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Biomedical subjects

L M Hutt-Fletcher

Publications and source records attributed to L M Hutt-Fletcher.

40 records · Page 3Linked to original sources
PubMed1983

Studies of the Epstein-Barr virus receptor found on Raji cells. I. Extraction of receptor and preparation of anti-receptor antibody.

Raji, a human lymphoblastoid cell line, expresses a membrane receptor (EBVR) specific for Epstein Barr virus (EBV). A component that binds EBV was extracted from this cell line by treatment of the cells for 3 hr on ice with Tris buffer containing 10% glycerol. The treatment reduced the capacity of the cells to bind virus, and after concentration the receptor extract (RE) inhibited both EBV binding and superinfection of fresh Raji cells. Similarly prepared extracts of EBVR- cells lacked such activity. An antibody was made to the extract (anti-RE), which after absorption with EBVR- cells, bound to the same percentages of EBVR+ lymphoblastoid cell lines, EBVR+ human/mouse somatic cell hybrids, and fresh peripheral B cells as the virus did. In reciprocal assays, preincubation of EBVR+ cells with anti-RE inhibited virus binding. Doubly stained patches were observed on membranes of EBVR+ cells that had been incubated simultaneously with virus and anti-RE and stained respectively with rhodaminated and fluoresceinated reagents. The major polypeptide immunoprecipitated by anti-RE from radiolabeled Raji cells had an approximate calculated m.w. of 150,000.

Animals↗
PubMed1981

Interferon production and activation of non-specific effector cells by stimulation with lymphoblastoid cell lines in vitro.

A population of non-specific effector lymphocytes is generated in response to stimulation with lymphoblastoid cell lines (LCL). These cytotoxic cells have an activity analogous to that exhibited by natural killer (NK) cells. When lymphoid cells lines established by transformation with Epstein-Barr virus (EBV) are used to stimulate autochthonous T-cell-enriched lymphocytes, the activity against the NK-sensitive target, K562, is increased up to 14-fold. The stimulated T lymphocytes produce interferon, and this factor augments the cytotoxic activity of unstimulated cells. The size distribution of cytotoxic lymphocytes after stimulation with the autochthonous EBV line is unlike that of either T-cells or interferon-augmented T-cells. Autochthonous stimulated lymphocytes which kill K562 are of several size classes, and are included in populations containing large blast cells. In contrast, the K562 activity of both unstimulated T-cells and interferon-augmented T-cells is contained in a more discrete population of cells, just slightly larger than the majority of lymphocytes. Thus, the generation of non-specific effector cells during stimulation with lymphoblastoid cell lines appears to involve the activation of a population of blast-size cells in addition to those initially responsive to interferon augmentation.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1981

Diverse familial malignant tumors and Epstein-Barr virus.

Continued monitoring of a family for new malignant tumors has revealed diverse immunological and neoplastic disorders during a 15-year period. In 1966, the proband developed lymphoma. In 1975, his antibody titers to Epstein-Barr virus (EBV) became elevated, and again, he developed a malignant lymphoma. He also had borderline hypo-immunoglobulin A, died of glioblastoma multiforme in 1977, and at autopsy, had adenomatous colonic polyps. His eldest brother has normal immunoglobulin levels, but developed immune thrombocytopenia in 1973 and had elevated EBV antibody titers in 1980. Another brother had hypo-immunoglobulin A, thymoma in 1965, and adenomas and adenocarcinoma of the colon. Two other brothers succumbed to glioblastoma in 1968 and 1969. The father of the proband had bronchiectasis in 1952, hypo-immunoglobulin M documented in 1972, and elevated EBV antibody titers 5 years preceding development of a malignant lymphoma. The latter contained 10 EBV genome equivalents/cell by EBV viral DNA/DNA reassociation kinetics analysis. The proband's grandmother had died of an immunoglobulin G-secreting myeloma in 1977, and his grandfather had borderline low immunoglobulin M, elevated EBV antibody titers, and hypopharyngeal carcinoma in 1980. Predisposition to oncogenesis in this family was probably inherited.

Adenocarcinoma↗