Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “immunogenetics”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,621 records · Page 90Linked to original sources
PubMed1996

[Genetic features of the Brown Carpathian breed--a vanishing local breed of cattle in the Western Ukraine].

A wide range of variation in immunogenetic and biochemical markers was found in thoroughbred Brown Carpathian cattle. Comparative analysis of genetic structure of Brown Carpathian and Swiss cattle, as well as various hybrids of these two breeds, with respect to polymorphic biochemical systems, demonstrated that all hybrids having any gene admixture of the Brown Carpathian breed formed a single cluster in a dendrogram and were readily distinguishable from thoroughbred Swiss cattle. Originally, the Swiss breed participated in forming the gene pool of Brown Carpathian cattle. The selective advantage of some gene associations, which included the loci of the biochemical genetic systems studied, was suggested to be a specific characteristic of the Brown Carpathian breed. Genetic differentiation in the groups of hybrids bred in regions with different ecological conditions (high- and lowland) was revealed.

Animals↗
PubMed1995

Fast food arthritis--a clinico-pathologic study of post-Salmonella reactive arthritis.

OBJECTIVE: To study the clinical presentation, immunogenetics, and serum immune response to lipopolysaccharide (LPS) in a cohort of patients with post-Salmonella reactive arthritis (ReA). METHODS: A validate ReA screening questionnaire (Quest 2) was mailed to 919 individuals reporting symptoms of gastroenteritis to the health department after eating at a single restaurant. Three hundred twenty-one persons returned questionnaires; 170 reported symptoms outside the gastrointestinal tract; 23 of those 170 reporting persistent joint symptoms were seen 4 to 16 weeks after the outbreak and 5 of the 23 were seen in followup 12 to 20 weeks later. Clinical features, HLA Class I typing, serum soluble CD8 levels, and serum antibodies to gram negative LPS by ELISA were determined. RESULTS: Joint complaints were reported more frequently by individuals with a longer duration of diarrhea. Upper extremity joints were frequently involved, and 66% reported one or more extraarticular symptoms of Reiter's syndrome. Three of 5 typed individuals were HLA-B27 positive, including 3 of the 4 most severely involved. Serum soluble CD8 levels correlated poorly with disease activity measured either clinically or by C-reactive protein. Antibodies to Klebsiella and Shigella LPS rose over time, while antibodies to Salmonella LPS fell. CONCLUSION: The clinical picture of post-Salmonella ReA is less stereotyped than often assumed, although severity correlated with HLA-B27 status. The association of joint symptoms with duration of diarrhea and the kinetics of the anti-LPS antibody response support the hypothesis that abnormal gut permeability plays a role in the pathogenesis of post-Salmonella ReA.

Antibodies, Bacterial↗
PubMed1997

High affinity human antibodies by phage display.

The development of phage display has now made it possible to consider the isolation of human antibodies directly without immunization. Recent advances in the field of human immunogenetics and in phage technology have led to the assembly of 'naive' human repertoires in vitro whose complexity approach that of the natural immune system. Screening of these libraries has allowed the isolation in one step of antibodies with affinities in the nanomolar range.

Antibodies↗
PubMed1997

[Immunology in clinical practice. VII. Psoriasis].

A new hypothesis of the pathogenesis of psoriasis holds that psoriasis is an epidermal hyperproliferative disorder resulting from abnormal interaction between T cells and basal layer stem cell keratinocytes. New therapies aimed at reducing T cell activity are most successful, as exemplified by the efficacy of systemic cyclosporine in severe cases of psoriasis. New developments in immunogenetics and immunodermatology are anticipated and it is expected that they will fully explain the chain of pathological events.

Antibodies, Monoclonal↗
PubMedDate not supplied

[Genetic-physiologic mother-fetus relationships and their effect on the adaptive traits of the offspring].

Using our own data and literature, we present analysis of genetic-physiological mechanisms providing for stable reproduction of mammals. Using multiparous species (such as minks, mice, water voles), we demonstrate that embryonic and early postnatal mortality of the offspring makes a significant contribution to stabilization of the actual fertility rate at a level optimal for the species. Studies of phenogenetics of fertility of inbred mice and their hybrids have demonstrated the definitive role of immunogenetic relationships between mother and fetuses in establishing of vitally important characteristics of the offspring. Antigenic differences between mother and fetuses observed in crosses between different strains and in experiments on allogenic transplantation of embryos provide stimulate the hormonal support of pregnancy (increase the level of progesterone) and the rate of embryonic development. It has been shown that antigenic stimulation of mother's immune system has a modifying effect on physiological and behavioral characteristics of the offspring and specifically on certain components of their reproductive success. In studies of the olfactory choice of mating partners by mouse and water vole females we established that mammals are capable of "predicting" the optimal phenotypic combination of parents leading to the most effective development of the offspring.

