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D R Bainbridge

Publications and source records attributed to D R Bainbridge.

36 records · Page 2Linked to original sources
PubMed1983

Elimination of allogeneic lymphocytes by mice.

Two major classes of response to allogeneic lymphocytes can be detected in mice in vivo, based on injecting them intravenously with 51Cr-labelled lymph node cells and examining them in a short term assay. A natural immunity discriminating between allogeneic and syngeneic lymphocytes is seen in the lymph nodes (and to a lesser extent, the spleen), which has such close similarities to natural cell-mediated responses of the NK class as thymic-independence and radioresistance. However, it has immunological specificity of a conventional kind, probably towards serologically determined K/D antigens. There is also an active immune response, produced by immunisation with dissociated lymphoid cells or allografting, which consists of three elements: an IgG opsonising alloantibody response, diverting circulating lymphocytes to the liver; an IgM opsonin, localising them to the spleen; and a cell-mediated serum-dependent elimination mechanism that destroys cells entering the lymph nodes and spleen. Dose-response curves for the primary response show evidence of high-dose paralysis of elimination. Dose-time-response results for the secondary show a variety of unique characteristics; evidence is presented to suggest that several aspects of the phenomenon betray primitive features retained from an earlier stage in the evolution of the immunological system.

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PubMed1981

Nomarski differential interference contrast studies of murine lymphocytes.

Nomarski differential interference contrast microscopy (DIC) of lymphocyte surface morphology was combined with immunofluorescence studies on T and B cell markers on the thymus, lymph nodes, spleen, peripheral blood lymphocytes and thoracic duct lymph of female CBA mice. DIC identified smooth cells and several categories of villous cells; more extreme forms were present in lymph. Most B cells seemed to belong to the smooth group and most peripheral T cells to the villous group. Thymus cells were almost entirely smooth, but treatment with cortisone increased the proportion of villous cells to 50%. The surface morphology of lymphocytes was highly labile preventing direct identification or separation of T and B cells. In vivo removal of T cells by adult thymectomy, lethal irradiation and bone marrow reconstitution caused the villous cells to decrease. During recovery from irradiation, T lymphocytes tended to parallel villous cells, B lymphocytes smooth cells, but were differences between the spleen and lymph nodes. Mice deprived of T1 cells by adult thymectomy showed a modest decrease of smooth cells in the spleen and blood; mice depleted of T2 cells by anti-lymphocyte serum, or which were naturally deficient in T2 cells, were markedly lacking in villous cells. Thoracic duct lymph, which is rich in T2 cells, had a high proportion of extremely villous lymphocytes. Exposure to lymph induced extreme villous features in lymph node cells, and it was found that the thoracic duct lymph was markedly hypertonic to serum, although varying in osmolarity throughout the day. It is suggested that the villous shape of T2 cells is a circulatory adaptation, necessitated by the peculiar character of the lymphatic system in mice.

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PubMed1980

Studies on transplantation immunity. IV. Murine natural immunity to lymphoid cells in vivo.

A natural response acting to discriminate between allogeneic and syngeneic lymphocytes in vivo is described for normal mice. Eighteen to 24 h after systemic injections of low doses of 51Cr-labeled cells, less radioactivity is found in the lymph nodes after allogeneic transfer. The spleen but not the liver participates in the response. It can be abolished by neonatal induction of transplantation tolerance, is shown to be immunologically specific, and is resistant to irradiation up to 1000 rd, although a radiosensitive phase occurs during recovery from sublethal irradiation. The response is cell-mediated but depends upon cooperation from a factor present in normal serum. It is thymus-independent: this clearly distinguishes it from the superficially similar immune response acquired by immunization and aligns it with the class of responses to which the hybrid histocompatibility response and natural killer-like phenomena belong. Unlike these, however, it is present at birth and directed primarily against H-2 antigens. It appears to follow the classical transplantation rules in a limited range of strains. Some of the difficulties inherent in this type of study are discussed.

Aging↗
PubMed1979

Identification of a defence mechanism in vivo against the leakage of enterokinase into the blood.

1. The serum proteinase inhibitors alpha 1-antitrypsin, alpha 2-macroglobulin, inter-alpha-trypsin inhibitor and C1-esterase inhibitor were found not to affect the catalytic activity of human enterokinase, whereas bovine trypsin activity was modified essentially as expected. Enterokinase was also not inhibited by Trasylol (trypsin inhibitor from bovine lung) or bovine pancreatic trypsin inhibitor. No other component in human or mouse serum complexing with enterokinase was identified. 2. Human enterokinase administered intravenously into mice was rapidly cleared from the circulation with a half-life of 2.5 min. This removal was not the result of the difference in species, since partially purified mouse enterokinase was cleared at the same rate as the human enzyme. Clearance was mediated by recognition of the carbohydrate portion of enterokinase and not through specific recognition of its catalytic site. Immunofluorescent staining showed that the enzyme accumulated in the liver. Attempts to block the clearance by the simultaneous infusion of competing glycoproteins suggested that enterokinase was taken up by hepatocytes. Of the glycoproteins tested only two, human lactoferrin (terminal fucosyl alpha 1 leads to 3 N-acetylglucosamine) and bovine asialo-fetuin (terminal galactosyl beta 1 leads to 4 N-acetylglucosamine) were weakly competitive. Two inhibitors of endocytosis, Intralipid and Triton WR1339, failed to delay the removal of enterokinase. It is proposed that enterokinase is cleared from the circulation by an as yet uncharacterized hepatocyte receptor.

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PubMed1977

Cell-mediated immunity to Sendai virus infection in mice.

The development of a cell-mediated immune response to Sendai virus infection in mice was examined by the use of a 51Cr release assay of cytotoxicity. A low level of "background cytotoxicity" to Sendai virus-infected L cells was found in the spleens of uninfected CBA mice. Spleen cells from Sendai-infected mice showed an elevated level of cytotoxicity against these target cells for a period of 5 weeks, commencing 4 days after infection of the mice. A more transient response was observed in the spleens of mice infected with a serologically distinct virus, the Kunz strain of influenza. This cross-reacting, cell-mediated immune response was intermediate between that observed in unsensitized and Sendai-sensitized spleen cells. The relevance of these cell-mediated immune responses to respiratory tract virus infections is discussed.

Animals↗
PubMed1976

Use of (75Se)L-Selenomethionine as a label for lymphoid cells.

[75Se]L-selenomethionine can be employed as a label for following lymphocytes in vivo. Its properties are broadly similar to those of 51Cr with regard to uptake, release of the isotope on cell death and reutilization; thus relatively high levels of 75Se in lymphoid tissue indicate the presence of viable labelled cells. It differs from 51Cr in that active release of selenium occurs from the labelled cells when the ambient cell concentration is low. No significant reutilization of leaked label occurs. Leakage of 75Se label occurs in vivo; this differs in the spleen and lymph nodes. Evidence is presented to suggest that 75Se losses reflect the transit times of cells through lymphoid organs.

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