PubMed Health⌕ Search

Biomedical subjects

A S Edelman

Publications and source records attributed to A S Edelman.

14 recordsLinked to original sources
PubMed1991

Proliferative response of mononuclear cells from HIV-infected patients to B-cell mitogens: effects of lymphocyte subset frequency, T-cell defects and prostaglandins.

Proliferative responses of mononuclear cells from patients seropositive for human immunodeficiency virus to B-cell mitogens are severely depressed compared with those of controls. The role of several immunoregulatory phenomena was analyzed. Experimental results show that addition of exogenous lymphokines to cultures increases responses to anti-mu and SAC. Addition of indomethacin to cultures greatly increases the SAC response and causes a smaller increase in the pokeweed mitogen (PWM) response. When both exogenous lymphokines and indomethacin are present in cultures, responses of patients' cells to all three mitogens are positively correlated with the percentage of CD4+ T cells and negatively correlated with the percentage of CD8+ T cells. Responses to anti-mu and SAC are also positively correlated with the percentage of B cells in these cultures. On the basis of these correlations between B-cell responses and lymphocyte subset frequency, patients' B-cell responses can be mathematically corrected to estimate the responsiveness of the B cells in the presence of normal numbers of CD4+ and CD8+ cells. These corrected responses for all three mitogens are virtually identical to control responses. Furthermore, responses of enriched B-cell populations from HIV+ subjects and normal controls to SAC were not significantly different when assays were performed in the presence of indomethacin and exogenous lymphokines. These results suggest that B cells from HIV+ patients are inherently normal in their responsiveness to B-cell mitogens. The depressed function is imposed upon them as a result of the abnormal frequency of lymphocyte subsets in the blood, by increased prostaglandin production, and deficient lymphokine production.

B-Lymphocytes↗
PubMed1990

Solitary splenic metastasis of an adenocarcinoma of the lung.

Splenic metastasis of solid tumors is a rare event, most often diagnosed at the time of autopsy. Whereas in cases of widely disseminated cancer, splenic involvement may be fairly common, solitary splenic metastasis in the absence of other metastases is exceedingly rare. The authors report a case of a 63-year-old woman in whom the sole detectable distant metastasis of a lung carcinoma was a splenic mass. The splenic lesion was detected before the resection of the primary lung lesion during a complete metastatic work-up. At that time, however, it was considered unlikely that the mass in the spleen represented a metastasis because of the lack of metastatic disease elsewhere.

Adenocarcinoma↗
PubMed1990

Response of mononuclear cells from HIV-infected patients to B-cell mitogens: correlation with immunological and clinical features of disease progression.

Proliferation of mononuclear cells from HIV-seropositive patients to B-cell mitogens was studied in the absence and presence of mixed lymphocyte culture supernatants (MLC-sup). The results show: (1) patients' responses to B-cell mitogens overlap with normal responses but are, on average, consistently lower than normal; (2) the addition of MLC-sup increases the proliferative responses to T-cell-independent mitogens, but does not bring patient's responses up to control levels; (3) HIV-positive patients in all clinical categories have decreased responses to B-cell mitogens. Although some patients with AIDS Centers for Disease Control (CDC) group IVC and IVD have the lowest responses, asymptomatic (CDC group II) and AIDS-related complex (ARC; CDC groups III/IVA and IVB) patients also show significant defects. (4) The same patients were recategorized using an immunological staging system. Those patients with more normal immunohematological parameters have significantly greater responses to mitogens compared with patients with more abnormal immunological parameters. The data suggest that immunological staging could provide more information than clinical classification with respect to the underlying immunopathogenic events occurring in HIV infection.

AIDS-Related Complex↗
PubMed1989

AIDS: a syndrome of immune dysregulation, dysfunction, and deficiency.

Acquired immune deficiency syndrome (AIDS) is a disease caused by the human immunodeficiency virus (HIV) in which cellular immune functions are severely impaired. Acute infection and subsequent destruction of helper T cells, although occurring readily in cell cultures, do not appear to be the only mechanisms mediating helper T cell loss. Other mechanisms that may account for the loss of helper T cells include: T cell syncytia formation, decreased T cell production, and autoimmune-related destruction of helper T cells. Immune abnormalities seen early in the course of HIV infection include immune hyperactivation and autoimmune phenomena suggestive of immune dysregulation rather than immune deficiency. Many changes in immune function are, in fact, seen in HIV-seropositive patients who possess a normal number of helper T cells. Mechanisms (other than the loss of helper T cells) that may contribute to the immune abnormalities seen in these patients include noninfectious effects of HIV and HIV proteins, effects of HIV on non-T cells, autoimmune-related manifestations of HIV infection, and HIV-induced activation of normal immunosuppressive circuits.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Suppressor T cells with histamine type II receptors in chickens bearing chemically induced fibrosarcomas.

