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Biomedical subjects

H Friedman

Publications and source records attributed to H Friedman.

At least 451 records · Page 25Linked to original sources
PubMed1977

Prolonged immunotherapy with alum-precipitated pyridine ragweed extracts-a clinical and immunological study.

In 18 ragweed hay fever patients who received injections of alum-precipitated pyridine (Allpyral) ragweed extracts in maintenance doses of between 6000 and 8000 P.N.U. at intervals of between two and four months over a two-year period, the prolonged interval did not seem to influence either the clinical response or the tendency to reaction, or result in significant change in immunological tolerance as determined by antibody studies, which included fluorescent antibody assays, as well as hemagglutination and RAST technics.

Adult↗
PubMed1976

Cellular events involved in the true primary immune response of splenocytes in vitro.

An antibody response showing characteristics of a "true" primary response was readily induced in vitro with splenocytes from normal non-immunized animals cultured with strongly immunogenic Vibrio cholerae somatic antigens. Prior studies have shown that the response to vibrios in intact animals appeared to be a true primary response since no pre-existing antibody forming cells were present in non-immunized animals and the antigen induced response, following a lag of two days, resulted thereafter in a rapid stepwise increase in the number of specific PFCs, reaching a peak at 12 to 14 days. Using the Marbrook culture system for antibody formation a readily detected immunocyte response to vibrios was induced with splenocytes from normal non-immunized animals. No background antibody forming cells developed to the organisms without addition of vibrios in vitro. After in vitro immunization with 10(6) bacteria significant numbers of IgM PFCs appeared with a peak response on days 7 to 8. Splenocyte cultures from mice primed earlier with vibrios developed a marked secondary response, with appearance of both IgM and IgG PFCs. Large numbers of both classes of PFCs developed, with peak responses on days 6 to 7, similar to the "primary" response to sheep erythrocytes. However, significant numbers of PFCs to vibrios developed in cultures of vibrio-primed cultures even in the absence of vibrios during the 12 day culture period. The availability of a completely in vitro model system to induce a true primary immune response without the complication of pre-existing background antibody forming cells will be of value for further studies concerning various cellular pathways and interactions during the immune response to small amounts of strongly immunogenic bacterial antigens.

Animals↗
PubMed1976

Modulation of the immune response in vitro and in vivo by splenocytes from tumor-bearing mice.

Immunosuppression in mice infected with either a leukemia virus (Friend virus) or bearing a rapidly growing transplantable tumor (either a plasmacytoma or mastocytoma) was studied at the level of individual immunocytes to sheep erythrocytes both in vivo and in vitro. Immunization of mice with progressing tumors showed markedly depressed hemolytic antibody plaque responses in the spleen. Furthermore, spleen cell cultures derived from immunodepressed mice with the tumors revealed the continued impairment of antibody formation in vitro. Relatively small numbers of splenocytes from the tumor-bearing mice suppressed larger numbers of normal spleen cells from control mice. Immunosuppression in all three tumor systems could be related to subcellular factors in that cell-free extracts of the spleens and tumor bearing mice or even ascites fluid or plasma could suppress the normal antibody responsiveness of normal spleen cell cultures. The virus per se or a virus associated factor seemed important in the leukemia virus model but non-virus tumor associated or related substances seemed to be involved in the immunosuppression induced by the plasmacytoma or mastocytoma. Such results support the view that tumor related subcellular factors may be important mediators of immunologic impairment of a host's immune defense mechanism to a neoplasm.

Animals↗
PubMed1976

RES blockade: effects on immunity and tolerance.

Reticuloendothelial cell blockade has been studied for decades in regards to physiological and immunological effects. "Overloading" of RE cells with inert colloidal particles, such as carbon or other particulate substances, has often been used to analyze the role of phagocytic activities in antibody formation, often with contrasting results. In the present studies the effects of colloidal carbon treatment of mice on immunologic responsiveness to sheep erythrocytes was investigated. Pre-treatment of mice with carbon shortly before either primary or secondary immunization with SRBCs markedly suppressed the expected antibody response, as shown by depressed numbers of hemolytic antibody plaque forming cells. Carbon treatment did not affect antibody forming cells per se as shown by lack of an effect on plaque forming cells when carbon was given after SRBCs, either in vivo or in vitro. Carbon injection before primary immunization prevented development of "immunologic memory," as shown by an altered secondary immune response. Mice given carbon and SRBC several weeks before secondary immunization with RBCs developed a primary type antibody response characterized by appearance of 19S antibody with little or no 7S hemolysins, characteristic of a secondary response. Furthermore, by appropriate treatment of mice with carbon and SRBC, immunologic unresponsiveness to SRBCs could also be induced, as evident by absence of both 19S and 7S antibody formation after subsequent challenge immunization with sheep erythrocytes. The mechanisms involved in RE "blockade" induced aberrations of normal immune responses may be related to effects on macrophages or soluble humoral factors, or both. It is unlikely that carbon treatment affects immunocytes directly. Further studies concerning the nature and mechanism of RE blockade on cellular and humoral components of the immune response mechanisms seem warranted and should provide more insight concerning the role of macrophages in antibody formation.

