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M A Axelrad

Publications and source records attributed to M A Axelrad.

12 recordsLinked to original sources
PubMed1979

The effect of a liver protein synthesis inhibitor on plasma SAA levels in a model of accelerated amyloid deposition.

Animals treated with AgNO3 and amyloid-enhancing factor deposit large quantities of splenic amyloid in 48 hours. The kinetics of SAA production was examined in such a model in the presence and absence of an inhibitor of liver protein synthesis (ethionine). Ethionine had little effect on splenic protein synthesis but inhibited both the production of SAA and liver protein synthesis. When experiments were performed with fed mice, ethionine induced an inhibition of liver protein synthesis lasting 16 hours. Thereafter, liver protein synthesis began to recover, accompanied by a rise in plasma SAA levels. These results are consistent with hepatic but not splenic synthesis of SAA.

Amyloid↗
PubMed1975

Rosette-forming ability of thymus-derived lymphocytes in cell-mediated immunity. I. Delayed hypersensitivity and in vitro cytotoxicity.

Effector cells in delayed hypersensitivity and in vitro cytotoxicity were studied in lymph node cells from animals immunized with sheep erythrocytes (SRBC) in complete Freund's adjuvant. Delayed hypersensitivity response (DHR) was assayed by the increase in foot pad swelling after the intrafoot pad injection of immune cells plus antigen. Cell-mediated cytotoxicity against SRBC was assayed by a microcytotoxicity test with sheep fibroblasts as target cells. Effector cells were antigen specific, sensitive to anti-theta serum plus complement (C), and insensitive to anti-Ig serum plus C. A nonrosette-forming (non-RFC) small lymphocyte effector T cell and a rosette-forming medium lymphocyte effector T cell were isolated by velocity sedimentation. The small lymphocyte non-RFC required a longer time than the medium lymphocyte RFC effector cell to produce maximum activity. Buoyant density failed to distinguish medium lymphocyte effector cells in DHR and in vitro cytotoxicity.

Animals↗
PubMed1973

Thymus-derived rosettes are not "helper" cells.

Rosettes against SRBC were made from normal spleen cells. Although T rosettes tend to dissociate, they could be stabilized with 0.05% sodium azide. A clear separation of nonrosettes, T rosettes, and B rosettes was obtained by subjecting the suspension of splenic rosettes to velocity sedimentation at unit gravity. Each fraction was injected with either normal bone marrow cells or normal thymus cells with antigen into 650-R-irradiated hosts. Direct plaque-forming cells (PFC) were assayed in the spleens 7 days later. Synergism with thymus cells occurred only in the B-rosette fraction; PFC precursors therefore sedimented as B rosettes. Synergism with bone marrow cells occurred only in the nonrosette small lymphocyte fraction; helper cells therefore did not bind detectable numbers of sheep red blood cells (SRBC). Thus T rosettes are not helper cells in the direct PFC response of bone marrow B cells to SRBC.

Animals↗
PubMed1972

Classification of thymus-derived and marrow-derived lymphocytes by demonstration of their antigen-binding characteristics.

Antigen-binding cells of T and B origin can readily be determined by quantitating the number of sheep erythrocytes per rosette after glutaraldehyde fixation. The T(1) and T(2) populations have low antigen-binding properties and are very unstable without fixation. The B(1) and B(2) populations are stable and correlate with precursor and secretory cells. Fixation of rosettes permits a sensitive test for studying differentiation of T and B cells.

Animals↗
PubMed1971

Immunological memory in vitro.

The immune responses to sheep erythrocytes of mouse spleen cell suspensions from immune and nonimmune donors were compared in vitro. In vivo immunity was only transiently reflected in vitro, and 8 wk after in vivo immunization the responses of cultures from immunized and nonimmunized mice were virtually identical. There appeared to be two mechanisms for an antibody response to sheep erythrocytes. The first was responsible for the early primary response and is unmodified in the immune animal though contributing little to subsequent in vivo responses due to its suppressibility by specific antibody. The second was expressed in the in vivo secondary response but not on in vitro challenge of spleen cells from mice immunized many weeks previously; spleen cell cultures from such immune mice, freed from the antibody of the in vivo environment, once again demonstrate a pure primary-type response.

Animals↗
PubMed1971

Suppression of memory by passive immunization late in the primary response.

The acquisition of a capacity to respond well to sheep erythrocytes in the presence of anti-SRBC antibody was taken as an indication of the presence of immunological memory. By the use of passive immunization, both the primary IgG plaque-forming cell response and the establishment of memory were abolished, despite occurrence of a full peak IgM PFC response. Evidence for regarding the aquisition of memory and the IgM PFC and IgG PFC responses as three separate processes was presented. Antibody on day 3 of the response to 1.5 x 10(8) SRBC abolished formation of memory; this effect was less if passive immunization was further delayed and absent by day 10.

Animals↗