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Biomedical subjects

R H Keller

Publications and source records attributed to R H Keller.

5 recordsLinked to original sources
PubMed1978

Malignant lymphoma of plasmablastic identity. A neoplasm with both "immunoblastic" and plasma cellular features.

A solitary extramedullary lymphoid neoplasm had characteristics of plasma cell precursors or plasmablasts. Conventional microscopic study classified this tumor as a diffuse large cell lymphoma of "immunoblastic sarcoma" type. Immunologic cell surface markers could not be detected, but cytoplasmic immunoglobulin G (IgG)-kappa was demonstrated by immunoperoxidase technic, and IgG was present in the supernatant of the tumor tissue culture. The distinction between lymphoid and plasma cellular neoplasms is made.

Aged↗
PubMed1976

Alpha-fetoprotein synthesis by murine lymphoid cells in allogeneic reactions.

Surface-bound alpha-fetoprotein (AFP) was demonstrated by immunofluorescence on approximately 1/3 of splenic lymphocytes in chronic murine graft vs. host (GVH) reactions. Splenic lymphocytes were also shown to have a suppressed phytohemagglutinin (PHA) response compared to controls while lymph node cells from the same GVH animals revealed no surface AFP and had normal PHA responses. Splenic lymphocytes showed marked synthesis of AFP in the GVH and mixed lymphocyte culture (MLC) reactions by [14C]leucine incorporation and by radioimmunoassay in MLC supernates. Lymph node cells, however, demonstrated less synthetic activity and 14C counts in their membrane fractions were not markedly elevated.

Animals↗
PubMed1976

Lymphocyte cytotoxicity and inhibition studied with autologous liver cells: observations in chronic active liver disease and the primary biliary cirrhosis syndrome.

A method is described for determining the cytotoxicity of normal and autologous lymphocytes for 51Cr-labeled isolated parenchymal liver cells in a low aggressor to target cell ratio. Results were compared from patients with chronic active liver disease (CALD), chronic persistent hepatitis (CPH), miscellaneous liver diseases, or primary biliary cirrhosis (PBC). In 53% of CALD patients, lymphocytes showed greater cytotoxicity for hepatic cells than did normal allogenic lymphocytes, but in 32% there was significantly less 51Cr release than normal; in the remainder, results were in the normal range. Lymphocyte cytotoxicity was greater in patients with disease of short duration and less in those treated with corticosteroids. In untreated CALD, decreased 51Cr release was associated with the presence of plasma factor(s) inhibiting phytohemagglutinin (PHA)-induced transformation of normal lymphocytes. Lymphocytes from approximately 50% of the patients with PBC exhibited cytotoxicity for hepatic cells but 25% showed less 51Cr release than controls and the remaining patients had results in the normal range. Lymphocyte cytotoxicity was also greater during the earlier stage of PBC. In contrast to CALD, decreased 51Cr release was not associated with the presence of plasma factor(s) inhibiting PHA-induced transformation of normal lymphocytes. Our findings support the hypothesis of in vivo lymphocyte-mediated liver cell damage in CALD and PBC, suggesting a potentially important role for lymphocyte suppression in the pathogenesis of both diseases.

Adult↗