Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immune-mediated diseases affect up to 5% of the population and are a major cause of morbidity and mortality. These diseases can be organ specific, such as insulin-dependent diabetes (IDDM) and non-organ specific, such as Rheumatoid Arthritis (RA). Identical and non-identical twins have been used to establish whether these diseases are determined by genetic or environmental factors. The results of these studies have been collated in a new section of the Mendel Institute in Rome. Diseases included in these studies included IDDM, RA, Systemic Lupus Erythematosus (SLE), Multiple Sclerosis (MS) and Myasthenia. Striking differences in concordance rates between identical and non-identical twins in all these studies suggest that genetic factors are important in causing these diseases. All the diseases are known to be associated with HLA genes on chromosome 6 which may account for some or all of the genetic susceptibility. However, in the majority of pairs the affected twin has an unaffected co-twin. These observations suggest that non-genetically determined factors, probably environmental factors and not somatic mutations, are critical. The study of unaffected co-twins, who are at high disease-risk, has allowed the identification of changes which precede and predict the clinical disease. The immune-mediated destruction in many of these diseases is probably caused by T-lymphocytes. Twin studies have shown the importance of genetic factors in determining T-cell responses. Identical twins should, therefore, provide the perfect test bed to assess the role of T-cells in immune-mediated diseases.
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PMID:Twin studies in auto-immune disease. 784 25

The presentation shows the survey of diseases the pathogenesis of which might be connected with the existence of Heat Shock Proteins (HSPs). We discuss the data referring to the influence of the HSPs upon the occurrence and progression of the following diseases: systemic lupus erythematosus, reactive arthritis, rheumatoid arthritis, insulin dependent diabetes mellitus, schizophrenia and Alzheimer's disease. There is also indicated a possible activity of HSPs in the pathogenesis of neoplasia, organ ischaemia and inflammation or degeneration.
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PMID:[Clinical significance of heat shock proteins. Influence of heat shock proteins on the pathomechanism of selected diseases]. 787 Dec 4

1. Graft survival was similar at one year for the various diseases, but at 3 years, a 16% divergence was noted among diseases. IGAN patients had the highest graft survival rate. 2. Graft survival rates of IGAN, ALP, and PC in Black and White patients were similar, but in all other diseases, a high loss rate was seen after one year among Black patients. 3. Patient survival was almost identical for the various diseases among Whites and Blacks. 4. SLE patients with DR2 or DR3 had higher graft survival rates than SLE patients without these groups (p < 0.05 in Whites). 5. IDDM patients with DR3 or DR4 had higher graft survival rates than IDDM patients without these groups (p < 0.05 in Whites, p = ns in Blacks). 6. Nephrosclerosis patients with DR2 or DR4 had higher graft survival rates than those who did not (p = ns in Whites, p < 0.05 in Blacks). 7. CGN patients with DR1 had higher graft survival rates than CGN patients without DR1 (p < 0.00005 in Whites). 8. IDDM patients with SPK transplants had higher graft survival rates than IDDM patients grafted with a KAT (p < 0.000001). In recent years, almost 30% of IDDM patients had SPK transplants. 9. Patients with SPK grafts compared to KAT were younger, White, were more often DR3/4, and worked full-time. 10. The SPK effect was seen only at the excellent centers. At all other centers, SPK and KAT patients had the same graft survival rates.
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PMID:The long-term effect of primary disease on cadaver-donor renal transplant recipients. 791 83

Epidemiological and experimental evidence suggested that denial of dietary cow milk protein early in life protects genetically susceptible children and animals from insulin-dependent diabetes (IDDM). Bovine serum albumin (BSA) was proposed as a candidate milk-borne mimicry antigen responsible for the diabetogenic cow milk effect. Elevated anti-BSA antibodies have been observed in patients and diabetic rodents, and these antibodies precipitate p69 from islet cell lysates. IDDM is a T cell mediated disorder but efforts to detect BSA-specific T cells in diabetic children have so far failed. We describe here a culture system which allowed the detection of BSA-specific T cells and we mapped this response to the ABBOS peptide (pre-BSA position 152-169) previously identified as a possible mimicry epitope. ABBOS-sensitized T cells were found in 28/31 children with recent onset IDDM but not in non-diabetic controls nor in children with SLE or JRA. T cell proliferative responses declined within the first few years of diabetes diagnosis. Although no effector cell role for BSA/ABBOS specific T lymphocytes has been demonstrated, the presence of BSA peptide-specific T cells strengthens the postulated link between a cow milk protein and IDDM.
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PMID:T cells from children with IDDM are sensitized to bovine serum albumin. 799 51