Adaptation, Physiological↗
PubMed1993

Role of predisposing and protective HLA-DQA and HLA-DQB alleles in Sardinian multiple sclerosis.

OBJECTIVE: To study the role of HLA genes in susceptibility and resistance to multiple sclerosis (MS) in Sardinian patients. To verify whether HLA-DQA and HLA-DQB genes differed between unrelated (MSU) and related (MSR) patients, and whether relapsing-remitting and chronic progressive forms of MS are immunogenetically distinct entities. DESIGN: Case-control study of HLA-DQA and HLA-DQB gene frequency. SETTING: All patients investigated were followed up by our MS referral centers. PATIENTS: The study involved 116 MSU patients, 67 of whom had a relapsing-remitting form (MSr), 28 of whom had a chronic progressive from-the-onset form (MSc), and 21 of whom had a benign form (MSb), 32 patients with MSR, 19 parents and 27 healthy siblings of patients with MSR, and 86 controls. Selection of patients was random, while control subjects came from families without known immunologic diseases. All patients had definite MS. MAIN OUTCOME MEASURE: Statistical analysis of gene frequencies was conducted with the chi 2 test with correction (Pc) for the alleles investigated, as was decided before the study began. RESULTS: The DQA1*0301 allele was found to be increased in patients (MSU vs controls, Pc = .008; patients with MSc vs controls, Pc = .001; patients with MSR vs controls, Pc = .02; and parents vs controls, Pc = .04), while the DQA1*0102 allele was found to be diminished in patients with MSr vs controls (Pc = .001). Among the DQB genes, the DQB1*0502 allele was diminished in patients with MSr vs controls (Pc = .04), while the sum of DQB1*0201 and *0302 alleles was significantly increased in patients with MSR vs controls (Pc = .003). CONCLUSION: Both HLA-DQA and HLA-DQB genes influence genetic susceptibility and resistance to MS. The roles of these genes differ in the various forms of MS. Patients with MSU and MSR both share HLA-DQA susceptibility genes.

Adolescent↗
PubMed1997

HLA typing in acute optic neuritis. Relation to multiple sclerosis and magnetic resonance imaging findings.

OBJECTIVE: To study the association of brain magnetic resonance imaging (MRI) findings and HLA findings to clarify the relationship between monosymptomatic optic neuritis (ON) and ON as part of clinically definite multiple sclerosis (CDMS). DESIGN: Population-based cohort of patients with ON referred prospectively during 6 years by neurologists and ophthalmologists within 4 weeks of onset of ON. SETTING: Referral center in the general community of greater Copenhagen (Denmark) (population, 1.5 million). PATIENTS: A consecutive sample of 199 patients aged 12 to 59 years with ON (133 with idiopathic ON, 66 with ON + CDMS), ethnically matched with 192 healthy volunteers. MAIN OUTCOME MEASURES: Relation between the HLA-DR15, -DR17, -DQA-1B, and -DQB-1B polymorphisms as defined by restriction fragment length polymorphism analysis, and presence of plaques on T2-weighted brain MRI. RESULTS: The frequency of HLA-DR15 was significantly increased in patients with ON + CDMS (52%) and ON (47%) compared with control subjects (31%). The frequency of HLA-DR17 was almost equal in the ON + CDMS (18%), ON (23%), and control (23%) groups. The frequencies of HLA-DQA-1B (55% in ON + CDMS, 58% in ON) and HLA-DQB-1B (49% in ON + CDMS, 59% in ON) were significantly increased compared with control subjects (41%, HLA-DQA-1B; 37%, HLA-DQB-1B). Brain MRI was abnormal in 48 of 56 examined patients with ON + CDMS and in 64 of 120 examined patients with ON (P < .001). In contrast, the frequencies of HLA alleles did not differ between patients with and without demyelinating lesions. However, patients with ON and normal MRI findings did not show association with HLA-DR15. CONCLUSIONS: The frequencies of alleles were similar in patients with ON and ON + CDMS, confirming that they are not 2 immunogenetically distinct disease entities. The heterogeneity within the group of patients with ON suggests that the HLA-DR15 molecule is involved in susceptibility to initial demyelinating lesion formation.

Acute Disease↗
PubMed1998

Molecular immunology and genetics of inflammatory muscle diseases.

