Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Histocompatibility Testing”

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 595 records · Page 33Linked to original sources
PubMed1998

Absence of linkage between MHC and a gene involved in susceptibility to human schistosomiasis.

Six hundred million people are at risk of infection by Schistosoma mansoni. MHC haplotypes have been reported to segregate with susceptibility to schistosomiasis in murine models. In humans, a major gene related to susceptibility/resistance to infection by S. mansoni (SM1) and displaying the mean fecal egg count as phenotype was detected by segregation analysis. This gene displayed a codominant mode of inheritance with an estimated frequency of 0.20-0.25 for the deleterious allele and accounted for more than 50% of the variance of infection levels. To determine if the SM1 gene segregates with the human MHC chromosomal region, we performed a linkage study by the lod score method. We typed for HLA-A, B, C, DR and DQ antigens in 11 informative families from an endemic area for schistosomiasis in Bahia, Brazil, by the microlymphocytotoxicity technique. HLA-DR typing by the polymerase chain reaction with sequence-specific primers (PCR-SSP) and HLA-DQ were confirmed by PCR-sequence-specific oligonucleotide probes (PCR-SSOP). The lod scores for the different theta values obtained clearly indicate that there is no physical linkage between HLA and SM1 genes. Thus, susceptibility or resistance to schistosomiasis, as defined by mean fecal egg count, is not primarily dependent on the host's HLA profile. However, if the HLA molecule plays an important role in specific immune responses to S. mansoni, this may involve the development of the different clinical aspects of the disease such as granuloma formation and development of hepatosplenomegaly.

Animals↗
PubMed1999

Thymic disorders and myasthenia gravis: genetic aspects.

Myasthenia gravis (MG) is an autoimmune disease characterized by production of antibodies to acetylcholine receptor at the motor end-plate responsible for impairment of neuromuscular transmission. There is general agreement about the involvement of the thymus in the pathogenesis of MG, and thymic pathological changes are commonly found in MG patients. Genetic factors seem to play an important role in susceptibility to MG. As with other autoimmune diseases, genetic predisposition to MG probably involves multiple genes. Ample evidence suggests that genes within the major histocompatibility complex (MHC) are involved in susceptibility to autoimmune diseases. Both data from the literature and our findings indicate that different genes within the MHC could predispose to various forms of MG, and that particularly the tumour necrosis factor genes may play a role in the association between the different thymic disorders and MG.

Case-Control Studies↗
PubMed1979

[Blood groups].

Explore the source record for details and available documents.

ABO Blood-Group System↗
PubMed1999

History of DNA typing for the human MHC.

The last twenty years have seen an exponential growth in the application of DNA technology to the field of Histocompatibility and Immunogenetics (H&I). Initially, this was confined to a few research laboratories. However, the development and application of several different DNA methods by many laboratories has led to the situation whereby nearly every H&I laboratory performs some DNA typing for the detection of HLA alleles. It would not be unfair to say that H&I has shown diagnostic laboratories in other disciplines how useful the DNA techniques can be. This review attempts to summarise the history and application of DNA methods in the field of Histocompatibility (Table 1).

DNA↗
PubMed1999

Molecular typing for the MHC with PCR-SSP.

Sequence-specific amplification (SSP) is simply a form of polymerase chain reaction (PCR) which involves designing one or both primers so that they will or will not allow amplification (the 3'-mismatch principle). Its origins are probably legion, i.e. many people probably thought of it at the same time. For example, in 1988 a group from Guy's Hospital, London, described a form of SSP for HLA-DR4 detection and in the same year a group from Upjohn described its use at the American Society of Histocompatibility and Immunogenetics (ASHI). Both are published in abstract form (British Society of Rheumatology and ASHI). The 3'-mismatch principle can be used to identify virtually any single nucleotide point mutation (SNP) within one or two PCR-SSP reactions and the first peer-reviewed statements of this came in 1989 (1, 2). Thus, although the use of SSP probably began around 1990, it was 5 years before its popularity erupted, mainly due to the work of Olerup & Zetterquist (3, 4), who defined its potential for solid organ transplantation. It is now the method of choice for high resolution HLA typing in many laboratories. In addition, over a thousand applications for genes outside the MHC are in the literature.