The particular histocompatability antigen (HLA) gene(s) that may confer systemic lupus erythematosus (SLE) susceptibility remains unknown. In the present study, 58 unrelated patients and 69 controls have been analyzed for their class I and class II serologic antigens, class II (DR and DQ) DNA restriction fragment length polymorphism, their deduced DQA1 and B1 exon 2 nucleotide sequences and their corresponding amino acid residues. By using the etiologic fraction (delta) as an almost absolute measure of the strongest linkage disequilibrium of an HLA marker to the putative SLE susceptibility locus, it has been found that the strength of association of the HLA marker may be quantified as follows: DQA1*0501 (associated to DR3) or DQB1*0201 (associated to DR3) > non Asp 57 beta DQ/Arg 52 alpha DQ > DR3 > non Asp 57 beta DQ. Thus, molecular HLA DQ markers tend to be more accurate as susceptibility markers than the classical serologic markers (DR3). However, dominant or recessive non Asp 57 beta DQ susceptibility theories, as previously postulated for insulin-dependent diabetes mellitus, do not hold in our SLE nephritic population; indeed, three patients bear neither Arg 52 alpha DQ nor Asp 57 beta DQ suscepibility factors. On the other hand, nonsusceptibility factors are included in our population in the A30B18CF130-DR3DQ2(Dw25) haplotype and not in A1B8CS01-DR3DQ2(Dw24); this distinctive association has also been recorded in type I diabetes mellitus and may reflect the existence of common pathogenic HLA-linked factors for both diseases only in the A30B18CF10DR3DQ2(Dw25) haplotype. Finally, the observed increase of deleted C4 genes (and not 'null' C4 proteins) in nephritic patients shows that C4 genes are disease markers, but probably without a pathogenic role.
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PMID:Differential contribution of C4 and HLA-DQ genes to systemic lupus erythematosus susceptibility. 810 32

Fourteen examples of lymphocytic mastitis (LM) with epithelioid stromal cells characterized by formation of a palpable, hard breast mass composed of a predominantly lobulocentric lymphocytic infiltrate, stromal fibrosis, and an unusual stromal infiltrate of epithelioid cells are presented. The epithelioid cells were so prominent and abundant that the possibility of an infiltrating carcinoma was raised in three cases, and a fourth case was misinterpreted as a granular cell tumor. Interestingly, eight of the 12 women and the only male patient had long standing, insulin dependent diabetes mellitus (IDDM), whereas two had IDDM and hypothyroidism, one had hypothyroidism alone, and one had systemic lupus erythematosus. Contrary to the conclusions in a recent report, our findings indicate that these mammary changes are not exclusive to patients with IDDM, and may also occur in nondiabetic patients particularly those with autoimmune disorders. The morphologic features of the epithelioid stromal cells which have been mistaken for infiltrating carcinoma are emphasized; immunohistochemical and ultrastructural findings favoring their myofibroblastic nature are presented.
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PMID:Epithelioid stromal cells in lymphocytic mastitis--a source of confusion with invasive carcinoma. 815 52

Few treated chronic conditions preclude the ability of a mother to conceive. However, consequences of the condition may undermine the pregnancy or aggravate maternal disease. Most chronic conditions require nutritional intervention beyond the normal needs of pregnancy. Insulin-dependent diabetes mellitus (IDDM) and systemic lupus erythematosus (SLE) are two common autoimmune disorders that affect women of childbearing age. Little has been published about the long-term consequences of current medication regimens for SLE and their interactions with either nutrient metabolism or requirements. More information is available on macronutrient dietary needs and metabolism during pregnancy and lactation in women with IDDM, but little is published about the metabolism of other nutrients in this condition. Thus, the nutritional consequences of treating these diseases during pregnancy and lactation must be evaluated continually.
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PMID:Nutritional consequences of chronic maternal conditions during pregnancy and lactation: lupus and diabetes. 830 84

