Biomedical subjects
Publications and source records attributed to J Jouquan.
The adenosine deaminase gene frequencies were calculated in 405 subjects randomly chosen from the Bigouden district. A rather high frequency (0.0765 +/- 0.0093) was found for the ADA2 gene. The possible effect of Celtic influences is considered.
Sera from 367 patients with rheumatoid arthritis (RA) and from 102 patients with other non-organ-specific (NOS) autoimmune diseases were examined for the presence of organ-specific (OS) autoantibodies. The incidence of these OS autoantibodies was not increased in patients with NOS autoimmune diseases with the exception of thyroglobulin antibodies, which were significantly more frequent in RA (P less than 0.001) and in Sjögren's syndrome (P less than 0.05) patients than in normal controls. Investigation of 169 patients with OS autoimmune diseases did not reveal an increased prevalence of NOS autoantibodies. In RA patients, OS autoantibodies correlated with NOS autoantibodies (P less than 0.04) and with HLA-DR3 antigen (P less than 0.01).
CD5 molecules present on human T cells are detectable but weakly expressed on some human B cells. We have increased the sensitivity of their detection by treating the B enriched cells with phorbol myristic acetate (PMA), a tumour promoting agent. The numbers of CD5+ B cells in the blood of patients with rheumatoid arthritis (RA) were higher than in control blood, and after PMA treatment this was statistically significant. CD5+ B cells were also increased in tonsils, lymph nodes, and spleens after PMA activation. There were no significant differences between the percentages of B cells carrying chi or lambda light chains in their expression of CD5 molecules in patients with RA.
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The bactericidal action of neutrophil polynuclear cells (NP) is significantly lower in the presence of diclofenac than in the presence of ketoprofen in patients with rheumatoid polyarthritis. This effect perhaps takes place through a serum factor, since the bactericidal action of normal NPs is diminished when the cells are incubated in the serum of patients treated with diclofenac or in the serum of healthy individuals after ingestion of diclofenac, but it is not decreased when the cells are incubated in the serum of patients treated with ketoprofen or the serum of healthy volunteers after ingestion of ketoprofen.
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Molecules recognised by the monoclonal antibodies Leu 1 - OKT 1 - Mid 5 (CD5 molecules) were originally shown on human T cells and are equivalent to Lyt-1 molecules in the mouse. These surface molecules are detectable on some human B cells, but are weakly expressed. We have therefore tested the effects of the tumour-promoter, phorbol myristic acetate (PMA) on expression of these molecules on B cells. Sheep red blood cell rosette-depleted lymphoid organ or blood cells from 8 controls and 10 rheumatoid arthritis (RA) patients were examined fresh and cultured with PMA for 48 hours and the cells stained with Leu 1 or Mid 5 by indirect immunofluorescence. Cells were analysed by UV microscopy or flow cytometry. More RA blood B cells were positive for Leu 1 than normals before culture. Following incubation with PMA, the percentage of positive cells increased in all cell populations (1-49% in RA patients and 5-26% in controls). There was no difference in the expression of Leu 1 on Kappa--or lambda--positive cells before and after culture in PMA. Leu 1 positive cells were under-represented in Epstein-Barr virus-driven cell lines.
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13 autoantibodies were sought in 23-26 elderly people and in 47-118 young controls. We found at least one autoantibody (mainly rheumatoid factor, RF, and anti-nuclear antibodies in 17/23 elderly (i.e., 17%) and in 7/45 young controls (i.e., 16%). Autologous rosette-forming cells and Leu-7 positive cells (Natural Killer Cells?) were higher, and OKT4 and OKT8 positive cells lower in the former than in the latter group. We show that elderly have a high proportion of CD5 positive B cells, compared with young controls, following phorbol myristic acetate activation in vitro. This abnormality might account for the discrepancy in production of RF compared to other autoantibodies.
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Clinical, biological and evolutive profiles of rheumatoid polyarthritis (RP) associated or not with a Gougerot-Sjögren syndrome (GSS) were compared in two series of 27 patients matched according sex and age, and recruited among 158 patients examined during a period of 36 months. The GSS was defined by the presence, in addition to RP, of xerophthalmia (Schirmer and Rose Bengal tests were positive) and/or salivary glands disorders (histological abnormalities at stages III or IV of Chisholm classification). The evolution of RP and the importance of articular or extra-articular involvement of the disease are identical in both groups. Biologically, the prevalence of agglutinating rheumatoid factors, antinuclear antibodies and specific organ antibodies, is not different from one group to the other. Only the serum levels of gammaglobulins and circulating immune complexes are higher in the presence of a GSS. Finally, it was not necessary to resort more often to steroid therapy and/or immunosuppressors for RP with GSS than for isolated RP. In summary, in the same age group and same sex, RP associated to a GSS do not appear to have a fundamentally different profile, contrary to what might have been suggested by previous studies.
In most of the cases, once a given endocrine gland is involved, the corresponding specific autoantibody may be detected; for example, anti-islet cell antibodies are produced within the first few years, after onset of symptoms in insulin-dependent diabetes (DID). Accompanying autoantibodies are quite frequently found in the patient himself. In Schmidt's syndrome (thyroid and adrenal glands are involved and associated to IDD in 30% of the cases) thyroid microsomal antibodies are found in 38% of the cases, thyroglobulin antibodies in 11% of the cases, islet-cell antibodies in 7% of the cases and steroid cell antibodies in 17% of the cases. Associations are also possible in patient family members. Aberrant expression of HLA-DR molecules at the membrane of follicular thyroid cells (as of any other endocrine gland), following a viral aggression, could well account for the endocrinopathy combinations, but alternative mechanisms should be discussed.