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R A Robins

Publications and source records attributed to R A Robins.

123 records · Page 7Linked to original sources
PubMed1976

Severe combined immunodeficiency with B lymphocytes: in vitro correction of defective immunoglobulin production by addition of normal T lymphocytes.

A 6 1/2-month-old male with severe combined immunodeficiency (SCID) had a low percentage and number of T cells (11%; 241/mm3) and a high percentage and number of B cells (52%; 1187/mm3) and null cells (37%; 868/mm3). In vitro studies were performed to determine if this child's primary defect involved differentiation of both T and B lymphocytes or if failure of B lymphocytes to differentiate into immunoglobulin producing cells was secondary to T lymphocyte abnormalities. Immunoglobulin production by lymphocytes in response to polyclonal mitogens (pokeweed mitogen and foetal calf serum) was measured by pulse-labelling cells with 3H-leucine and then precipitating cytoplasmic and secreted immunoglobulins with polyvalent anti-human immunoglobulin and S. aureus (Cowan strain I) protein A. The patient's lymphocytes did not synthesize immunoglobulins in vitro in response to mitogens. They did not suppress synthesis of immunoglobulins by normal lymphocytes. However, addition of normal purified T cells, which themselves did not synthesize immunoglobulins, enabled the patient's B lymphocytes to become immunoglobulin synthesizing and secreting cells. Gamma, mu, and light chains were secreted. This suggests that the primary abnormality was in the T-cell axis at the level of lymphoid stem cells or prothymocytes and that failure of B lymphocytes to become immunoglobulin-producing cells was secondary to this defect.

Antibody-Producing Cells↗
PubMed1975

Subpopulations of multiparous rat lymph-node cells cytotoxic for rat tumour cells and capable of suppressing cytotoxicity in vitro.

Lymph-node cells (LNC) from multiparous pregnant rats were separated on columns prepared from nylon wool, and tested for cytotoxicity against target tumour cells. Reactivity of LNC towards hepatoma D23 and mammary carcinoma AAF57 was demonstrated in cell populations retained on the nylon wool, and not with cells eluted from the column. Although only 25% of the samples of unfractionated LNC were cytotoxic for tumour cells, retained cell fractions were cytotoxic in 11 out of 12 tests (p = less than 0.05). Similarly retained LNC were also cytotoxic for 15-day-old embryo cells but not for normal adult rat fibroblasts. Using multiparous rat serum it was shown that the reactivity of the retained LNC population could be abrogated in eight out of 11 tests (p = less than 0.05). The LNC population recovered from the nylon wool constituted 28 to 35% of the original LNC preparation, and consisted of 60-70% Ig-bearing cells together with a subpopulation of cells responding to soluble PHA. Separation of multiparous LNC on glass beads coated with rat Ig and then rabbit anti-rat Ig (in excess) also demonstrated the retained cell population to be cytotoxic against tumour cells. Approximately 17-20% of the original cell population was recovered from cells retained on the column, and consisted of an enriched Ig-bearing cell population (65-80% Ig-bearing cells) and LNC responsive to PHA. Carbonyl iron treatment of multiparous rat LNC was found to remove detectable cytotoxicity from multiparous rat LNC preparations. The cytotoxicity of multiparous rat LNC retained on nylon wool was also abolished following incubation with carbonyl iron. Definite conclusions as to the nature of the effector cell cannot be drawn from this test, since carbonyl iron treatment was found to remove not only phagocytic cells from LNC preparations but also a proportion of other cell populations including Ig-bearing lymphocytes... In addition to detecting a cytotoxic LNC population reactive towards tumour-associated embryonic antigens (retained fractions from nylon-wool column separation), a subpopulation of multiparous rat LNC was demonstrated in cell fractions eluted from the nylon wool which was shown to suppress the cytotoxicity of the retained multiparous LNC population. The exact nature of this subpopulation of LNC and the mechanism of action is at present not known.

Animals↗
PubMed1975

Serum factors modifying cell mediated immunity to rat hepatoma d23 correlated with tumour growth.

Sera from rats bearing a progressively growing transplanted aminoazo-dye-induced hepatoma (hepatoma D23) have been examined for the presence of hepatoma D23-specfic antigen, antibody and immune complexes throughout the course of tumour growth. The levels of these factors have been correlated with the in vitro blocking and inhibition of cytotoxic lymph-node cells from immunized animals for cultured tumour cells. Sera from animals bearing small tumours (7-14 days after tumour implantation contain free tumour-specific antigen whilst immune complexes could not be detected. Although these sera were neither blocking nor inhibitory under the normal conditions of the test, when concentrated two and fourfold, inhibition but not blocking of lymph-node cell cytotoxicity could be detected. In comparison sera from animals bearing large tumours (24-28 days) blocked but did no inhibit in vitro lymph-node cell cytotoxicity and this correlates with the presence of tumour-specific immune complexes in antibody excess. Animals with intermediate-sized tumours had high levels of both blocking and inbibitory activity in the serum, these effects becoming apparent when neither free antibody nor free antigen could be detected. The relevance of these findings to the mechanism by which a growing tumour may escape specific cellular immune destruction is discussed.

Animals↗
PubMed1975

Serum antibody responses to an ascitic variant of rat hepatoma D23.

Antibody was detected by membrane immunofluorescence tests in sera of rats bearing an ascitic variant of a transplanted hepatoma, and in concentrated cell-free ascitic fluid. Ascites hepatoma cells were also shown to have immunoglobulin, possibly tumour specific antibody, bound to their surface. The kinetics of antibody responses to ascites hepatoma and hepatoma cells from solid tumours were compared: both tumour types gave positive reactions by the third day after implantation; antibody was present throughout subsequent tumour growth with the ascites whereas antibody was not detected after tumour became palpable in rats injected with hepatoma cells from solid tumour. Antibody responses to ascites tumour were investigated in rats bearing solid hepatoma tumour. Subcutaneous hepatoma did not influence the antibody response to ascites, but rats bearing intraperitoneal tumours showed a diminished serum antibody response to ascitic hepatoma.

Animals↗