HL‐A8 and LD‐8a in Patients with Myasthenia Gravis

Möller, Erna; Hammarström, Lennart; Smith, Edvard; Matell, G.

doi:10.1111/j.1399-0039.1976.tb01027.x

Cited by 32 publications

(1 citation statement)

References 12 publications

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“…It is striking that there is an increased frequency of HLA-Dw3 in patients with juvenile rheumatoid arthritis presenting with polyarticular disease. HLA-Dw3 has been associated with several other dysimmune diseases including myasthenia gravis, celiac sprue and chronic active liver disease (Keuning et al 1976, Moller et al 1976, Opelz et al 1977. However, in contrast to the present studies, all previous associations of HLA-Dw3 were present in diseases that were also associated with HLA-B8.…”

Section: Discussioncontrasting

confidence: 99%

Frequency of HLA‐Dw3 in Juvenile Rheumatoid Arthritis

Gershwin

Opelz²,

Terasaki³

et al. 1977

Tissue Antigens

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We have prospectively examined 46 consecutive unrelated children with JRA, 28 females and 18 males, for HLA‐A, ‐B, ‐Dw1, and ‐Dw3 antigens. The data were analyzed according to mode and age of onset, as well as presence of extraarticular features. Patients with JRA were found to have an elevated frequency of HLA‐B27 (26% vs. 8% of controls, P < 0.01). This elevated frequency of HLA‐B27 was noted in patients with either a pauciarticular or polyarticular onset and consistent with previous observations, was more common in males than females. However, the most striking associations in JRA were apparent when the MLC‐defined locus HLA‐Dw3 was studied. The total patient population had a 46% frequency of HLA‐Dw3 as compared with 24% in controls (P < 0.01). Moreover, when the group of 46 children was subdivided, the HLA‐Dw3 frequency of patients with polyarticular disease was 64% as compared with 21% in pauciarticular disease (P < 0.01). Further, although the frequency of HLA‐B8 was similar in JRA to that in the control panel, a significant degree of linkage disequilibrium was shown to exist between HLA‐B8 and HLA‐Dw3. No such linkage was shown to exist between HLA‐B27 and either HLA‐Dw1 or Dw3. Although we have not multiplied the P value by the number of HLA‐A, ‐B and ‐D antigens, we suggest that the presence of the MLC‐defined locus HLA‐Dw3 is significantly elevated in children with polyarticular mode of onset of JRA and suggest that further definition of lymphocyte‐dependent loci may aid in understanding the mechanism of pathogenesis as well as the classification and prognosis of childhood onset arthritis.

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Section: Discussioncontrasting

confidence: 99%

Frequency of HLA‐Dw3 in Juvenile Rheumatoid Arthritis

Gershwin

Opelz²,

Terasaki³

et al. 1977

Tissue Antigens

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Acetylcholine Receptor Antibody Titer and HLA-B8 Antigen in Myasthenia Gravis

Keesey

Naiem

Lindstrom

et al. 1982

Archives of Neurology

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Cytokines and the pathogenesis of myasthenia gravis

1997

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Myasthenia gravis (MG) and its animal model experimental autoimmune myasthenia gravis (EAMG) are caused by autoantibodies against nicotinic acetylcholine receptor (AChR) in skeletal muscle. The production of anti‐AChR antibodies is mediated by cytokines produced by CD4+ and CD8+ T helper (Th) cells. Emerging investigations of the roles of cytokines in MG and EAMG have revealed that the Th2 cell related cytokine interleukin 4 (IL‐4), an efficient growth promoter for B‐cell proliferation and differentiation, is important for anti‐AChR antibody production. IL‐6 and IL‐10 have similar effects. The Th1 cytokine IFN‐γ is important in inducing B‐cell maturation and in helping anti‐AChR antibody production and, thereby, for induction of clinical signs and symptoms. Results from studies of time kinetics of cytokines imply that IFN‐γ is more agile at the onset of EAMG, probably being one of the initiating factors in the induction of the disease, and IL‐4 may be mainly responsible for disease progression and persistance. Even though other Th1 cytokines like IL‐2, tumor necrosis factor α (TNF‐α), and TNF‐β as well as the cytolytic compound perforin do not directly play a role in T‐cell‐mediated help for anti‐AChR antibody production, they are actually involved in the development of both EAMG and MG, probably by acting in concert with other cytokines within the cytokine network. In contrast, transforming growth factor β (TGF‐β) exerts immunosuppressive effects which include the down‐regulation of both Th1 and Th2 cytokines in MG as well as EAMG. Suppressive effects are also exerted by interferon α (IFN‐α). Based on elucidation of the role of cytokines in EAMG and MG, treatments that up‐modulate TGF‐β or IFN‐α and/or suppress cytokines that help B‐cell proliferation could be useful to improve the clinical outcome. © 1997 John Wiley & Sons, Inc. Muscle Nerve, 20, 543–551, 1997

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HL‐A8 and LD‐8a in Patients with Myasthenia Gravis

Cited by 32 publications

References 12 publications

Frequency of HLA‐Dw3 in Juvenile Rheumatoid Arthritis

Frequency of HLA‐Dw3 in Juvenile Rheumatoid Arthritis

Acetylcholine Receptor Antibody Titer and HLA-B8 Antigen in Myasthenia Gravis

Cytokines and the pathogenesis of myasthenia gravis

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