Animals↗
PubMed1976

A simplified procedure for in vitro immunization of dispersed spleen cell cultures.

Dispersed spleen cell suspensions from normal mice were immunized with sheep erythrocytes in flat bottom vial tubes containing a relatively small amount of tissue culture medium fortified with a 'nutrient cocktail'. The magnitude of the number of antibody plaque forming cells appearing in such tube cultures was equivalent or greater than that obtained in Marbrook vessels in the Mishell--Dutton system. Omission of the nutrient cocktail on the day of culture initiation, or the use of round bottom vials, resulted in much lower PFC responses.

Animals↗
PubMed1976

Acute and chronic single dose effects of LSD-25 on visual discrimination in rats.

Rats subjected to either a frontal cortex lesion or to a sham operation were trained to discriminate between a lighted and unlit alley to escape shock. Following intubation with either placebo or LSD-25 (1.0 mg/kg), they were given discrimination trials 2 hr, 1 week, and 1 month later, but with an increased level of task difficulty. Single dose effects of LSD-25 were observed acutely in a transient impairment of visual discrimination accuracy, and more chronically in slower running time. Although no significant drug-lesion interactions were noted, the results were in the direction of a combinatory effect. The value of increasing the level of post-treatment task was confirmed.

Animals↗
PubMed1976

Immunosuppression induced in vitro by cell-free extracts of Friend leukemia virusinfected splenocytes.

The immunologic responsiveness by normal BALB/c spleen lymphocytes immunized in vitro with sheep erythrocytes was markedly suppressed by calrified cell-free homogenates of Friend leukemia virus (FLV)-infected mouse spleens. Suppression was achieved with a 3,000Xg supernatant of FLV-containing homogenates freed of cellular debris but not with crude unclarified homogenates or pelleted material after centrifugation. The immunosuppressive effects of the virus were dose dependent, whether the virus was added directly to the target spleen cells or separated from them by a 0.4mu Nuclepore filter. Suppression was prevented by heating of the virus at 100 degrees C for 10 minutes or by neutralization with antiserum to FLV. Addition of the virus as late as 48 hours after in vitro immunization of splenocytes affected the immune response. However, suppression was maximum when the clarified virus was added to the splenocytes 1 or 2 days before immunization. The agent in the FLV-infected spleen homogenates responsible for immunosuppression appeared to be the virus per se; however, virus-associated soluble factor(s) might have been involved.

Animals↗
PubMed1976

Altered immunologic responsiveness in mastocytoma-bearing mice.

Immune responses to sheep erythrocytes were enhanced in mice bearing small mastocytomas soon after injection of a few tumor cells. In contrast, mice with larger tumors after transfer of a greater number of mastocytoma cells and those in the later stages of tumor development after transfer of small numbers of tumor cells showed moderately suppressed immune responses. Transfer of spleen cells from mastocytoma-bearing mice to irradiated recipients resulted in more antibody-forming cells as compared to transfer of splenocytes from normal donor mice. The addition of graded numbers of mastocytoma cells to a constant amount of normal spleen cells transferred to irradiated mice also resulted in enhanced responses and increased spleen weights in the recipients. This increase, in direct proportion to the number of mastocytoma cells transferred, also occurred when Escherichia coli lipopolysaccharide (a T-cell independent antigen) was used to immunize animals given spleen cells from normal mice and mastocytoma cells. Mastocytoma cell-free homogenates or X-irradiated tumor cells also heightened immune responses in recipient mice, which indicated that viable cells were not needed for the effect. Such homogenates, as well as the tumor cells per se, stimulated increased lactate dehydrogenase (LDH) activity in the sera of recipient mice. However, tumor cells passaged in tissue culture for several months, those derived from mice bearing a mastocytoma cell line with a low LDH-stimulatory activity, or UV-irradiated mastocytoma cells with a high LDH-stimulatory activity did not induce enhanced plaque-forming cell responses.