Histocompatibility Testing↗
PubMed1999

The human leucocyte antigens and clinical medicine: an overview.

The Major Histocompatibility Complex (MHC) occupies 4-6 megabases on the short arm of chromosome 6 and is the most intensively studied segment of the human genome. This region was first discovered through its influence on transplantation rejection and on antigen-specific immune responses. The most important genes for managing these functions encode the HLA molecules (human leucocyte antigens) which are highly polymorphic in human populations. HLA typing for these polymorphisms is widely used in clinical medicine when identifying optimal organ donors or recipients and in assessing the risk of diseases such as narcolepsy, hereditary hemochromatosis, ankylosing spondylitis and certain autoimmune disorders. As new genes are identified in the MHC, the clinical impact of this genetic region is likely to assume further importance as outlined in this review.

Antigen Presentation↗
PubMedDate not supplied

Endocrine autoimmunity in young patients with juvenile chronic arthritis.

OBJECTIVE: The aim of our study was to investigate the coexistence of autoimmune diseases (autoimmune thyroid disease and type 1 diabetes mellitus, T1DM) in patients affected by Juvenile Chronic Arthritis (JCA). METHODS: We studied 66 patients affected by JCA, 42 females and 24 males: 42/66 patients had a pauciarticular form of JCA, 13/66 had a polyarticular form and 11/66 had a systemic form. All the patients underwent autoimmune thyroid screening through determination of anti-thyroglobulin (TgA) and anti-peroxidase (TPOA) autoantibodies. Patients with TgA and/ or TPOA, underwent thyroid sonography. T1DM screening included determination of anti-glutamic acid decarboxylase (GADA), anti-insulin (IAA), anti-tyrosine phosphatase-like protein (IA-2A) and anti-islet cell (ICA) autoantibodies. Oral glucose tolerance test (OGTT) was performed only in patients with autoantibody positive values. HLA typing for risk of T1DM was performed in 43 patients. RESULTS: Nine female patients (14%) showed anti-thyroid autoantibodies, in particular: TgA in 3 cases, TPOA in 5, TgA and TPOA in only 1. In 3 of these patients, ultrasound examinations showed thyroid abnormal pattern, suggesting Hashimoto's thyroiditis. As regards T1DM, only 2 patients showed positive levels of GADA. As regards HLA typing, one or more T1DM susceptibility heterodimers were detected in 20 patients (46%) (13 with 1 heterodimer, 7 with 2 heterodimers). CONCLUSION: Our study showed that anti-thyroid autoantibody frequency (9/66, 14%) was higher in JCA than in the general population, while T1DM markers (islet autoantibodies and genetic markers) were not frequent. These results suggest to investigate specific markers of thyroid autoimmunity in patients with JCA, in particular in females with JCA pauciarticular form.

Adolescent↗
PubMed1975

Single donor, HL-A matched platelet transfusions for thrombocytopenic patients undergoing surgery.

Thrombocytopenic patients, who displayed hemostatic disorders and had been previously sensitized by repeated blood transfusions and/or pregnancies, were supported for surgical procedures by platelet transfusions obtained from a single ABO and HL-A matched donor by the use of continuous collection centrifugation. Because of the low incidence of HL-A identical donors, compatibility was assessed by known serological cross-reactivity of the HL-A determinants. In three cases repeated platelet transfusions had excellent in vivo survival, and sensitization could not be detected by a battery of immunological assays. In one case there was immune sensitization and refractoriness to repeated platelet transfusion, as documented by accelerated in vivo destruction of donor and third-party platelets bearing the disparate factor HL-A8. Although serologic tests for lymphocytotoxic and leukoagglutinating antibodies were negative, the patient displayed cellular immunity in leukocyte aggregation and cell-mediated plateletolysis tests. The single donor, continuous collection technique appears to have the technical advantage of rapid, efficient collection and the immunological benefit of a restricted spectrum of allosensitization.

ABO Blood-Group System↗