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PubMed1991

An immunogenetically defined and immunodominant Trypanosoma cruzi antigen.

Two strains of mice, A. SW (H-2s) and A.CA (H-2f), were immunized with live trypomastigotes or epimastigotes of the Tulahuen strain of Trypanosoma cruzi or with their sonicates. By immunowestern blotting, sera from A.SW mice, but not from A.CA, recognized, in an immunodominant fashion, a 45 kDal polypeptide (Tc45) present in both epimastigotes and trypomastigotes. Since A.SW and A.CA strains are congenic for the major histocompatibility H-2 complex, recognition of Tc45 seems to be controlled by this genetic region or by gene(s) located in its immediate vicinity. Subcellular fractionation revealed that Tc45 is mainly present at the cytoplasmic compartment.

Animals↗
PubMed1984

Primary Sjögren's syndrome and other autoimmune diseases in families. Prevalence and immunogenetic studies in six kindreds.

The relationships of human leukocyte antigen (HLA) and heavy chain immunoglobulin (Gm) haplotypes to disease and autoantibody expression were examined in six large kindreds, each having one or more members with primary Sjögren's syndrome. Various other autoimmune diseases and autoantibodies occurred among the 117 relatives in these families. The HLA and Gm haplotypes did not necessarily segregate persons into those with Sjögren's syndrome, other autoimmune disorders, or serologic abnormalities, but HLA alleles DR3 and DR2 occurred in significant excess in relatives with Sjögren's syndrome, irrespective of HLA haplotype. Segregation analysis suggested a Mendelian dominant genetic defect common to the many autoimmune diseases and serologic reactions that was not linked to HLA or Gm. A significant effect of female sex was also documented. These studies suggest that Sjögren's syndrome results from the interaction of several HLA-linked and non-HLA-linked genes.

Adult↗
PubMed1981

Gold-induced thrombocytopenia. A clinical and immunogenetic study of twenty-three patients.

Thrombocytopenia developed in 23 patients with rheumatoid arthritis treated with gold salts over 25 years. All patients recovered, and there were no episodes of life-threatening hemorrhage; four patients eventually needed splenectomy. The clinical presentation of gold-induced thrombocytopenia and its treatment and outcome are reviewed. Because gold-induced thrombocytopenia is believed to have an immunologic basis, we sought an association between this complication and antigens of the human leukocyte antigen (HLA) region. The most significant finding was the association of the HLA-DR3 alloantigen in 12 of 15 of these patients compared with 26 of 84 in a control population (x2 12.9, p less than 0.001). This study provides further evidence that gold-induced thrombocytopenia is immunologically mediated and that genes of the major histocompatibility complex are involved.

Adult↗
PubMed1983

Immunogenetics of the neonatal lupus syndrome.

Infants with neonatal lupus erythematosus have congenital heart block, transient cutaneous lesions, or both. Mothers of these infants have SSA/Ro autoantibodies that are passed across the placenta to the fetus and that have been temporarily associated with the syndrome. Six families with neonatal lupus were studied by HLA typing. All seven infants had transient cutaneous lesions, congenital heart block, or both. Five of six mothers were asymptomatic and one had Sjögren's syndrome. Six of seven infants and all six mothers had antibodies to SSA/Ro in their sera. The infants became seronegative by age 8 months. Five mothers were positive for HLA-DR3, five for HLA-MB2, six for HLA-MT2, and six for HLA-B8. No HLA associations were seen in infants. Gene products of the DR or similar regions may be associated with autoantibody production but not with other events in tissue injury.

Antibodies, Antinuclear↗
PubMed1999

Genetic analysis of disease subtypes and sexual dimorphisms in mouse experimental allergic encephalomyelitis (EAE): relapsing/remitting and monophasic remitting/nonrelapsing EAE are immunogenetically distinct.

Experimental allergic encephalomyelitis (EAE) is the principal animal model of multiple sclerosis (MS), the major inflammatory disease of the central nervous system. Murine EAE is generally either an acute monophasic or relapsing disease. Because the clinical spectrum of MS is more diverse, the limited range of disease subtypes observed in EAE has raised concern regarding its relevance as a model for MS. During the generation of a large F2 mapping population between the EAE-susceptible SJL/J and EAE-resistant B10.S/DvTe inbred lines, we identified four distinct subtypes of murine EAE resembling clinical subtypes seen in MS. We observed acute progressive, chronic/nonremitting, remitting/relapsing, and monophasic remitting/nonrelapsing EAE. An additional subtype, benign EAE, was identified after histologic examination revealed that some mice had inflammatory infiltrates of the central nervous system, but did not show clinical signs of EAE. Genome exclusion mapping was performed to identify the loci controlling susceptibility to each disease subtype. We report three novel EAE-modifying loci on chromosomes 16, 7, and 13 (eae11-13, respectively). Additionally, unique loci with gender-specific effects govern susceptibility to remitting/relapsing (eae12) and monophasic remitting/nonrelapsing (eae7 and 13) EAE.

