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Biomedical subjects

A Lamour

Publications and source records attributed to A Lamour.

At least 37 records · Page 2Linked to original sources
PubMed1993

Prognostic significance of cytotoxic T cells in individuals infected with human immunodeficiency virus.

Nine dual-fluorescence combinations were used to enumerate T-cell subsets in 112 human immunodeficiency virus type 1-infected patients. Two blood samples were analyzed, with a 6-month interval between the tests, in 53 of these 112 patients. The alteration in CD4 over this period of time correlated with the change in CD8 and CD8S6F1 (P < 0.02 and P < 0.01), irrespective of the disease stage. Two groups of patients were defined by the CD8S6F1 subset at the first normal levels. Changes in numbers of CD4, CD4CD45RA, and CD4CD29 were significantly higher in group B than in group A patients. The absolute count of CD8S6F1 could thus serve as an indicator of the ensuing depletion of the CD4 population, as well as the CD4 subsets.

Adolescent↗
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↗
PubMed1993

Expression of CD5 and CD72 on T and B cell subsets in rheumatoid arthritis and Sjögren's syndrome.

A minority of B cells express the CD5 marker, which is found on virtually all T cells, and CD72 has been defined as the CD5 ligand on the B cell membrane. The mean fluorescence intensity (MFI) of the CD5 molecules was shown to be higher on CD4+CD29+ than CD4+CD45RA+ in peripheral blood (PB) and synovial fluid (SF) of rheumatoid arthritis (RA) patients (P < 0.0001 and < 0.001), and PB of Sjögren's syndrome (SS) patients and normal controls (P < 0.02 and < 0.03). This MFI declined once the CD4 expressed HLA-DR in PB of SS patients (P < 0.004) and normal controls (P < 0.02) or CD25 in PB of RA (P < 0.004) and SS patients (P < 0.0004). There was a correlation between the CD5 MFI on CD4+CD45RA+ and CD4+CD29+ in RA (P < 0.001) as well as SS (P < 0.0007) PB. The CD72 MFI was impressively higher on CD5+ than CD5- B cells in PB and SF of RA patients (P < 0.0001 and P < 0.005) and PB of SS patients (P < 0.005) and normal controls (P < 0.005). Our data suggest that, in association with CD4CD29, CD5 is involved in CD5+B/CD5+ B cell interactions in non-organ-specific autoimmune diseases.

Adult↗
PubMed1993

Fc-gamma receptor III shedding by polymorphonuclear cells in primary Sjögren's syndrome.

A sandwich enzyme-linked immunosorbent assay was developed to assess Fc-gamma receptor III (Fc gamma RIII), based on a combination of two non-competing monoclonal antibodies. This receptor was detectable in the serum of eight out of 23 patients with primary Sjögren's syndrome and two out of 23 normal controls. The proportion of Fc gamma RIII-carrying polymorphonuclear (PMN) cells was lower (P < 0.05) in the patients with cell-free Fc gamma RIII (90.4 +/- 7.5%) than in the remainder (84.8 +/- 8.3%). The PMN cell functions were evaluated and the diminished adherence (71.7, geometric mean) and chemotaxis (1.23) paralleled the Fc gamma RIII release. The relative inefficiency of PMN cells in SS might be due to phagocytosis of immune complexes.

Adult↗
PubMed1993

Human CD5-positive B cells in lymphoid malignancy and connective tissue diseases.

The current literature on human CD5-positive B cells (CD5 + B cells) has been analysed, with a special emphasis on non organ-specific auto-immune diseases. Malignant cells of most of the chronic lymphoid leukaemias of the B cell lineage express the CD5 molecule. Antibodies of the IgM class produced by leukaemic B cells are multispecific auto-antibodies. The CD5 + B cell subset may be expanded in non organ-specific autoimmune diseases, such as rheumatoid arthritis, primary Sjögren's syndrome, systemic lupus erythematosus. This holds true for various conditions, including organ-specific auto-immune diseases. Since auto-immune features are common in lymphoproliferative disorders, and the latter be a complication in non organ-specific auto-immune diseases, CD5 + B cells may represent an intermediary between these auto-immune diseases and B cell lymphoproliferations. Studies on the regulation of CD5 + B cell production and function are likely to shed light on the aetiology of, and pathogenetic mechanisms operating in the different disease states.

Antigens, CD↗
PubMed1993

[Infectious origin of rheumatoid arthritis].

Three preliminary concepts are developed: antigen presentation, "peptidic self" and superantigen. Several infectious contenders for rheumatoid arthritis (RA) are then reviewed: Epstein-Barr virus, mycobacteria, parvovirus, proteus and streptococcus. Finally, the most important hypotheses are discussed: microbe present and still accessible, microbe present but hidden, microbe absent but perpetuated by the immune system. In the latest case, molecular mimicry could possibly be the mechanism operating in RA.

Animals↗
PubMed1992

Conjunctival epithelial cells from patients with Sjögren's syndrome inappropriately express major histocompatibility complex molecules, La(SSB) antigen, and heat-shock proteins.

The La(SSB) antigen has been detected within the cytoplasm and on the membrane of conjunctival cells (CC) from patients with Sjögren's syndrome, whereas it was weakly expressed in the nucleus of normal cells. The diseased CC were shown to overproduce major histocompatibility complex (MHC) class I antigens and express MHC class II antigens. Anti-heat-shock protein monoclonal antibody bound to the cell membrane in patients but not in normal controls.

Autoantigens↗
PubMed1992

Cell-free CD5 in patients with rheumatic diseases.

