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Results for “Human leukocyte antigen”

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At least 19 recordsLinked to original sources
PubMed1979

Hypertrophic cardiomyopathy and human leukocyte antigen linkage: differentiation of two forms of hypertrophic cardiomyopathy.

To determine whether hypertrophic cardiomyopathy is associated with a human leukocyte antigen (HLA) phenotype, we tissue-typed 70 unrelated afflicted patients and 86 of their asymptomatic family members (from nine separate kindreds). Forty-five per cent of the white patients had B-12 antigen as compared to 23 per cent in matched control subjects; 69 per cent of black patients had a B-5-complex antigen as compared to 33 per cent in matched controls. Patients with a B-12 or B-5-complex antigen were nonhypertensive and had family members with the disease. Patients without these antigens were severely hypertensive and had no affected family members. Linkage analysis of six families revealed a lod score of 7.7 for asymmetric septal hypertrophy and the HLA region of chromosome 6. We conclude that there is a heritable, nonhypertensive form of hypertrophic cardiomyopathy linked to the HLA loci on chromosome 6 and that a sporadic form is associated with severe, systemic hypertension.

Adult↗
PubMed1977

Association of human leukocyte antigen (HLA)-B5 and -BW22-J with hepatic cirrhosis of apparently unknown etiology.

The majority of patients with hepatic cirrhosis in Japan do not have a history of acute hepatitis or alcoholism. Twenty-nine patients with hepatic cirrhosis which were thought as random samples from cirrhotic patients without a history of acute hepatitis or alcoholism were Human Leukocyte Antigen (HLA) typed. Association of HLA-B5 and -BW22-J with hepatic cirrhosis of apparently unknown etiology was found in p less than 0.003, and p less than 0.01, respectively (128 controls). A predisposition linked to HLA-B5 or -BW22-J related gene or genes seems to play a role in the development of hepatic cirrhosis, at least in a substantial part of patients with hepatic cirrhosis of apparently unknown etiology in Japan.

Adult↗
PubMed1979

Human leukocyte antigen system not closely linked to or associated with bipolar manic-depressive illness.

An association and linkage study of the HLA system and bipolar affective illness is reported. HLA B-14 showed an increased frequency and HLA-Bw27 a decreased frequency in 92 bipolar patients compared to 210 controls, but significance is not reached when appropriate statistical corrections are made. It is shown that ethnological differences can lead to sampling biases; a purported increased frequency of HLA-Bw 16 in Ashkenazi Jewish bipolar patients is negated when ethnologically similar controls are used. The transmission of HLA alleles in nine families with at least two generations of affective illness revealed independent assortment, and nonlinkage to either locus A or B was demonstrated using a multigenerational method of linkage analysis. The nonreplicability of the HLA association studies, and the failure to demonstrate linkage of the HLA loci with afe development of affective illness, although further analyses are necessary.

Adult↗
PubMed1977

Influenza virus antigens in human leukocytes after oral administration of live tissue culture influenza A monovaccine.

Influenza A virus antigens were detected in leukocytes by immunofluorescence. After intravenous inoculation of the A/Moscow/16/65 (H2N2) vaccine strain to chickens, cytoplasmic antigens of the virus were observed in mononuclear leukocytes from 24 to 72 hours post inoculation (p.i.). The course of antigen detectability was similar after two repeated inoculations of the virus. After oral vaccination of human volunteers with a live tissue culture influenza A monovaccine from the X-47 (H3N2) recombinant viral antigens were also found in mononuclears; the maximal number of antigen-positive cells was observed at 24 hours p.i. The method of membrane immunofluorescence proved to be the most sensitive for antigen detection; it revealed a considerable decrease in the number of antigen-positive cells after repeated administration of the virus to volunteers. This fact may possibly reflect the development of antiviral resistance in the process of vaccination.

Administration, Oral↗
PubMed1979

Adherent cell function in murine T-lymphocyte antigen recognition. IV. Enhancement of murine T-cell antigen recognition by human leukocytic pyrogen.

A macrophage-dependent, antigen-specific murine T-cell proliferation assay was utilized to examine the role of soluble products of murine and human adherent cells in the activation of T lymphocytes. Highly purified human leukocytic pyrogen, and supernates from both murine and human mononuclear phagocytes-macrophages stimulated the immune T-cell proliferative response to the multideterminant antigens dinitrophenyl-ovalbumin and keyhole limpet hemocyanin. The implications of these studies and the relationship of leukocytic pyrogen to human lymphocyte-activating factor are discussed.

Animals↗
PubMed2026

Immunodominant Tuberculosis Antigens Recognized by Human CD4+ and CD8+ T Cells.

Tuberculosis (TB), caused by infection with Mycobacterium tuberculosis (MTB), represents an important cause of morbidity and mortality worldwide for which an improved vaccine and immunodiagnostics are urgently needed. CD4+ and CD8+ T cells play an important role in host defense to TB. Definition of the immunodominant antigens recognized by these T cells is critical for improved understanding of the immunobiology of TB and for development of vaccines and diagnostics. Herein, we review antigens and epitopes recognized by classically human leukocyte antigen (HLA) class I- and class II-restricted CD4+ and CD8+ T cells in humans infected with MTB, as defined using either targeted or genome-wide approaches. We address the extent to which these antigens have been defined as immunodominant, protective, and/or specific to disease stages in humans and, with particular relevance to CD8+ T-cell recognition, whether these antigens are displayed by MTB-infected cells.

Journal Article↗
PubMed1975

Modulation of HL-A antigens by anti-HLA antiserum: effects on the cytotoxicity assay and mixed leukocyte reaction.

Modulation of human leukocyte antigen (HLA) was attempted by treating leukocytes with specific anti-HLA antiserum or by their passage through columns coated with anti-HLA or a double layer of HLA-anti-HLA. The modulated cells were resistant to the cytotoxic effects of the anti-HLA, and they were poor stimulators and good responders to allogeneic cells in the unidirectional mixed leukocyte reaction. Modulated cells regained their HLA 16 hr after modulation if kept in cell suspension alone. The proliferative responses of modulated cells to mitogens were as good as non-modulated cells, indicating that modulation was probably not caused by depletion of lymphoid cells. Supernatants of modulated cells that were incubated overnight or preformed HLA-anti-HLA complexes were capable of suppressing and enhancing the MLR of specific cells depending on the dose used. The similarities of modulation of HLA to other lymphocyte receptors and the limitation of application of the modulation phenomenon to transplantation of allogeneic cells are discussed.

Antibody Specificity↗
PubMed1975

Investigation of the nature of Australia antigen. I: The absence of biological activity of Australia antigen in human blood leukocyte culture.

Purified and concentrated preparations of Australia antigen had no stimulating effect on leukocytes of human subjects under study when tested either on DNA-polymerase activity, 3H-thymidine uptake or chromosomal alterations. Moreover, in patients with chronic hepatitis and cirrhosis of the liver no correlation between antigenemia and chromosome aberrations in blood leukocyte cultures could be detected. On the other hand, a serum obtained from a virus hepatitis patient with Australia antigen in the blood was found to stimulate leukocyte cultures from one patient with Down's syndrome and antigenemia, one mentally retarded patient and three normal donors. This stimulating agent is obviously not associated with Australia antigen.

Adolescent↗