients with pSS might prevent the recognition of IgA by receptors that are responsible for their clearance, resulting in an excess of serum IgA and related immune complexes.

Adult↗
PubMed2000

CD5-positive B cells at the crossroads of B cell malignancy and nonorgan-specific autoimmunity.

The CD5 glycoprotein is detectable on a minute fraction of circulating B cells. The number of CD5+ B cells (B1 cells) is increased in patients with autoimmune disorders and these cells, similar to those leading to chronic lymphocytic leukemia (CLL), may be induced to produce multispecific autoantibodies. CD5 is associated with the B cell antigen receptor, and the induction of apoptosis depends on the activation state of the cells. Defective regulation of this phenomenon might result in the production of autoantibodies and/or the development of CD5+ B cell tumors. We have proposed that there may be different B1 populations in man, which depend on the consequence of CD5 ligation on their surface: 'natural' or 'classical' CD5+ B cells, and 'induced' CD5+ B cells.

Apoptosis↗
PubMed1999

CD5 expression in human B-cell populations.

The origin of CD5+ B cells remains controversial. The differential response to ligation of CD5 resulting in apoptosis or proliferation provides insight into its roles in distinct human B cells. Here, Pierre Youinou, Christophe Jamin and Peter Lydyard review current knowledge of B-1 and B-2 cells, and propose that CD5 has different functions when expressed by different B-cell subpopulations.

Animals↗
PubMed1999

Glycosylation of immunoglobulin A influences its receptor binding.

Immunoglobulin A (IgA), which is heavily glycosylated, interacts with a variety of receptors, e.g. the asialoglycoprotein receptor (ASGP-R), which binds terminal galactose residues, and the Fcalpha receptor (FcalphaRI). It has thus been proposed that elevated serum levels of IgA in primary Sjögren's syndrome (pSS) are caused by its defective clearance. To test this hypothesis, we developed a method (based on sialyl transferases eluted from a hepatoma cell line) to increase the amount of sialic acid (SA) on IgA, and used a battery of IgA1- and IgA2-specific glycosidases to reduce this amount. Binding of IgA1 and IgA2 to ASGP-R and FcalphaRI was found to be sugar dependent because oversialylated IgA bound less than native or desialylated IgA. However, individual sugars did not play a direct role in this binding. Given that IgA are oversialylated in pSS, defective clearance of IgA may indeed be ascribed to an excess of SA in IgA1 and IgA2.

Acetylgalactosamine↗
PubMed1999

CD5 B cells and B-cell malignancies.

Over the past year, progress has been made in understanding of the physiology and disease associations of CD5+ (B1) B cells, although their exact role in pathogenesis remains unclear. Earlier studies on the negative function of CD5 within the B-cell receptor complex have been substantiated, and it seems likely that soon the signaling pathways used by this coreceptor will be elucidated. Progress in diagnosis, physiology, and etiopathogenesis of CD5+ malignancies has been made, particularly in B-cell chronic lymphocytic leukemia. The low-level expression of surface immunoglobulin has been explained by the mutations that occur in the associated CD79b. Two new potential tumor-suppressor genes have been identified in the hot spot of chromosome 13q, which provides an exciting step forward in understanding of the etiopathogenesis of some B-cell chronic lymphocytic leukemia. Activated signal transducers for activation of transcription factors molecules have been shown to be phosphorylated on different amino acids in B1 and chronic lymphocytic leukemia tumors, although the significance of this is, as yet, unclear. Finally, aberrant expression of CD40L by chronic lymphocytic leukemia T cells may contribute to the immunodeficiency that develops in these patients.

Apoptosis↗
PubMed1999

The role of CD5-expressing B cells in health and disease (review).

The CD5(+) B cell population is prominent in early life and produce low avidity and, thereby, polyreactive antibodies. CD5(+) B cells are receptive to cytokines and interleukin-10 seems to be influential in the regulation of some of these CD5(+) B cells. The question of whether CD5 is a marker of activation or a molecule specific for a B cell lineage remains unresolved because evidence in support or against a separate lineage are still a matter for debate. However, we suggest the possibility of different kind of CD5(+) B cells. Indeed, activated CD5(+) B cells do proliferate, following CD5 engagement, while resting CD5(+) B cells do not. Moreover, three ligands for CD5 have, thus far, been identified but their functional effects are yet unknown. CD5(+) B cells probably play a role in setting up the idiotype network, antigen presentation and tolerance induction. B cells of most of the chronic lymphoid leukemias express CD5 molecules and, surprisingly, these cells may be expanded in non-organ-specific autoimmune diseases, such as rheumatoid arthritis or primary Sjögren's syndrome. CD5(+) B cells seems to be involved in the autoantibody production (this does not necessarily imply that pathogenic autoantibodies are produced by CD5(+) B cells) in autoimmune disease and particularly susceptible to transformation in lymphoproliferative disorders. Thus, this B cell population appears to play a key role at the crossroad of the non-organ-specific autoimmune diseases and B lymphoproliferative disorders.

Animals↗
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↗