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Biomedical subjects

H Friedman

Publications and source records attributed to H Friedman.

At least 487 records · Page 27Linked to original sources
PubMed1975

Failure of peritoneal exudate macrophages to reverse immunologic impairment by Friend leukemia virus.

Transfer experiments with peritoneal exudate macrophages from normal donor mice were performed to determine if a defect of normal macrophage function or activity was a major or contributing factor to the immunosuppression characterizing leukemia virus infection of mice. Challenge immunization of Friend leukemia virus-infected mice with sheep erythrocytes resulted in markedly depressed hemolytic antibody responses, as compared to responses of normal noninfected mice. When PE cell suspensions rich in macrophages were transferred from normal donor mice to leukemia virus infected recipients there was no affect on the FLV-induced impairment of the immune response. Similar transfer of PE cells to normal uninfected mice generally resulted in a moderate depression of the expected immune response. In no case did the PE cells enhance the immune responses in normal or virus-infected mice.

Animals↗
PubMed1975

Immunosuppression by leukemia viruses. Effect of Friend leukemia virus on humoral immune competence of leukemia-resistant C57BL/6 mice.

Infection of genetically resistant C57BL/6 mice with Friend leukemia virus resulted in a marked but transient immunodepression of the humoral immune response to sheep erythrocytes. The primary immune response to sheep erythrocytes was depressed in mice infected 1 or 3 days before challenge immunization, but no suppression was observed when the interval was greater. The suppression coincided with the time of transient viremia in the mice. The secondary immune response to sheep erythrocytes was inhibited when virus was injected within a few days before booster immunization. Induction of immunologic "memory" to sheep erythrocytes was also blocked in C57BL/6 mice given virus before priming with the SRBC. The immunosuppressive activity appeared due to a marked but transient effect of the virus on antibody precursor cells, as ascertained by cell transfer experiments. These observations are pertinent to the general question to the cellular site of action of immunosuppressive tumor viruses and the relationship between immunosuppression and the neoplastic properties of the RNA viruses.

Animals↗
PubMed1975

Modulation of in vivo antibody responses by cholera toxin.

Treatment of mice with an exotoxin (0.01 mug to 1.0 mug) purified from Vibrio cholerae culture filtrates markedly influenced the immune response to sheep erythrocytes (SRBC) and the Escherichia coli lipopolysaccharide (LPS). Simultaneous administration of the toxin (CT) with antigen resulted in a delayed appearance of antibody plaque-forming cells (PFC) during the first few days after immunization, followed by a marked enhancement of both IgM and IgG PFC. The secondary immune response to SRBC was also similarly affected when CT was given together with a second inoculation of SRBC; i.e., a delay in appearance of hemolytic PFC followed by a markedly enhanced IgM and IgG PFC response. Treatment of mice with cholera toxin 1 to 3 days before SRBC or LPS was immunosuppressive. The effect of CT on the level of splenic cyclic AMP appeared related to the effects on antibody formation.

Adjuvants, Immunologic↗
PubMed1975

Vibriolytic IgG immunocyte response of mice after primary and secondary immunization with cholera somatic antigens.

Antibody plaque-forming cells (FC) to the somatic antigens of Vibrio cholerae were enumerated in the spleen of mice after primary and secondary immunization with a heat-killed vaccine prepared from the vibrios. Immunocytes releasing both high efficiency IgM and low efficiency IgG antibody were readily detected using a direct and facilitated plaque procedure in agar gel. Whereas the peak numbers of IgM-PFC after primary immunization occurred on days 12 to 14, the peak IgG-PFC response developed somewhat later (16-18 days). After a second injection of vaccine larger numbers of both IgM- and IgG-PFE appeared in the mouse spleens, with peak responses for both occurring between days 5 and 8. The largest number of IgG-PFC developed in spleens of mice given a second injection of vaccine 6-8 weeks after primary immunization. The dose of killed vibrios used for priming markedly affected both the magnitude and the class of antibody-forming cells appearing during the secondary response; 1--10 mug vaccine was more effective than higher or lower doses for priming the mice to a heightened secondary response. Furthermore, the antigenic specificity of both the IgM- and IgG-PFC appearing after secondary immunization was directly related to the strain of cholera bacilli used for priming. When mice were immunized with the Ogawa strains of cholera most of the secondary PFC after booster immunization with the serologically distinct Inaba strain was directed towards the common antigen shared by both strains and not to the type specific antigen of the Inaba vibrios. The specificity of the anti-vibrio PFC during both the primary and secondary responses was readily demonstrable by inhibition experiments using sonicated or soluble cholera antigens. Prior incubation of these antigens with test spleen cells in the agar gel effictively inhibited development of the vibriolytic plaques, regardless of antibody class. Similar antigen extracts from toher bacteria had no effect. The immunoglobulin nature of the plaques was also demonstrable by inhibition with low dilutions of rabbit anti-mouse globulin serum incorporated into the agar plates prior to testing; both IgM and IgG plaues were inhibited.

Animals↗
PubMed1975

Immunosuppression induced in vitro by mastocytoma tumor cells and cell-free extracts.

Suppressed anti-sheep RBC responses occurred when spleen cells from mastocytoma-bearing mice were incubated in vitro and immunized with red blood cells. Marked immunosuppression also occurred when mastocytoma cells were added to spleen cell cultures from normal mice immunized in vitro with the sheep RBC. Suppressed immune responses also occurred when the mastocytoma cells were separated from the normal cells by 0.4-mu nucleopore membranes, but not by dialysis membranes in double chambered culture vessels. Cell-free homogenates prepared from mastocytoma cells, as well as ascitic fluid from tumor-bearing mice, also impaired the responsiveness of normal splenocytes to the SRBC. The suppressive activity of the cell-free homogenates was abolished by heating at 56 degrees C for 30 min. The immunosuppressive activity, however, was retained in supernatant ultracentrifugates of the cell-free homogenate after 100,000 times G for 90 min. Immunosuppression was most evident when mastocytoma extracts were added to cultures of normal splenocytes at the time of in vitro immunization and culture initiation. Suppression was not reversed by washing of the cultured cells and addition of fresh medium. Immunosuppression also occurred when mastocytoma extracts were incubated with spleen cells from allogeneic tumor resistant C57BL/6 mice. Additional physicochemical analyses should provide information as to the nature and specificty of the inhibitory factor(s) and its role as an immunoregulatory substance important in the host-tumor relationship.

Animals↗
PubMed1975

Restoration of in vitro immune responsiveness of mastocytoma-suppressed splenocytes by activated T cells.

Spleen cells from normal DBA/2 mice pretreated with a soluble factor from mastocytoma cells or from ascitic fluid of mastocytoma-bearing mice were markedly impaired in terms of antibody formation to SRBC in vitro. Such immunosuppression by mastocytoma homogenates or ascitic fluid was reversed when syngeneic T cells activated to SRBC were added to the cultures, but not when peritoneal exudate cells or anti-theta-treated normal splenocytes were used. Activated T cells, as well as normal B lymphocytes prepared from spleens of lethally irradiated mice reconstituted with bone marrow cells, were less sensitive to the immunosuppressive factor than non-activated T cells. The ability of educated T cells to restore immunocompetence of suppressed spleen cells in vitro suggests that the target of the immunosuppressive factor from mastocytoma cells may be non-activated T cells, especially those involved in T cell helper function.

Animals↗