Animals↗
PubMedDate not supplied

[The immunomodulator ximedon lowers the level of induced DNA damages in bone marrow and peripheral blood cells: the possibilities for immunogenetic correction].

It was established in experiments on albino unbred mice and during treatment of patients with osteomyelitis that 30 mg/kg of ximidon suppresses the formation of micronuclear polychromatophilic erythrocytes found in the bone marrow of mice and peripheral blood of patients with chronic osteomyelitis. The interrelationship of the results obtained with the modulating effect of ximidon on the mitochondrial, thiol, and adenylate cyclase-dependent mechanisms of cell regulation is discussed.

4-Aminobenzoic Acid↗
PubMed1999

[Immunology in medical practice. XXVI. Immunogenetics of chronic inflammatory bowel diseases].

Epidemiological and family studies have shown that the inflammatory bowel diseases (IBD), encompassing ulcerative colitis and Crohn's disease, are in large part genetically determined. This genetic susceptibility is complex and does not follow Mendelian inheritance patterns. The search for susceptibility genes is further complicated by genetic and clinical heterogeneity. Recent developments in molecular biology have enabled the identification of chromosomal regions and genes underlying IBD. Genetic association studies have established a role of HLA genes and cytokine gene polymorphisms in the pathogenesis of IBD. Whole genome linkage analysis studies using microsatellite markers and affected sib-pair analysis have identified two chromosomal locations (IBD1 on chromosome 16 and IBD2 on chromosome 12) associated with IBD. Recent investigations have shown that some chromosomal regions play a role in several autoimmune disorders. This suggests the presence of two types of genes in these diseases: genes that encode proteins that play a key role in the immune response and predisposing for autoimmune diseases in general, and disease-specific genes that are responsible for the phenotype and the severity of the disease.

Chromosomes, Human, Pair 12↗
PubMed2000

Anti-ganglioside antibodies in a large cohort of European patients with systemic lupus erythematosus: clinical, serological, and HLA class II gene associations. European Concerted Action on the Immunogenetics of SLE.

OBJECTIVE: To assay anti-ganglioside antibodies (aGM1) in sera of a large cohort of European patients with systemic lupus erythematosus (SLE) to define the prevalence of these autoantibodies in SLE; to evaluate the association of aGM1 with clinical manifestations and other autoantibodies found in SLE; and to search for aGM1 association with HLA class II alleles. METHODS: Four hundred forty-eight patients with SLE were consecutively enrolled in 8 centers from 6 European countries. All sera were tested for antinuclear antibodies by immunofluorescence on HEp-2 cells as substrate, anti-dsDNA, aGM1, aCL, abeta2-glycoprotein I (abeta2-GPI) antibodies by ELISA, and antineutrophil cytoplasmic antibodies (ANCA) by immunofluorescence and by ELISA. Genomic typing for HLA class II loci was performed by polymerase chain reaction-sequence specific oligonucleotide probe method. Clinical assessment was done at the time of enrolment. RESULTS: We found 41.9% of patients with clinical signs of neuropsychiatric involvement; 15.5% of patients were positive for aGM1, 8% of the IgG isotype and 8.6% of the IgM isotype; aGM1-IgG were associated with neuropsychiatric manifestations (NPM) (RR = 3.7), with migraine (RR = 2.4), with OBS (RR = 7.3), and with peripheral neuropathy (RR = 8.5). aGM1-IgM were associated with NPM (RR = 4) and with depression (RR = 3.4). Furthermore, the genetic study showed that aGM1-IgG were associated with HLA-DQB1*0404 (RR = 7.2) while aGM1-IgM were associated with HLA-DQB1*0605 (RR = 33.3). No associations were found between aGM1 and anti-dsDNA, aCL, abeta2GP1, or ANCA. CONCLUSION: Our results show aGM1 can be found in patients with SLE. aGM1 may play a pathogenetic role for some NPM in this condition.

Adolescent↗
PubMed1999

Anticardiolipin and anti-beta2GPI antibodies in a large series of European patients with systemic lupus erythematosus. Prevalence and clinical associations. European Concerted Action on the Immunogenetics of SLE.

