HLA-D identity in a family with multiple cases of multibacillary leprosy

Haregewoin, Abebe; Yemane-Berhan, T; Aredath, Sarojini Peringali; E, Fekete; Mock, Barbara

doi:10.5935/0305-7518.19840007

Cited by 3 publications

(2 citation statements)

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“…Il existe une grande similarité entre les manifestations articulaire de la lèpre et la PR. Les deux affections sont sous-tendues par des mécanismes dysimmunitaires proches, en effet, il a été rapporté que l'haplotype HLA-DR4 est corrélé à une réactivité altérée aux antigènes mycobactériens (tuberculose, lèpre...) et à une forme sévère de la PR [21][22][23][24][25][26][27][28]. Notre patient avait présenté des poussées d'arthrites accompagnées de fièvre, parfois d'adénopathies, de pointe de rate et d'un syndrome inflammatoire biologique en rapport avec des réactions d'une scléromégalie modérée, ce qui est concordant aux données de la littérature [4].…”

Section: Discussionunclassified

Rhumatisme inflammatoire chronique révélant une lèpre « border-line »

Miladi

Feki

Bahloul

et al. 2006

Revue du Rhumatisme

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Section: Discussionunclassified

Rhumatisme inflammatoire chronique révélant une lèpre « border-line »

Miladi

Feki

Bahloul

et al. 2006

Revue du Rhumatisme

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“…suggest that T-cell activation by AP-MT is due in large part, to response to the 65 kDa mycobacterial heal shock protein. This heat shock protein is capable of activation of gamma/delta T-eell receptor-positive lymphocytes [6]. An enrichment of these cells in patient synovial fluids [2].…”

Section: Discussronmentioning

confidence: 99%

Mechanism of T‐Cell Activation by Mycobacterial Antigens in Inflammatory Synovitis

1991

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Earlier studies demonstrated enhanced proliferative responses to an acetone precipitable Mycobacterium tuberculosis (AP-MT) antigenic complex by T lymphocytes from the synovial fluid, compared with the peripheral blood, of patients with inflammatory synovitis, including rheumatoid arthritis. In contrast, decreased proliferation and interleukin 2 (IL-2) production in response to mitogens by synovial fluid lymphocytes from patients with rheumatoid arthritis has been demonstrated. In order to determine if IL-2 was produced in response to AP-MT, the peripheral blood and synovial fluid of patients with inflammatory arthritis were analysed by measuring proliferation and IL-2 production in response to AP-MT and tetanus toxoid. A reduction of IL-2 production relative to proliferation was observed in some, but not all, synovial fluids of patients who responded to the AP-MT. Nevertheless, antibodies to IL-2 as well as interleukin 4 (IL-4), significantly inhibited proliferation of synovial fluid lymphocytes by AP-MT. There was no inhibition by antibodies to interleukin 6 (IL-6). We conclude that AP-MT induced proliferation by synovial fluid lymphocytes is mediated by both IL-2 and IL-4.

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