Polymyositis, dermatomyositis, and inclusion body myositis, although immunopathologically distinct, share 3 dominant histological features: inflammation, fibrosis, and loss of muscle fibers. Progress in molecular immunology and immunogenetics has enhanced our understanding of these cellular processes. Based on the T-cell receptor gene rearrangement, the autoinvasive CD8+ T cells in polymyositis and inclusion body myositis, but not dermatomyositis, are specifically selected and clonally expanded in situ by heretofore unknown muscle-specific autoantigens. The messenger RNA of cytokines is variably expressed, except for a persistent up-regulation of interleukin 1beta in inclusion body myositis and transforming growth factor beta in dermatomyositis. In inclusion body myositis, the interleukin 1, secreted by the chronically activated endomysial inflammatory cells, may participate in the formation of amyloid because it up-regulates beta-amyloid precursor protein (beta-APP) gene expression and beta-APP promoter and colocalizes with beta-APP within the vacuolated muscle fibers. In dermatomyositis, transforming growth factor beta is overexpressed in the perimysial connective tissue but is down-regulated after successful immunotherapy and reduction of inflammation and fibrosis. The degenerating muscle fibers express several antiapoptotic molecules, such as Bcl-2, and resist apoptosis-mediated cell death. In myositis, several of the identified molecules and adhesion receptors play a role in the process of inflammation, fibrosis, and muscle fiber loss, and could be targets for the design of semispecific therapeutic interventions.

Apoptosis↗
PubMed1979

HLA antigens in ocular cicatricial pemphigoid.

HLA antigen frequencies were studied in 45 patients with ocular cicatricial pemphigoid. HLA-B12 was found to have an increased frequency of 44.4% in patients with ocular cicatricial pemphigoid, which was statistically significant when compared with a frequency of 19.6% in the control population (P less than .001 or P less than .031 when corrected for the number of antigens tested). The results of this study suggest that there is an immunogenetic susceptibility to the development of ocular cicatricial pemphigoid.

Eye Diseases↗
PubMed1982

HLA antigens in Stevens-Johnson syndrome with ocular involvement.

Fifteen white patients and three black patients with Stevens-Johnson syndrome (SJS) with ocular involvement had HLA typing performed. The HLA-Bw44 antigen was found to have an increased frequency of 66.7% in white patients with SJS with ocular involvement, which was statistically significant when compared with a frequency of 20.4% in the white control population. The results of this study suggest that there is an immunogenetic susceptibility to the development of SJS with ocular manifestations in white patients.

Adolescent↗
PubMed1982

Close association of HLA-Bw51 with Behçet's disease.

Frequency of HLA-A, B, and C antigens was studied in 184 patients with Behçet's disease to investigate the immunogenetically determined predisposition to this disease. A statistically significant increased incidence of HLA-B5 or Bw51 was noted in the patients as compared with the normal control subjects. No significant difference was observed in the distribution of other HLA antigens. On the basis of HLA studies, it seems likely that the susceptibility genes to Behçet's disease closely linked to HLA-Bw51 may have been spread by the old nomadic tribes or the Turks via the Silk Route.

Behcet Syndrome↗
PubMed1990

HLA-B7 and HLA-DR2 antigens and acute posterior multifocal placoid pigment epitheliopathy.

Acute posterior multifocal placoid pigment epitheliopathy is a chorioretinal inflammatory disease occurring in young, healthy adults. Its cause is unknown, although it frequently follows a flulike illness. We reexamined 30 patients with documented acute posterior multifocal placoid pigment epitheliopathy to determine their HLA class I antigen (A and B) and class II antigen (DR and DQ) distribution. The HLA class I antigen B7 was found in 12 patients (40.0%) compared with 63 controls (16.6%) (relative risk, 3.38). The class II antigen DR2 was present in 17 patients (56.7%) compared with 107 controls (28.2%) (relative risk, 3.34). The specific role of HLA antigens in uveitis is unknown, but the finding of an increased prevalence of HLA-B7 and HLA-DR2 antigens in patients with acute posterior multifocal placoid pigment epitheliopathy suggests an immunogenetic predisposition to acquiring this disease.

Chorioretinitis↗
PubMed1991

Association of HLA antigens with Vogt-Koyanagi-Harada syndrome in a Han Chinese population.

Vogt-Koyanagi-Harada syndrome, or the uveomeningitis syndrome, is one of the most commonly identified types of endogenous uveitis diagnosed in China. Because its incidence is higher in Orientals than in whites, immunogenetic background [corrected] may be an important factor in its incidence. We performed HLA-A, -B, and -DR typing on 25 patients with Vogt-Koyanagi-Harada syndrome and on 65 healthy control subjects from the Han Chinese population. The results showed that HLA-DR4 and -Dw53 were closely associated with Vogt-Koyanagi-Harada syndrome (P less than .001 [relative risk = 16.0] and P less than .001 [relative risk = 34.2], respectively). This association is similar to that reported in patients with Vogt-Koyanagi-Harada syndrome in Japan, suggesting that DR4 and DRw53 may play important roles in the development of Vogt-Koyanagi-Harada syndrome in Oriental populations.

