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Biomedical subjects

M O Jauberteau-Marchan

Publications and source records attributed to M O Jauberteau-Marchan.

7 recordsLinked to original sources

The protective role of Langerhans' cells and sunlight in multiple sclerosis.

The low prevalence of multiple sclerosis in equatorial areas may be the consequence of a physiological immunosuppression induced by ultraviolet radiation on the epidermal Langerhans' cells, which are the antigen-presenting cells. Multiple sclerosis appears to be the consequence of an immune response to an environmental antigen during childhood in the absence of two protective factors: a genetic factor conferred by the HLA haplotypes of Langerhans' cells, and an environmental factor conferred by ultraviolet radiation in sunlight. In the presence of these two factors, T lymphocytes are physiologically immunosuppressed. Their association may play a key role in protection against multiple sclerosis. The varying combinations of these two factors may provide an explanation for the differences in incidence and prevalence of the disease noted within a single region or from one region to another throughout the globe. The hypothetical pathogenic mechanism developed in this article opens up new fields of research, particularly those concerning its therapeutic applications.

Humans↗

[Immunohistochemical study of lesions in Horton's temporal arteritis before and during corticotherapy].

The immunohistochemical study was performed on temporal artery biopsies from eight patients with giant cell (temporal) arteritis: three before treatment, four after a short period of corticosteroid therapy (from 1 day to 7 days) and one during relapse occurring after a treatment of 9 years; from four subjects with clinical symptoms but without histological features of giant cell arteritis and from five negative controls. Before treatment, biopsies of patients with temporal arteritis showed an inflammatory infiltrate with macrophages and T cells, essentially CD4+ and memory T cells (CD45 RO+), expressing the markers of activation IL2 receptor and HLA DR. Few B and NK cells were also detected. Adhesion molecules, LFA1 and I-CAM1, were strongly expressed by T cells and macrophages. In contrast, the ligand to the CD2, the CD58 marker, was rarely detected. These immunohistochemical features were also observed after a short corticosteroid treatment (by intravenous methylprednisolone or oral prednisone), with presence of activated T cells, memory T cells, macrophages and I-CAM1 and LFA1 expressing cells in the infiltrate. A temporal biopsy, performed after a long time of corticosteroid therapy, showed activated T cells, macrophages and memory cells in o,ne arteriole. In controls, this study showed some mononuclear cells dispersed in intima and adventia, but without activated or memory T cells. Our results support the presence of immune local response in temporal arteritis, incompletely improved by a short corticosteroid treatment.

Adrenal Cortex Hormones↗

[Anticardiolipin antibodies and Horton disease].

A prospective study, including 86 patients with giant cell arteritis proven by temporal artery biopsies, was performed to determine the prevalence of anticardiolipin antibodies, the antibody isotype, the relationship of antibodies to ischemic involvement and their evolution during corticosteroid treatment. Controls were obtained from 50 subjects without vasculitis or autoimmune disorders. Before treatment, 50% of patients' sera contained anti-cardiolipin antibodies (vs 8% in controls, p < 0.0001). These antibodies were IgG-ACL in 36% of patients and IgM-ACL in 17% of patients (vs respectively, 4% and 2% in controls). No significant association was observed between the incidence of ischemic ocular complications and the levels of anti-cardiolipin antibodies. During corticosteroid treatment, the level of anti-cardiolipin antibodies, mostly IgG class, decreased to become negative in 2 months. An increase of these antibodies was observed with the occurrence of relapses in four patients, after the end of corticosteroid therapy. The significance of IgG and IgM antibodies is different in giant cell arteritis. IgG antibodies may be markers of the course of this vasculitis.

Adrenal Cortex Hormones↗

[Systemic signs of primary Gougerot-Sjögren syndrome. 48 cases].

Forty-eight patients with primary Sjögren syndrome are documented together with the results of their baseline investigations. The majority of patients were female (44 out of 48) and mean age was 63.2 years. Common clinical features included 20 parenchymal lung disease, among which 4 had interstitial pulmonary fibrosis and 2 lymphocytic interstitial pneumonitis, 12 neurologic manifestations, 16 Raynaud's phenomenon, 12 arthritis, and 3 gastrointestinal involvement. Haematological features occurred in 15 patients and another autoimmune disease was encountered in 13 cases. These extraglandular manifestations were the dominating reasons for hospital referral in 43.5% of cases, the sicca syndrome were most often only mentioned by the patients after special questioning which explain considerable delay before the diagnosis.

Adult↗

Human African trypanosomiasis: presence of antibodies to galactocerebrosides.

Improvements were made in the immunodetection of anti-galactocerebroside (anti-GalC) antibody in sera of patients with human African trypanosomiasis by thin-layer chromatography, enzyme-linked immunosorbent assay, and immunoadsorption. Rabbit anti-GalC antibodies were used to standardize these techniques and demonstrate their specificity. Anti-GalC antibodies were found in the sera of 42.8% of 63 patients with human African trypanosomiasis. Thirty-four control subjects living in the same endemic area were also tested. Anti-GalC levels were higher in human African trypanosomiasis patients with neurologic disturbances compared with patients without such disturbances. These antibodies were distributed mainly between the IgG and IgM classes, but 28% of the patients with human African trypanosomiasis had increased IgA levels without anti-GalC antibody activity.

Agglutination Tests↗

[Anti-cardiolipin antibodies in Horton's disease].

A prospective study on 11 patients with temporal artery biopsy-proven arteritis examined the frequency and significance of anti-cardiolipin antibodies. Antibody levels in 7 patients were higher than 20 units but were not correlated with an inflammatory syndrome, as assessed by measurement of 4 inflammatory proteins (fibrinogen, C-reactive protein, orosomucoid and haptoglobin). These 7 patients were treated with steroids and their antibody levels returned to the normal range after 4 to 16 weeks of therapy, later than the inflammatory proteins. Two patients had slight increases of their anti-cardiolipin antibody levels, but no signs of clinical relapse or increases of inflammatory proteins were observed. In this study, no correlation was found between the presence of anti-cardiolipin antibodies and the occurrence of ischemic complications in 6 of the 11 patients.

Aged↗