Animals↗
PubMed1976

Discussion paper: impairment of B-lymphocyte functions in concanavalin A-treated friend virus infected mice.

Friend leukemia virus (FLV) leukemogenesis was prevented by treatment of the virus with Concanavalin A (Con A). Mice infected with the lectin-treated virus, however, showed evidence of a dormant infection since infectious virus could be recovered for as long as 100 days. Humoral immune responses to sheep erythrocytes (SRBC), a thymus-dependent antigen, and to E. coli lipopolysaccharide (LPS), a thymus-independent antigen, were depressed (approximately 80-90%) in mice given the Con A-treated FLV. Cell transfer studies indicated that the impaired responsiveness to SRBC was related to a defect in B-lymphocyte function, similar to the impairment in mice infected with untreated FLV. The mitogenic response of splenocytes from Con A-FLV mice to E. coli LPS was also depressed as was the ability of Ig-bearing spleen cells to redistribute these immunoglobulin receptors into polar caps. The impaired immune responsiveness in the Con A-FLV infected mice appeared associated with the persistent virus infection and not to neoplastic transformation generally associated with leukemogenic process.

Animals↗
PubMed1976

Discussion paper: protective immunity in leukemic mice treated with specific "immunogenic" RNA.

Mice were actively immunized against Friend leukemia virus tumorigenesis by vaccination with cell-free homogenates derived from infected splenocytes emulsified in Freund's adjuvant. Adoptive immunity was also achieved by transferring splenocytes from actively immunized donor animals intravenously into syngeneic recipient animals challenged with the virus. Furthermore, RNA-rich extracts derived from spleens of actively immunized donor animals were capable of transferring immunity to FLV leukemia when injected into recipient animals challenged with the virus. The "immune RNA," when incubated with normal splenocytes in vitro, followed by washing, resulted in a cell population that also induced adoptive immunity after transfer to normal animals challenged with virus either before, simultaneously with, or after injection of the treated splenocytes. RNase, but not DNase or other enzymes, inactivated the biologie activity of the protective RNA from immune donors. In addition, isogeneic mouse serum that contained neutralizing antibody to FLV also inhibited the protective effect of the specific RNA; sera from control mice immunized with unrelated antigens failed to neutralize the specific RNA. These results indicate that an RNA extract that contains a virus-associated or -induced antigen is formed in the spleens of actively immunized animals and possesses the ability to either directly induce protective immunity in recipient animals challenged with virus or, indirectly, to convert normal splenocytes in vitro to adoptively confer immunity to similar recipients. Further investigations concerning the mechanism by which such immunogenic RNA functions in vivo and in vitro, as well as the physicochemical nature of the RNA complex, especially that portion associated with the tumor virus-associated antigen, are needed.

Animals↗
PubMed1976

Immunodepression by Rowson-Parr virus in mice; lymphocyte markers and capping response of spleen and lymph node cells after infection.

Infection with Rowson-Parr virus (RPV) induced a rapid reduction in the number of immunoglobulin-positive and theta antigen-positive cells detectable by immunofluorescence in the spleens of susceptible BALB/c mice. The changes produced by RPV infection in the lymph nodes were different, since the number of immunoglobulin-positive cells was increased and the proportion of theta-positive cells remained unchanged. However, the ability of immunoglobulin-bearing cells to redistribute their receptors into caps was reduced in both types of lymphoid tissue. A similar pattern of changes was produced by infection with Friend leukemia complex, from which RPV was originally obtained. These effects of RPV and Friend leukemia complex may contribute to the immunodepressed state of infected mice.

Animals↗
PubMed1976

Restoration of leukemia virus-suppressed immunocytes in vitro by peritoneal exudate cells.

Depressed antibody responsiveness to sheep erythrocytes in mice infected with Friend leukemia virus continued in vitro when spleen cell cultures from infected animals were cultured in the presence of antigen. Addition of PE cells from normal donor mice to the immunologically depressed splenocyte cultures resulted in a marked restoration of antibody responsiveness. Restoration of the immune response was PE cell dose-dependent; a ratio of 1 PE cell per 10 splenocytes resulted in the largest numbers of PFC's. These results suggest that impaired antibody responsiveness by spleen cell cultures from FLV-infected mice may be due, in part, to effects on antigen-processing macrophages, since restoration of immune responsiveness occurs by PE cell supplements.

Animals↗