Adolescent↗
PubMed1998

The role of the HLA-DQA1 gene in resistance to atrophic gastritis and gastric adenocarcinoma induced by Helicobacter pylori infection.

BACKGROUND: It has been suggested that immunogenetic factors for susceptibility or resistance to disease caused by Helicobacter pylori exist in the host. To examine host genetic factors that increase the risk of gastric adenocarcinoma among H. pylori-infected persons, the HLA-DQA1 locus was examined in patients with gastric adenocarcinoma. METHODS: Eighty-two gastric adenocarcinoma patients and 167 unrelated controls were examined for H. pylori infection and HLA-DQA1 genotyping. In addition, serum pepsinogen A (PGA) and pepsinogen C (PGC) values and the PGA/PGC ratio, which have been characterized as markers of gastric mucosal atrophy, also were analyzed. RESULTS: Of the 167 controls, 121 were H. pylori positive (+) and 46 were H. pylori negative (-). All H. pylori (-) individuals had normal endoscopic and histologic findings. Among the 121 H. pylori (+) controls, 36 had superficial gastritis and 85 had atrophic gastritis. The allele frequency of DQA1*0102 was significantly lower in the H. pylori (+) atrophic gastritis group than in the H. pylori (+) superficial gastritis and H. pylori (-) normal control groups. In addition, the allele frequency of DQA1*0102 also was significantly lower in the H. pylori (+) intestinal type gastric adenocarcinoma group than in the H. pylori (-) normal control, H. pylori (+) superficial gastritis, and H. pylori (-) diffuse type gastric adenocarcinoma groups. Serum PGA and PGC values and the PGA/PGC ratio did not differ significantly among HLA-DQA1 genotypes; however, the PGA/PGC ratio was significantly lower in the H. pylori (+) atrophic gastritis and H. pylori (+) intestinal type gastric adenocarcinoma groups than in the H. pylori (-) normal control and H. pylori (+) superficial gastritis groups. CONCLUSIONS: The DQA1*0102 allele may contribute to resistance against H. pylori-associated gastric atrophy and its association with intestinal type gastric adenocarcinoma, whereas the absence of DQA1*0102 may be a host genetic risk factor for H. pylori-associated atrophic gastritis and intestinal type gastric adenocarcinoma.

Adenocarcinoma↗
PubMed1998

HPV 16 infection and progression of cervical intra-epithelial neoplasia: analysis of HLA polymorphism and HPV 16 E6 sequence variants.

High-risk human papillomavirus (HPV) infection plays an important role in cervical intra-epithelial neoplasia (CIN), but HPV infection alone is not sufficient for progression to cervical cancer. Several lines of evidence suggest that cellular immune surveillance is important in the control of HPV infection and the development of CIN. The presentation to T cells of target viral peptides in the context of HLA molecules is influenced by the genetic polymorphisms of both HPV and HLA and thereby influences the host immune response and clinical outcome of HPV infection. HLA class I and II polymorphism in susceptibility for HPV 16 infection, development and progression of CIN was analyzed in a group of 118 patients participating in a prospective study of women with initial abnormal cytology. Patients were stratified according to HPV status and course of the disease. HLA-B*44 frequency was increased in the small group of patients with a lesion that showed clinical progression during follow-up [OR = 9.0 (4.6-17.5), p = 0.007]. HLA-DRB1*07 frequency was increased among HPV 16-positive patients compared with patients who were negative for all HPV types [OR = 5.9 (3.0-11.3), p = 0.02]. Our results are consistent with the immunogenetic factors associated with disease progression being different from those associated with susceptibility to HPV 16 infection. Sequencing of the HPV 16 E6 and E7 open reading frames of a subset of these patients (n = 40) showed the frequency of HPV 16 variants to be similar to other studies. However, there was no significant correlation between variant incidence and disease progression or viral persistence and no significant correlation with any HLA allele. It appears that multiple HLA types can influence HPV 16-associated cervical dysplasia but the role of HPV 16 variants in disease progression and susceptibility in relation to HLA polymorphism remains unclear.

Adult↗
PubMed1999

Geographic diversity of adult t-cell leukemia/lymphoma in Brazil. The Brazilian ATLL Study Group.

