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At least 865 records · Page 48Linked to original sources
PubMed1986

[Does seronegative chronic polyarthritis have a special place? Clinical, biochemical and immunogenetic profile of early seronegative seropositive chronic polyarthritis].

In the framework of an early-diagnosis out-patients clinic 100 patients (mean age 51 years), 82 of them female, were identified as highly suspicious of having chronic rheumatoid arthritis of recent onset (2-12 months). Five or more ARA criteria were present in 77 patients. IgM rheumatic factor was present in serum of 51 patients (latex-fixation test). A Waaler-Rose test of greater than or equal to 32 IU/ml was present in 21. After adjusting for alpha errors, there was a significantly higher prevalence of HLA-DR4 among those seropositive in the latex fixation test (64 vs 29%). A further 19 constitutional, anamnestic, clinical, biochemical and psychosocial criteria failed to reveal any different distribution between seropositive and seronegative cases. Using the specific definition of seropositivity in the Waaler-Rose test eliminated HLA-DR4 differences. The latter did not serve as a distinguishing criterion. There was only a marginal difference between DR4-positive and negative patients. These results fail to lend support to recent views of a special position of seronegative chronic rheumatoid arthritis.

Arthritis, Rheumatoid↗
PubMed2006

Immunogenetics of pemphigus: an update.

Pemphigus are rare but informative models of organ-specific autoimmune diseases, resulting from the interplay of environmental, genetic and stochastic factors. There are many arguments to consider that pemphigus have a genetic basis involving, as many other autoimmune diseases, several different genes with additive or synergistic effects. So far, the unique strategy used to identify the contributive loci has been direct analysis of candidate genes through conventional case-control association studies. The major histocompatibility complex in particular the class II locus was demonstrated to be associated with pemphigus with a high rate of replicability. The progresses in the understanding of pemphigus physiopathology and the development of new molecular tools offer new perspectives to unveiled the genetic basis of this group of autoimmune blistering diseases, as shown by recent studies of candidate genes expressed at different levels of the autoimmune process.

Animals↗
PubMed1983

Transplantation: immunogenetic and clinical aspects--part II.

The ultimate goal is not merely to find a better way of treating acute rejection; efforts are now concentrated on prophylactic immunosuppression with low-dose regimens of azathioprine and steroids. In the wings is cyclosporine, a fungal polypeptide that shows great promise in clinical trials. And on the horizon there is hope that monoclonal antibodies may hold the key to prevention.

Adult↗
PubMed1995

Progress in the immunogenetics of rheumatoid arthritis.

Although much remains to be learned about environmental factors and putative pathogens, significant strides have been made on the genetic front. Genes appear to have a greater role in determining disease severity than disease risk. In particular, patients who are heterozygous for two HLA-DR4 subtypes are prone to severe erosive disease, making them candidates for early, aggressive therapy.

Alleles↗
PubMed1987

A new human Duffy blood group specificity defined by a murine monoclonal antibody. Immunogenetics and association with susceptibility to Plasmodium vivax.

A new Duffy specificity, Fy6, defined by a murine monoclonal antibody of the IgG1 kappa class, is related to susceptibility to malarial invasion. In humans, Fy6 is present on the red cells of all persons except those of the Fy(a-b-) type, a distribution resembling that of Fy3. However proteolytic enzyme treatment of red cells enhances the reactivity of Fy3, whereas Fy6, like Fya and Fyb, is susceptible to degradation by this process. The number of Fy6 sites on human red cells was found to be 12,200 per cell, in close agreement with earlier estimates of the number of Fya sites. Anti-Fy6 reacted in western blots with a membrane glycoprotein of approximately 46,000 Mr, not significantly different from that of a molecule known to bear the Fya determinant. The Fy6 epitope is shown to be present on the red cells of some but not all nonhuman primate species, where it has a distribution not only distinctly different from Fya, Fyb, and Fy3, but in close accordance with susceptibility to penetration by Plasmodium vivax. Thus, the red cells of two species of macaques (Macaca mulatta and M. fascicularis), which are invaded by Plasmodium knowlesi but not by P. vivax are shown to have other Duffy antigens but to be devoid of Fy6. It appears, therefore, that the red cell epitopes used by these closely related species are distinct, and that susceptibility to P. vivax merozoite penetration is dependent on the presence of Fy6.

Animals↗
PubMed2000

Analysis of candidate-host immunogenetic determinants in herpes simplex virus-associated Mollaret's meningitis.

