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J M Puck

Publications and source records attributed to J M Puck.

95 records · Page 6Linked to original sources
PubMed1980

Role of Ia-positive cells in induction of secondary human immune responses to haptens in vitro.

We have described techniques for induction of primary and secondary human immune responses in vitro to lymphoid cells modified with trinitrophenyl, dinitrophenyl, and fluorescein isothiocyanate. Optimal secondary proliferative responses required the presentation of hapten on stimulator cells that shared HLA-D region determinants with the responder cell and/or the original stimulator cell. In contrast, hapten-specific cytotoxic responses assessed on modified allogeneic targets with no detected HLA homology with the responder were comparable in magnitude to those detected on modified autologous targets. Furthermore, secondary proliferative, but not cytotoxic, responses required presentation of Ia+ stimulator populations. Modified B cells, surface-immunoglobulin-negative, non T cells (null-cells), and Ia+ activated T cells all induced proliferative responses at least as effectively as equal numbers of hapten-conjugated macrophage/monocytes. Conversely, Ia(-) null cells and macrophages were entirely unable to stimulate. The data thus suggest that for proliferative responses, primed human T cells respond to modified lymphoid cells only when hapten is recognized in the context of Ia molecules.

Cytotoxicity, Immunologic↗
PubMed1980

Protection of infants from infection with influenza A virus by transplacentally acquired antibody.

Transplacentally acquired antibody to influenza A virus was measured by a microneutralization test and a radioimmunoprecipitation assay in cord blood obtained from infants at a large urban county hospital in 1975-1978. Random samples tested before epidemic periods were a measure of susceptibility of the population. Twenty-six infants from whom cord sera were available had culture-documented infections with influenza A/Victoria (H3N2) virus when younger than four months. The direct correlation between age at the time of infection and level of antibody measured in cord serum (P less than 0.002) suggested a protective effect of transplacentally acquired antibody. None of fourteen acute-phase serum specimens obtained early in the course of culture-positive infections of young infants had detectable antibody to influenza A viral hemagglutinin by the sensitive radioimmunoprecipitation test. Because passively transferred maternal antibody to influenza virus may prevent symptomatic infection in young infants, vaccination of pregnant women could be beneficial.

Antibodies, Viral↗
PubMedDate not supplied

Isolation of cDNA clones encoding the 20K non-glycosylated polypeptide chain of the human T-cell receptor/T3 complex.

The antigen receptor on human T lymphocytes consists of two variable immunoglobulin-like glycoproteins, alpha and beta, which occur in association with three invariable T3 membrane proteins. In humans two of these proteins, T3-gamma and T3-delta, are glycoproteins of relative molecular mass (Mr) 25,000 (25K) and 20,000 (20K), respectively, while the third, T3-epsilon, is a 20K non-glycosylated protein. On the surface of murine T cells, a non-glycosylated protein dimer composed of 17K subunits (T3-zeta) is found associated with the T-cell receptor alpha and beta chains and the three T3-like polypeptide chains. It is generally accepted that major histocompatibility complex-restricted antigen recognition is a function of the alpha-beta heterodimer. This has led to the postulation that the proteins of the T3 complex are involved in the signal transduction that immediately follows antigen recognition via the antigen receptor. Events believed to be involved in early T-cell activation, such as rapid increases in phosphatidylinositol turnover and free intracellular calcium, can be triggered by antibodies directed against either the T3 complex or the clonotypic receptor. We have previously reported our findings on the cloning of the complementary DNA and genomic structure encoding both the human and murine 20K glycoprotein, T3-delta (refs 11-13). We now present our results on the cloning of the cDNA encoding the human 20K non-glycosylated chain, T3-epsilon.

Amino Acid Sequence↗
PubMedDate not supplied

Analphoid marker chromosome in a patient with hyper-IgE syndrome, autism, and mild mental retardation.

Hyper-IgE syndrome with recurrent infections (HIES) is a primary immunodeficiency disease characterized by recurrent skin and lung abscesses and extreme elevations of serum IgE, but also involving dentition, bones, and connective tissue. Although the etiology of HIES is unknown, autosomal dominant inheritance has been observed in multiple kindreds. A 17 year old male with sporadic HIES, autism, and mild mental retardation was found to have a supernumerary marker chromosome in peripheral blood lymphocytes and skin fibroblasts. Microdissection and FISH analysis of the marker chromosome showed that it was derived from a small interstitial deletion of one homologue of chromosome 4q21. Lack of hybridization of probes specific for telomeres and alphoid centromeres, including a centromere 4 specific probe, established that the marker was an analphoid ring chromosome. Comparative genotyping of transformed B-cell subclones with (M+) and without (M-) the marker chromosome showed loss of the maternal alleles in M- cells between markers D4S1569 and D4S3010. FISH using YAC clones from 4q21 confirmed the size and location of the interstitial deletion. Thus our patient's phenotypes were associated with de novo formation of a marker chromosome containing 15-20 cM of DNA deleted from his maternally derived chromosome 4. Proximal chromosome 4q therefore is a candidate region for disease genes for both HIES and autism. Identification of genes disrupted or lost during the formation of the marker chromosome as well as linkage studies in kindreds with HIES or autism may help us to understand the etiology of these complex phenotypes.

Abnormalities, Multiple↗