We describe 195 cases of adult T-cell leukemia/lymphoma (ATLL) reported to the national registry of T-cell malignancies in Brazil between 1994 and 1998. We compared the effect of demographic differences and clinical features of 150 consecutive ATLL cases in different regions of this diverse country. At diagnosis, the predominant clinical sub-type was the acute type (60%), followed by lymphoma (22%), chronic (10%) and smoldering (8%) types. Although we expected that different sub-types would be present in different regions, on the basis of immunogenetic factors determined by ethnicity, we did not demonstrate these differences. There were no significant differences among ATLL subtypes by age or gender. No ethnic group predominated in the total population of patients, but significant differences were noted when examining ethnic distribution by region. Reflecting the general population distribution, white patients were seen more often in São Paulo and black patients in Bahia, than in other regions. In most regions, cases were equally distributed between blacks and mulattos, except in Pernambuco, where blacks were less frequent. The main clinical features were lymphadenopathy, skin lesions, hypercalcemia and hepatomegaly. Fourteen patients (9%) suffered from HTLV-I-associated myelopathy (HAM/TSP), either at diagnosis or during follow-up of ATLL. All cases but one had antibodies to HTLV-I, with concordant results with ELISA, WB and PCR analyses. For the antibody-negative case, pol and tax gene sequences were present in tumor cells when subjected to PCR analyses. The prognosis was generally poor, suggesting that the disease in Brazil behaves in similar fashion regardless of ethnic or geographical differences.

Adolescent↗
PubMed1996

Cellular immune reactions in brain transplantation: effects of graft pooling and immunosuppression in the 6-hydroxydopamine rat model of Parkinson's disease.

We used high immunogenic mouse and low immunogenic rat brain transplants to investigate the effect of pooling of tissue with immunogenetic disparity on cellular immune reactions. Foetal xenogenic mouse striatum and allogenic rat substantia nigra were implanted into i) the 6-hydroxydopamine lesioned striatum of outbred female Sprague-Dawley rats as a pooled cell suspension, or into ii) the unlesioned and lesioned striata as non-pooled separate deposits, with or without immunosuppressive treatment with cyclosporin A (Cy A). In control animals, iii) mouse striatum was replaced by rat striatum, and iv) sham grafts with and without immunosuppression. Six weeks post grafting, brains were semiquantitatively processed using immunocytochemical markers for microglia, astrocytes, T-helper cells, and macrophages, major histocompatibility class (MHC) I and II expression. The total amount of immunoreactivity (PA) for microglial cells and astrocytes was pronounced and the PA for T-helper cells and macrophages was doubled in recipients of pooled rat and mouse cografts compared to non-pooled deposits, indicating ongoing immune reactions with participation of glial cells. MHC I expression was significantly increased in pooled xeno- and allogenic cografts with and without immunosuppression compared to allogenic controls. Expression of MHC II was significantly increased in pooled cografts without immunosuppression. In recipients of separate, non-pooled heteroimmunogenic cotransplants, MHC I and II expression was significantly increased in xenogenic deposits with and without immunosuppression. MHC II was as well significantly increased in allogenic deposits without immunosuppression. Immunosuppressed animals with non-pooled allogenic mouse cografts showed low levels of cellular immune parameters. In conclusion non-pooled heteroimmunogenic grafts lead to less pronounced immune reactions compared to pooled grafts and immunosuppressive treatment with Cy A has a beneficial effect on acute transplant-associated immune parameters.

Animals↗
PubMed1998

Contribution of T cells to the development of autoimmune diabetes in the NOD mouse model.

The nonobese diabetic (NOD) mouse spontaneously develops an autoimmune diabetes that shares many immunogenetic features with human insulin-dependent diabetes mellitus (IDDM), type 1 diabetes. The mononuclear cell infiltrates in the islet, which results in the development of insulitis (a prerequisite step for the development of diabetes) are primarily composed of T cells. It is now well accepted that these T cells play important roles in initiating and propagating an autoimmune process, which in turn destroys insulin-producing islet beta cells in the pancreas. T cells are subdivided into CD4+ helper T cells and CD8+ cytotoxic T cells. CD4+ T cells are further subdivided into Th1 and Th2 cells based on profiles of cytokine production, and these two T-cell populations counterregulate each other. Because many autoimmune diseases are Th1 T-cell mediated, current studies have focused on manipulating the Th1/Th2 imbalance to suppress the autoimmune process in the NOD model. Furthermore, the incidence of disease is much higher in females than that in males, suggesting an involvement of sex-steroid hormones in the development of diabetes. Understanding insights of the mechanism of immune-mediated islet cell destruction and the interaction between the immune and the neuroendocrine system may, therefore, provide new therapeutic means of preventing this chronic debilitating disease.

Animals↗