Presence of autoimmune diseases and relationship of autoantibody expression with HLA association has been studied in 44 multicase rheumatoid arthritis (RA) families of Asian Indian origin. An increased prevalence of systemic lupus erythematosus (SLE) was observed in relatives (2.3%). Although HLA-DR4 segregated preferentially with seropositivity in general, no difference was observed among seropositive versus seronegative RA. On the other hand, no HLA association was observed with ANF positivity in these families. An increased frequency of DR7 in the ANF negative and RF negative group of RA patients compared to positive groups suggests that it may act as protective element for the development of autoantibodies in RA. An increased occurrence of DR4 in relatives affected with SLE was observed. While RA segregated mostly with HLA-DR4 in these families, autoimmune thyroid disease and insulin dependent diabetes mellitus (IDDM) segregated with HLA-DR3 suggesting the involvement of at least two sets of HLA-linked autoimmunity favouring susceptibility genes in the Indian population.
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PMID:Occurrence of autoimmune diseases and relationship of autoantibody expression with HLA phenotypes in multicase rheumatoid arthritis families. 835 6

The involvement of autoantibodies in the extrathyroidal manifestations of Graves' disease has been the subject of extensive investigation, with fairly inconclusive results to date. We investigated the presence of immunoglobulin A (IgA) and IgG antibodies in patients with Graves' disease and pretibial myxedema (PTM; n = 21) as well as those with Graves' disease with thyroid-associated ophthalmopathy (TAO; n = 10), Graves' disease with no clinical evidence of extrathyroidal manifestations (n = 11), Hashimoto's thyroiditis (n = 9), type 1 diabetes mellitus (n = 10), systemic lupus erythematosus (n = 9) and normal individuals (n = 17). We looked for antibodies to both retroocular muscle and dermal fibroblasts as well as to thyroid peroxidase, thyroid microsomal antigen, thyroglobulin, and human eye muscle membranes. IgA class antibodies to microsomal antigen (30-50% of patients), thyroid peroxidase (5-20%), and human eye muscle membrane (0-26%) antigens were found in the various groups of patients with Graves' disease. With each of these antigens, serum from patients with PTM showed the greatest binding. Highly significant IgA binding was shown by PTM serum to both dermal (P < 0.001) and retroocular muscle (P < 0.001) fibroblasts from 12 different donors. Serum from Graves' patients with and without TAO and that from Hashimoto's thyroiditis patients reacted significantly with 4 of the 12 fibroblasts lines. In contrast, IgG binding was only found for 3 of the 12 fibroblast lines using patient serum. The IgA binding to fibroblasts shown by PTM patients was predominantly of the IgA2 subclass. The activity was absorbed out by both fibroblasts and thyroid cells. In immunoblotting studies, PTM patient serum reacted with a 54-kilodalton dermal fibroblast antigen and a 66-kilodalton retroocular fibroblast antigen. No binding to these antigens was seen with serum from normal controls or patients without PTM. Further elucidation of the nature of this fibroblast antigen will help to determine the role of IgA autoantibodies in the extrathyroidal manifestations of Graves' disease.
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PMID:Immunoglobulin A class fibroblast antibodies in patients with Graves' disease and pretibial myxedema. 853 May 78

SLE is dramatically more prevalent in persons of African descent than in other populations. Several genes in the class III region of the MHC have been considered as potential susceptibility loci for this disorder, but the primary association(s) remains unknown. The stress protein gene, hsp70-2, is of special interest in this regard because it encodes a protein functionally relevant to antigen processing and presentation and has itself been identified as a putative susceptibility locus in organ-specific autoimmune diseases in Caucasians. To clarify the relationship of the hsp70-2 gene to SLE in African Americans, genomic DNA from 46 patients and 42 appropriately matched control subjects was analyzed for an RFLP of the hsp70-2 gene using the probe pH2.3 and the restriction endonuclease PstI, which identifies alleles of 8.5 and 9.0 kb. The 8.5-kb hsp70-2 allele was associated with SLE in this population (X2 = 8.2473, p = 0.0044). This association was not due to linkage disequilibrium with the C4A deletion or with HLA-DR3, as has been reported in Caucasians with IDDM. These data suggest that the 8.5-kb hsp70-2 allele may be an independent susceptibility marker for SLE in African Americans.
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PMID:The 8.5-kb PstI allele of the stress protein gene, Hsp70-2: an independent risk factor for systemic lupus erythematosus in African Americans? 865 62


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