OBJECTIVE: To test the prevalences and the clinical associations of anticardiolipin (aCL) and anti-beta2GPI (abeta2GPI) antibodies in a large series of European patients with systemic lupus erythematosus (SLE). METHODS: 574 SLE patients from 7 European countries were tested for aCL and abeta2GPI by ELISA methods. RESULTS: aCL of IgG, IgM, and IgA isotypes were detected in 22.8%, 14%, and 13.9% of the patients, respectively. IgG and IgM abeta2GPI were detected in 20% of the patients. The presence of aCL was highly associated with the presence of abeta2GPI. Medium-high titer IgG aCL and abeta2GPI were associated with thrombosis, with similar sensitivity, specificity, and positive predictive value. When present at medium-high titer, IgG aCL were associated with thrombocytopenia, IgM aCL with hemolytic anemia, and cerebrovascular accidents. IgA aCL with livedo reticularis and Raynaud's phenomenon. CONCLUSIONS: aCL, when present at medium-high titer, are as important as abeta2GPI, as a risk factor for thrombosis. Medium-high titer aCL, but not abeta2GPI, are associated with other clinical features of the antiphospholipid syndrome.

Adolescent↗
PubMed1975

Immunogenetics of a thymus antigen in lymphoma-prone and lymphoma-resistant colonies of wild mice.

The Thy-1 (theta) antigen was identified in wild mice (Mus musculus), the frequency of its alleles was determined in two natural populations of wild mice, and the possible T-cell origin of spontaneous lymphomas was investigated in one of these populations. Reaction patterns for Thy-1 antigen with the use of direct cytoxicity and indirect absorption assays were identical in wild mice and inbred strains. Between 15 and 55 percent of viable spleen cells from healthy young or old wild mice were Thy-1 positive. Spleen, but not brain, cells from older wild mice were less strongly positive. Wild mice from the lymphoma-prone population were polymorphic for Thy-1alpha and Thy-1beta alleles, whereas wild mice from the lymphoma-resistant populations were homozygous for the Thy-1beta allele. Contrary to expectation, a higher frequency of the Thy-1beta allele was noted in the mice with lymphomas. Alleles at two other loci on chromosome number 9 (Mod-1alpha and Trfbeta) were fixed in both populations. The absence of detectable Thy-1 antigen on spleen cells (despite its detectability in undiminished titer in brain tissue) in 80 percent of mice with lymphomas, along with the absence of thymus involvement in the lymphomatous proliferations, suggested that these tumors are derived from an expansion of non-thymus-derived cells.

Absorption↗
PubMed1999

[The diagnostic significance of immunogenetic markers in vertebrogenic neurological syndromes].

A total of 116 patients presenting with different neurological syndromes of vertebral osteochondrosis were examined. More common in patients with reflex neurological manifestations of osteochondrosis compared with controls (n = 51) was a complete HLA phenotype (heterozygosity) determining better evolutional and biological resistance to injuring factors and ability to produce adequate adaptive and compensatory reactions. The diagnosing of incomplete phenotype in other groups indicated homozygosity of genes and suggested a high risk for development of the disorder. Criteria have been established for a relative risk of development of the disease for all six vertebrogenic neurological syndromes.

Biomarkers↗
PubMed2000

Clinico-immunogenetic characteristics of multiple sclerosis with optic neuritis in children.

The frequency of multiple sclerosis (MS) with clinical onset before 16 years of age in different regions of Russia fluctuates from 2 to 10% of all MS patients. One of the most frequent signs of MS manifestation and/or exacerbation at this age is optic neuritis (ON). Forty-seven children with MS were observed in Moscow. Diagnosis of MS in every case was clinically definite and proved by serial MRI. Clinico-tomographic dissociation was noticed: numerous large lesions, typical for MS on T2 images were often seen in children with mild or moderate residual neurological symptoms. All patients had relapsing/remitting MS course, mean EDSS was 2.24+/-0.26. Thirty-eight children (80%) had ON at least once, ten (21.3%) - twice or more times. In several cases ON had subclinical course or might be missed and the damage of the optic nerve with partial atrophy was found only after complex ophthalmological investigation including visual evoked potentials. Thus, the clinical course of MS and ON have some peculiarities in children and may be genetically based. Analyses of allelic polymorphisms of HLA-DR and TNF loci on chromosome 6 was performed. Data from children with MS were compared with data from their parents, healthy controls and other MS patients from the same ethnic group. Children with MS had increased frequency of DR2(15) and TNF-a11, but not TNF-a9 as adult MS patients from the same ethnic group. The presence of TNF-a7, rare in adult patients, could be proposed as a marker of early MS onset.

Adolescent↗