Infection due to herpes simplex virus (HSV) is associated with recurrent aseptic meningitis (Mollaret's meningitis); however, the neuropathogenesis of this disease remains unknown. We collected 20 cerebrospinal fluid (CSF) specimens that were positive for HSV DNA by using polymerase chain reaction (PCR) assay from patients with a clinical diagnosis of Mollaret's meningitis. Patients were predominantly female (female:male, 22:1), with an average age of 32.8 years (range, 18-46 years). Using direct sequence analysis of HSV PCR products obtained from the CSF, we determined that all of the patients were infected with HSV type 2. In addition, we evaluated polymorphisms in 2 human genomic loci, which are associated with either severe or recurrent microbial infections (interferon-gamma receptor [IFN-gammaR] and mannose binding lectin [MBL]); these host genes were also amplified directly from the CSF specimens. No mutations were found in exons 2 or 3 of the IFN-gammaR gene (n=20). In contrast, there were 4 (20%), 4 (20%), and 0 mutations found in codons 52, 54, and 57, respectively, in exon 1 of MBL (n=20). A significantly higher frequency of codon 52 mutations (P=.04) was observed, compared with racially matched control patients.

Adolescent↗
PubMed2006

Host immunogenetics and control of human herpesvirus-8 infection.

BACKGROUND: Kaposi sarcoma (KS) is primarily caused by human herpesvirus (HHV)-8 infection, and the risk is increased with high HHV-8 lytic or latent antibody titers or the detection of HHV-8 DNA in peripheral blood mononuclear cells (PBMCs). Host genes important for control of HHV-8 infection are not well characterized. METHODS: In 172 HHV-8 latent nuclear antigen (LANA)-seropositive adults in Italy without KS, we examined correlations of common variants in host immune genes with the detection of HHV-8 DNA in PBMCs and with high lytic and latent antibody titers. Twenty-eight single-nucleotide polymorphisms in 14 genes were analyzed. We detected HHV-8 DNA in PBMCs with real-time amplification of the K6 gene, anti-K8.1 (lytic) titers with enzyme-linked immunosorbent assay, and anti-LANA (latent) titers with immunofluorescence. RESULTS: Detection of HHV-8 DNA in PBMCs was not significantly related to any variant examined. In contrast, a 3-locus haplotype of IL4, which contains the -1098G allele (rs2243248), was overrepresented among subjects with high lytic titers (odds ratio [OR], 2.8 [95% confidence interval {CI}, 1.1-6.7]), compared with those with low titers, as was the functional promoter variant of IL6, C-236C (rs1800795) (OR, 3.7 [95% CI, 1.1-12.8]). Compared with subjects with low HHV-8 latent antibody titers, analysis of inferred haplotypes for IL12A revealed an overrepresentation of -798T/277A in subjects with high HHV-8 latent antibody titers (OR, 2.4 [95% CI, 1.1-5.2]). CONCLUSIONS: Our observations are the first to provide preliminary evidence suggesting that common variants in key host immune genes could influence the control of HHV-8 infection.

Adult↗
PubMed2006

Immunogenetics of CD4 lymphocyte count recovery during antiretroviral therapy: An AIDS Clinical Trials Group study.

During antiretroviral therapy, CD4 lymphocyte count increases are modest in some patients despite virologic control. We explored whether polymorphisms in genes important for T cell expansion, survival, and apoptosis are associated with the magnitude of CD4 lymphocyte count recovery during antiretroviral therapy. We studied treatment-naive individuals who achieved sustained control of plasma viremia (<400 HIV-1 RNA copies/mL) for at least 48 weeks after initiation of antiretroviral therapy and compared genotypes among individuals who had an increase of either <200 or > or =200 CD4 cells/mm3 from baseline. A total of 137 single-nucleotide polymorphisms across 17 genes were characterized in 873 study participants. In multivariate analyses that controlled for clinical variables, polymorphisms in genes encoding tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL), TNF- alpha , Bcl-2-interacting molecule (Bim), interleukin (IL)-15, and IL-15 receptor alpha chain (IL-15R alpha ) were associated with the magnitude of the increase in CD4 lymphocyte count, as were haplotypes in genes encoding interferon- alpha , IL-2, and IL-15R alpha (P < .05, for each). Multifactor dimensionality reduction identified a gene-gene interaction between IL-2/IL-15 receptor common beta chain and IL-2/IL-7/IL-15 receptor common gamma chain. Immune recovery during antiretroviral therapy is a complex phenotype that is influenced by multiple genetic variants. Future studies should validate these tentative associations and define underlying mechanisms.

Adult↗
PubMed2000

Immunogenetic therapy of human melanoma utilizing autologous tumor cells transduced to secrete granulocyte-macrophage colony-stimulating factor.

We performed a clinical study of five patients with melanoma to evaluate the immunobiological effects of retrovirally transduced autologous tumor cells given as a vaccine to prime draining lymph nodes. Patients were inoculated with both wild-type (WT) and GM-CSF gene-transduced tumor cells in different extremities. Approximately 7 days later, vaccine-primed lymph nodes (VPLNs) were removed. There was an increased infiltration of dendritic cells (DCs) in the GM-CSF-secreting vaccine sites compared with the WT vaccine sites. This resulted in a greater number of cells harvested from the GM-CSF-VPLNs compared with the WT-VPLNs at a time when serum levels of GM-CSF were not detectable. Four of five patients proceeded to have the adoptive transfer of GM-CSF-VPLN cells secondarily activated and expanded ex vivo with anti-CD3 MAb and IL-2. One patient had a durable complete remission of metastatic tumor. Utilizing cytokine (IFN-gamma, GM-CSF, IL-10) release assays, GM-CSF-VPLN T cells manifested diverse responses when exposed to tumor antigen in vitro. In two of two patients, GM-CSF-VPLN T cell responses were different from those of matched WT-VPLN cells. This study documents measurable immunobiologic differences of GM-CSF-transduced tumor cells given as a vaccine compared with WT tumor cells. The complete tumor remission in one patient provides a rationale to pursue this approach further.

