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Biomedical subjects

H A Stephens

Publications and source records attributed to H A Stephens.

30 records · Page 2Linked to original sources
PubMed1991

Analysis of HLA-DR and -DQ gene polymorphisms in Sudanese patients with type 1 (insulin-dependent) diabetes.

In this study we report for the first time, the molecular analysis of HLA-DR and -DQ gene frequencies in a large cohort of well characterized type 1 (insulin-dependent) diabetes mellitus (IDDM) patients (n = 72), and ethnically matched controls (n = 59) collected in sub-Saharan Africa. High molecular mass DNA was prepared and analyzed in Southern blots with DRB1, DQA1, and DQB1 probes. By identifying DR and DQ allele-specific restriction fragment length polymorphisms (RFLPs), we have shown a strong positive association between IDDM and the Asp 57- DQB1 allele *0201 (DQw2). A rare DR4, DQw2 haplotype was also identified at high frequency in the IDDM cohort. We can now confirm that the association between Asp 57-DQB1 alleles and IDDM, previously reported in ethnically diverse cohorts collected in Western Europe, North America, and South Asia, is also present in an IDDM cohort collected in Africa.

Adolescent↗
PubMed1990

Genes encoding the beta-chains of HLA-DR7 and HLA-DQw2 define major susceptibility determinants for idiopathic nephrotic syndrome.

1. We have investigated the frequencies of the major histocompatibility complex class II alleles by restriction fragment length polymorphism analysis, using DR, DQ and DP complementary DNA probes, in 40 Caucasoid steroid-sensitive nephrotic children. 2. A significant association with HLA-DR7 was demonstrated (P = 2 x 10(-5); aetiological fraction 0.6). The DQB1 gene of HLA-DQw2 was present in 83% of our patients (P = 2 x 10(-4); aetiological fraction 0.7). We present evidence that it contributes a second susceptibility allele. 3. A weak association between the uncommon HLA-DP-Cp63 allele and the disease was also observed. 4. Our data suggest that the immune events in steroid-sensitive nephrotic syndrome are defined by a particular immunogenetic background involving the beta-chain genes of HLA-DR7 and HLA-DQw2.

Adolescent↗
PubMed1989

Southern blot analysis of HLA-DP gene polymorphisms in Caucasoid rheumatoid arthritis (RA) patients and controls.

Despite extensive analysis of the incidence of HLA-DR and HLA-DQ allele frequencies in defined autoimmune disease groups, there is very little information available on HLA-DP allele frequencies. This is largely because HLA-DP typing has until recently been restricted to primed lymphocyte typing (PLT). However, allelic polymorphism of the HLA-DP subregion can now be studied by Southern blot analysis or genotyping with DPA1 and DPB1 probes. By direct counting of allele-specific DNA fragments, we have analyzed the frequencies of five major DP genotypes (DPw1, DPw2, DPw3/6, DPw4, and DPw5), in a large number of Caucasoid rheumatoid arthritis (RA) patients (n = 74), and controls (n = 91). The predicted frequency of DP alleles in both patient and control groups was comparable to PLT-determined DP allele frequencies in normal Caucasoids. However, the gene frequency of DPw4 was increased in the RA patients, with 51% of the patients studied scoring as DPw4, 4 homozygotes. With the exception of one possible combination (DPw5 and DRw6) in the controls, no significant linkage disequilibrium was detected between DP and DR alleles in either patient or control groups. Thus the prevalence of DPw4 in the RA patients is independent of any disease association with the DR loci, and may represent a new class II association with RA.

Arthritis, Rheumatoid↗
PubMed1985

Null cell immunoregulation in SLE.

Fresh normal T cells do not lyse MDA-157 target cells. Normal null cells, cultured for 4 days with MDA-157 stimulators, and then mixed overnight with fresh normal T cells, induce cytotoxicity on MDA-157 targets and suppressor activity in the T-cell acceptor population. With the same normal acceptor T cells, MDA-157 activated null cells from 13/18 patients with Systemic Lupus Erythematosus (SLE), unlike activated cells from a disease control population, induce little or no T-cell cytotoxicity or suppression. These results provide further evidence for abnormal null cell function in SLE.

Cells, Cultured↗
PubMed1983

Recognition of marrow elements by natural killer cells: are NK cells involved in haemopoietic regulation?

NK cells from young normal mice are cytolytic in vitro for a virus-induced tumour cell line, YAC-1. Cytotoxicity is inhibited by the addition of unlabelled homologous YAC-1 cells and by regenerating bone marrow cells from the spleens of lethally irradiated, bone-marrow-grafted mice. Quiescent marrow from syngeneic and allogeneic mice produces little or no competition. This suggests that NK cells recognize, and may regulate, marrow progenitor cells.

Animals↗
PubMed1982

Inhibition of proliferative and suppressor responses in the autologous mixed lymphocyte reaction by serum from patients with systemic lupus erythematosus.

Serum from patients with systemic lupus erythematosus (SLE) prevents the proliferative response of normal T cells when stimulated by autologous or allogeneic non-T cells. The abrogation of proliferation in an autologous mixed lymphocyte reaction (AMLR) with SLE serum is associated with a lack of suppressor T cell generation. Fractionation of SLE sera on sucrose gradients reveals an 18-12 S peak of Raji cell binding material. Fractions with an S value of </=12 S show inhibitory activity in an AMLR.

Adult↗
PubMed1982

Insensitivity to interferon of NK cells from patients with systemic lupus erythematosus.

Natural cytotoxicity (NK) by fresh E-rosette-negative (ER-) cells from normal donors was increased after overnight incubation with purified IFN alpha and with supernatants containing IFN gamma. ER- cells from 61% of 23 patients with systemic lupus erythematosus did not show increased cytotoxicity after treatment with IFN alpha. Similarly, ER- cells from nine of 18 patients that were treated with IFN gamma-containing supernatants failed to show increased cytotoxicity. The patients who did not show enhanced cytotoxic responses to IFN had higher mean indices of disease activity than responding patients.

Adult↗
PubMedDate not supplied

T cell receptor Vbeta gene usage in Thai children with dengue virus infection.

T lymphocyte activation during dengue is thought to contribute to the pathogenesis of dengue hemorrhagic fever (DHF). We examined the T cell receptor Vbeta gene usage by a reverse transcriptase-polymerase chain reaction assay during infection and after recovery in 13 children with DHF and 13 children with dengue fever (DF). There was no deletion of specific Vbeta gene families. We detected significant expansions in usage of single Vbeta families in six subjects with DHF and three subjects with DF over the course of infection, but these did not show an association with clinical diagnosis, viral serotype, or HLA alleles. Differences in Vbeta gene usage between subjects with DHF and subjects with DF were of borderline significance. These data suggest that the differences in T cell activation in DHF and DF are quantitative rather than qualitative and that T cells are activated by conventional antigen(s) and not a viral superantigen.

Adolescent↗