Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0024591 (malignant hyperthermia)
 2,353 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During the course of a routine H-2 alloimmunization, individual mice within a group of inbred animals produced anti-MHS antibodies of differing specificities. These different antibody populations were directed against various but probably cross-reacting components of complex HLA and H-2 gene products.
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PMID:Individual mice of one inbred strain produce anti-H-2 and anti-HLA antibodies of different specificities. 69 15

The present family investigation has shown that genes within the MHS are mainly responsible for the development of psoriasis or psoriasis-associated arthritic lesions (peripheral arthritis and sacroiliitis). We have hypothetically discussed the possibility that multiple genes, all located within the MHS, act in concert to increase the risk of developing disease to very high levels. This implies that at least two MHS linked genes act in complementary fashion for the development of disease, these genes seem to be able to operate both in the cis and in the trans position. One of these genes would be situated in the chromosomal portion of the MHS which carries the HLA-D locus. Families with a high incidence of disease would show inheritance according to the cis position of genes, when it can be shown that most of the carriers of the specific disease-associated haplotype are affected by disease, whereas in other families, complementarity between two distinct HLA haplotypes with genes acting in the trans position would result in disease.
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PMID:Psoriasis, sacro-iliitis and peripheral arthritis occurring in patients with the same HLA haplotype. A preliminary family report and a hypothetical explanation of the interaction between MHS products. 96 98

We have studied HLA haplotypes, autoimmune diseases and circulating autoantibodies in 23 families with multiple cases of rheumatoid arthritis; 76 per cent of rheumatoid arthritis and 70 per cent of non-rheumatoid individuals were positive for HLA-DR4. The haplotypes Bw44-Bf*S-DR4; B40-Bf*S-DR4; and B15-Bf*S-DR4 were found in 13, 9 and 7 per cent of probands respectively and the B15-Bf*S-DR4 haplotype was found between four and five times more frequently in DR4-positive rheumatoid arthritis than in DR4 positive, non-rheumatoid arthritis families. Rheumatoid arthritis segregated with a DR4 positive haplotype in 13 families and with a DR4 negative haplotype in seven. Analysis of HLA haplotype sharing showed greater than random sharing by affected siblings which is in keeping with genes within the MHS influencing susceptibility to rheumatoid arthritis. Autoimmune thyroid disorders were seen in 8 per cent of family members investigated. They were significantly more frequent in those families in which rheumatoid arthritis segregated with a non-DR4 bearing HLA haplotype. This suggests that genes for autoimmune thyroid disease might predispose to rheumatoid arthritis independently of DR4. These genes are probably not HLA-linked, as there was no trend for HLA haplotype sharing to be increased in sibling pairs with either rheumatoid arthritis and thyroid disease or rheumatoid arthritis and thyroid autoantibodies respectively.
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PMID:Clinical and immunogenetic studies in multicase rheumatoid families. 633 66