Adult↗
PubMed1975

Serum antigens of cattle. IV. Immunogenetics of a soluble antigenic determinant derived from lysed erythrocytes.

This paper describes an allotypic system in cattle called Ec (Erythrocyte cattle). The antigenic determinant is derived from red cells and is detected in lysates by gel precipitation with alloimmune serum. The Ecl specificity is controlled by an autosomal dominant gene and occurs with variable frequencies in different cattle breeds. The Ec system is a very useful genetic marker because the homozygous and heterozygous genotypes show a dosage effect and can be distinguished by the size of the precipitin rings in double diffusion gel precipitation tests.

Alleles↗
PubMed2006

Chlamydia trachomatis-associated tubal factor subfertility: Immunogenetic aspects and serological screening.

Chlamydia (C.) trachomatis female genital tract infections usually remain asymptomatic and untreated. Therefore, an adequate immune response, rather than antibiotic treatment, is essential to clear the pathogen. Most women will effectively clear C. trachomatis infections, but some will have persistent C. trachomatis infections, which may ascend to the upper genital tract and increase the risk of tubal factor subfertility. Pattern recognition receptors (PRRs) of the toll-like receptor (TLR) and nucleotide-binding oligomerization domain (NOD) families recognize C. trachomatis and initiate the immune response. Host immune factors are determinants of the course of C. trachomatis infections. Genetic variations in TLR and NOD genes may affect receptor function, leading to inadequate recognition of C. trachomatis, an inadequate immune response, and consequently an increased risk of persistence and late sequelae. For the risk assessment of tubal pathology in subfertile women, C. trachomatis immunoglobulin (Ig) G antibody testing (CAT) in serum is widely used. A positive CAT is indicative of a previous infection but not of a persistent infection. Measuring serological markers of persistence, of which C-reactive protein (CRP) seems promising, in CAT-positive women may identify a subgroup of subfertile women with persistent C. trachomatis infections and the highest risk of tubal pathology.

C-Reactive Protein↗
PubMed1988

Immunogenetic analysis of human tuberculosis.

An investigation was undertaken to determine if susceptibility and/or immune response to Mycobacterium tuberculosis was associated with histocompatible leukocyte antigen (HLA) phenotype frequencies of class I or II antigens. Comparisons of the HLA phenotypes of 51 Mexican-American patients with tuberculosis and 54 healthy subjects who differed in their skin-test reactivity to purified protein derivative (PPD) revealed that HLA-DR3 was significantly decreased in patients with tuberculosis, compared with healthy persons who were tuberculin skin-test positive. Although no association was observed between HLA phenotype and skin test reactivity to PPD in tuberculous patients, we did observe an increase in the HLA-A9-B40 phenotype in patients who manifested a strong in vitro proliferative response to PPD, whereas the HLA-B14-DR1 phenotype was increased in patients who exhibited a low proliferative response to this antigen.

Adult↗
PubMed1990

Immunogenetics of mycobacterial infections: mouse-human homologies.

In the mouse, innate resistance or susceptibility to infection with numerous mycobacteria is controlled by the Bcg host resistance locus located on the centromeric region of chromosome 1. The resistance/susceptibility phenotype is expressed by the mature tissue macrophage and Bcg has been identified as a locus that is involved in the regulation of macrophage activation and in the modulation of acquired immune responses to mycobacteria. Experiments aimed at the cloning of the Bcg gene via a "reverse genetics" approach have generated a detailed genetic map in the immediate vicinity of the locus, placing Bcg within the reach of long-range eukaryotic cloning techniques. The chromosomal segment around Bcg in the mouse is exactly conserved onto the long arm (q) of human chromosome 2. Linkage of genetic markers from human chromosome 2q with susceptibility to leprosy or tuberculosis would support both the existence of a susceptibility gene in humans and the contention that this susceptibility gene is a homologue of the mouse Bcg locus.

Animals↗
PubMed1976

Immunogenetic aspects of nasopharyngeal carcinoma. IV. Increased risk in Chinese of nasopharyngeal carcinoma associated with a Chinese-related HLA profile (A2, Singapore 2).

The results of this study of 110 Singapore Chinese with nasopharyngeal carcinoma (NPC) and 91 controls confirmed the association between the occurrence of HLA antigen Singapore 2 (Sin2) and NPC in the Chinese population, and indicated that their increased risk for NPC was confined to the joint occurrence of Sin 2 and A2 antigens. These findings suggested that the genotype of importance in susceptibility to NPC is the A2-Sin 2 haplotype.

Asian People↗