Since an increased frequency of CD5+ B cells has been reported in rheumatoid arthritis (RA) and primary Sjögren's syndrome (SS), and the expression of the molecule was reduced on the T cells of some SS patients, we hypothesised that there would be an accelerated turnover of CD5 in these disorders. We describe a novel enzyme-linked immunosorbent assay for measuring cell-free (CF) CD5, using rabbit F(ab')2 anti-CD5 antibody as capture agent and monoclonal anti-CD5 antibody as revealing agent. It was established that CF-CD5 was detectable in RA and SS sera, as opposed to sera from patients with ankylosing spondylitis and normal controls. The level of CF-CD5 did not correlate with rheumatoid factor in RA patients but was significantly higher (P less than 0.05) in SS patients with extraglandular manifestations than in those with glandular disease. Three of the latter patients with significantly increased levels of CD5-negative T cells did not have a particularly high proportion of CF-CD5 in these sera.

Antigens, CD↗
PubMed1992

Galactose terminating oligosaccharides of IgG in patients with primary Sjögren's syndrome.

Using a simple but novel ELISA, we have screened 40 serum samples from patients with primary Sjögren's syndrome and 34 normal controls for IgG glycosylation deficiencies, identified by their specific ricin binding. Elevated levels of asialylated IgG were detected in 24 patients. The extent of asialylation was significantly higher in the patients with extraglandular manifestations than in the others. Interestingly, the correlation of asialylated IgG was apparent only with Raynaud's phenomenon and arthritis, and not other extraglandular manifestations. Strong correlations (P less than 0.01) were noted between asialylated IgG and rheumatoid factor or IgA-containing immune complexes.

Adult↗
PubMed1992

Analysis of T cell receptors in rheumatoid arthritis: the increased expression of HLA-DR antigen on circulating gamma delta+ T cells is correlated with disease activity.

The phenotypic characteristics of peripheral blood T cells, isolated from 37 rheumatoid arthritis (RA) patients and 17 healthy controls were determined with special emphasis on gamma delta+ T cells and CD4-CD8- alpha beta+ T cells. Two- and three-colour automated flow cytometry analyses were performed using a panel of MoAbs directed against differentiation antigens and T cell receptor molecules. The results demonstrated: (i) no significant difference between the percentages of CD4-CD8- alpha beta+ T cells in patients and controls; (ii) a significant decrease of the gamma delta+ T cell level in the peripheral blood of RA patients relative to controls; (iii) phenotypic abnormalities of circulating gamma delta+ T cells in RA patients suggestive of an activation status in vivo. These abnormalities included a significant reduction in the density of the T cell differentiation antigen CD3 and an increase in the expression of HLA-DR antigen. The level of circulating HLA-DR+/gamma delta+ T cells was significantly higher in patients with active disease. HLA-DR+/gamma delta+ T cells were also present in the synovial fluid obtained from three patients with an active disease. In addition, preliminary experiments showed that the activated gamma delta+ T cells were predominantly V delta 1. Taken together, these data support the involvement of gamma delta+ T cells in the pathogenesis of RA.

Adult↗
PubMed1992

Anti-Epstein-Barr virus-nuclear antigen-1, -2A and -2B antibodies in rheumatoid arthritis patients and their relatives.

We have examined serum antibodies to Epstein-Barr virus Nuclear Antigen (EBNA)-1, -2A and -2B, in addition to antibodies to viral capsid antigen and early antigen in 100 rheumatoid arthritis patients and 50 of their relatives. Using indirect immunofluorescence on transfected cells and Western-blot technique, we have found increased frequency and titres of antibodies to EBNA-2B in patients and, to a lesser degree, in their family members, whereas other anti-Epstein-Barr virus antibodies appeared to be similar to controls. Cross-inhibition experiments were carried out and show that antibodies to EBNA-2A are distinct from those to -2B, and vice versa.

Adult↗
PubMed1992

Anti-neutrophil cytoplasm antibodies in patients with giant cell arteritis and/or polymyalgia rheumatica.

Anti-neutrophil cytoplasm antibodies (ANCA) were detected at low titers by indirect immunofluorescence in 1 out of 13 patients with giant cell arteritis (GCA) alone, 7 out of 30 with polymyalgia rheumatica (PMR) alone and 4 out of 15 with GCA plus PMR (8, 23 and 27%, respectively). Anti-myeloperoxidase antibodies were also demonstrated by an enzyme-linked immunosorbent assay in 4 patients with GCA alone (31%), 13 with PRM alone (42%) and 5 with GCA plus PRM (33%). The C-reactive protein response was significantly higher (p < 0.05) in ANCA-positive than in ANCA-negative patients.

Aged↗
PubMed1991

Anti-organelle and anti-cytoskeletal autoantibodies in the serum of Epstein-Barr virus-infected patients.

A number of non-organ-specific autoantibodies, such as antibodies to vimentin, centriole, the midbody of chromatin and the Golgi apparatus, were detected in the sera of patients with infectious mononucleosis or nasopharyngeal carcinoma, by using an indirect immunofluorescence technique. There was no significant correlation between the titers of anti-Epstein-Barr virus antibodies and those of autoantibodies. Our findings suggest that the autoantibody production is antigen-driven.

Autoantibodies↗
PubMed1991

[Free-flap coverage technique with double vascular bypass in the lower limb].

In thirteen patients, the repair of a soft tissue defect of the lower limb required a free tissue transfer revascularized by microvascular grafts. The indication of vascular grafting was either the absence of vessels or inadequate recipient vessels. Proximal anastomoses were performed on the femoral artery and the femoral vein or the long saphenous vein. All the transfers were done in one stage procedure. In two cases, a transitory arteriovenous shunt was established. Three flaps out of thirteen have been lost by thrombosis. The discussion concerns the causes of the failures and the indication of the establishment of a transitory or a temporary arterioveinous shunt prior to free flap transfer.

Adult↗