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Biomedical subjects

E Engleman

Publications and source records attributed to E Engleman.

23 records · Page 2Linked to original sources
PubMed1985

Transient antibody to lymphadenopathy-associated virus/human T-lymphotropic virus type III and T-lymphocyte abnormalities in the wife of a man who developed the acquired immunodeficiency syndrome.

We present evidence of transmission of lymphadenopathy-associated virus (LAV)/human T-lymphotropic virus type III (HTLV-III) from a man to his wife, and a return to a normal number of T-helper lymphocytes and loss of antibody after discontinuing sexual exposure to LAV/HTLV-III. The man had hemophilia A, and developed the lymphadenopathy syndrome, antibody to LAV, and a low number of T-helper lymphocytes. His wife, who had no risks for the acquired immunodeficiency syndrome other than sexual contact with him, developed LAV antibody (titer, 1:160) and a mildly decreased number of T-helper cells. The husband subsequently developed the syndrome and lost the LAV antibody. During 10 months of follow-up his wife remained clinically well, discontinued exposure to semen, and then lost the LAV antibody, and regained a normal number of T-helper cells.

Acquired Immunodeficiency Syndrome↗
PubMed1982

Protein A binding assay for the identification of HLA antigens on peripheral blood lymphocytes by monoclonal antibodies: application to HLA B27.

Splenocytes from mice immunized with purified, papain-solubilized HLA B27 antigen and/or human lymphocytes bearing the B27 specificity were fused with myeloma cell lines NSI or Sp2. The screening strategy employed a protein A binding assay in which various target cells were used. First, the hybrid cell supernatants were screened against B lymphocyte cell lines of known HLA specificities and the Daudi cell line, which does not express HLA-A, B, or C antigens. Second, a panel of PBLs were used as target cells. It was necessary to refine the protein A binding assay by preabsorbing the radiolabeled protein A with PBLs and by precoating the test wells with ovalbumin. Clones selected by these criteria were further tested by indirect immunoprecipitation and by inhibition of binding or microcytotoxicty to target call lines with purified HLA antigens or beta 2m. Forty-four clones were selected which showed varying degrees of specificity for allo- and nonallo-specific determinants and one clone was selected which was specific for beta 2m. Clone 27M1 which was previously shown to be specific or HLA-B27 as judged by conventional microcytotoxicity testing (Grumet et al., Lancet No. 8239, II:174, 1981) was compared with other clones using the above parameters for evaluation. Antibody from clone 27M1 showed preferential binding to B27 positive cell lines and PBLs, lesser binding to B7 positive target cells, and no binding to B40 positive target cells. Purified B27 antigen (papain) from two sources including the B27 target cell line, was able to inhibit the binding of antibodies from 27M1 to target cells. The extension of the protein A binding assay to PBLs has made it possible to more accurately quantitate the binding or inhibition of binding of antibodies to panels of PBLs.

Animals↗
PubMed1979

Significance of HLA antigens and the mixed lymphocyte reaction in psoriasis.

Human Major Histocompatibility (HLA) complex antigens B13, BW16, BW17, CW6 and D-MA are increased in frequency in patients with psoriasis. Of these, the strongest association is with HLA-CW6 and D-MA, with a relative risk of 10.4. Since no strong association with any HLA-A locus antigen is seen, it seems likely that the disease susceptibility gene for psoriasis lies close to the HLA-D locus, which is defined by the use of the mixed lymphocyte reaction (MLR). In the mouse, the Immune response (Ir) genes are found in the MLR region and it is thought that Ia antigens lie at a corresponding location in man. Recently, we have demonstrated that human epidermal cells cause stimulation in the mixed lymphocyte reaction. Lymphocyte antigens which stimulate in this reaction are known to be products of HLA genes and anti-HLA-D sera block stimulation by epidermal cells. It is possible that these antigens may be involved in the regulation of cell--cell communication. Psoriasis is a disease characterized by epidermal hyperproliferation. It is possible, therefore, that an HLA-linked deficiency of recognition between epidermal cells exists in patients with psoriasis and that this defect allows abnormal cellular proliferation to occur.

Animals↗
PubMedDate not supplied

In vivo persistence of donor cells following adoptive transfer of allogeneic dendritic cells in HIV-infected patients.

Peripheral blood samples from HIV-seropositive individuals enrolled in a pilot clinical trial investigating the use of allogeneic dendritic cell therapy were evaluated for mixed chimerism. In this study, dendritic cells from HLA-identical, HIV-seronegative siblings were used. Patients received an infusion of dendritic cells pulsed with HIV MN gp160 protein or with peptides from HLA-A2 restricted epitopes of env, gag, and pol proteins every month for 6-9 months. Of the five allogeneic dendritic cell recipients, two showed increases in HIV antigen-specific immune responses. Allele-specific polymorphisms were identified in three sib-pairs that allowed infused donor cells to be detected using sensitive PCR-based molecular methods. Analysis of blood samples from patients showed similar patterns of donor cell persistence after the first infusion, in that cells were detectable for at least 1 week. Also, differences were observed in the kinetics of cell survival between the first and subsequent infusion cycles in all three patients. This suggests variation in HIV-specific immune responses detected among these three patients was not due to differences in persistence of infused donor cells.

Adoptive Transfer↗