Immunity to a local (wing web) challenge with transplantable, chemically induced tumors, such as CHCT-NYU-4, can be transferred to histocompatible SC chickens with intravenously injected splenic T cells from tumor-immune chickens. Simultaneous iv injection of splenic T cells from chickens bearing progressively growing CHCT-NYU-4 prevents the expression of this adoptive systemic tumor immunity. The splenic suppressor T cells are B-L(Ia) positive and adhere to dishes coated with cimetidine-protein conjugate, suggesting that they bear type II histamine receptors (H2R). Intravenous injection of gamma-irradiated CHCT-NYU-4 cells 7 days prior to a local challenge with the same tumor promotes growth of a normally suboptimal tumor cell dose such that the incidence of progressive tumor growth is significantly increased. Concomitant treatment with the H2R antagonist, ranitidine, inhibits tumor growth of an optimal tumor dose challenge and promotes induction of tumor immunity. However, this drug cannot reverse the effect of iv injected tumor cells. Another drug with reported antisuppressor cell activity, cyclophosphamide (50 mg/kg), injected 1 day prior to challenge causes a transient inhibition of tumor growth. Injection of this drug on Day 7 does not have a significant effect by itself but, in combination with the Day-1 pretreatment, a significant inhibition of tumor growth by size and tumor incidence measurements is obtained. These results indicate that manipulation of immunity to transplantable fibrosarcomas in the chicken is possible with drugs acting on suppressor cells.

Animals↗
PubMed1985

Ability of chicken B cells from different compartments to respond to TNP-Ficoll.

The responsiveness of chicken B cells from various compartments to T-independent antigens was studied by immune transfers of spleen and bursa cells into immunosuppressed recipients. Bursa cells from 8- to 10-wk-old donors failed to respond to trinitrophenylated Ficoll (TNP-F) even when thymus cells or splenic T cells were added. Spleen cells from the same donors transferred responses, as judged both by anti-TNP plaque-forming cells (PFC) per spleen and serum anti-TNP titers. In contrast, responses to TNP-Brucella abortus (TNP-BA) were transferred at least as well as by bursa as by spleen cells. Rabbit anti-chicken T cell serum plus complement treatment of the spleen cells reduced their ability to transfer responses to sheep erythrocytes, but either did not affect or enhanced serum antibody responses to TNP-BA and TNP-F. In intact animals, responsiveness to i.v. injected TNP-F was found to develop slowly after hatching in the chicken. At the age of 2 and 3 mo, PFC/spleen on day 4 after TNP-F injection were only 20% and 40%, respectively, of the adult response. Thymectomy at hatching further delayed this development, resulting in 12% and 45% of the adult control response at ages of 3 and 4 mo. It is concluded that responsiveness to the TI-2 antigen, TNP-F, develops slower than that to the TI-1 antigen, TNP-BA, and is restricted to the splenic B cell compartment. In addition, this development appears to be faster in the presence rather than in the absence of the thymus. In view of the previously shown effect of thymus on bursa development, these data suggest that the maturation of TI-1 antigen (TNP-F)-respondent chicken B cells requires residence in both the bursa and spleen before the development of responsiveness to such antigens.

Animals↗
PubMed1985

Cross-reactive cellular and humoral immunity to carcinogen-induced chicken fibrosarcomas. I. Protective cross-immunity between transplantable tumor lines.

Dimethylbenz[a]anthracene (DMBA)-induced transplantable fibrosarcomas in B2 homozygous chickens (SC line) grow progressively in normal chickens, but are rejected by chickens immunized previously with irradiated tumor cells and Corynebacterium parvum. Tumor-immune chickens resist challenge by the immunizing tumor lines as well as by some, but not all, fibrosarcoma lines. The pattern of cross-reactivity between four DMBA-induced transplantable tumor lines was examined in detail. Ability to reject a tumor challenge correlated very well (p less than 0.001) with the presence of delayed-type hypersensitivity (DTH) to that tumor. Immunization with one of two of the DMBA-induced lines tested also caused rejection of transplantable tumors developed from methylcholanthrene-induced and benzo(a)pyrene-induced primary fibrosarcomas. Although immunization with tumor caused DTH to chicken embryo fibroblasts (CEF), immunization with CEF failed to cause protective immunity or DTH to tumors. Presence of protective immunity, where tested, also correlated with the ability of spleen cells from immune donors to inhibit tumor growth in Winn tests. Humoral immunity exhibited even greater cross-reactivity than did cellular immunity. Distinct patterns of cross-reactivity were nevertheless observed with respect to the serum antibodies as detected in ELISA. Two of these patterns were also observed in several sera from primary tumor-bearing chickens, both including reactivity with CEF. Such reactivity was absent from normal chicken sera.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1985

Cross-reactive cellular and humoral immunity to carcinogen-induced chicken fibrosarcomas. II. Effect of prior immunization with transplantable tumors on primary tumor incidence.

Primary carcinogen-induced (7,12-dimethyl-benz[a]anthracene; DMBA) tumor-bearing SC chickens (B2/B2) frequently showed antibodies in their sera which reacted with cells from their autochthonous tumors, chicken embryo fibroblasts (CEF), tumor cells from some transplantable tumor lines, and from approximately 10% of other primary tumors. Similar results were obtained by ELISA on glutaraldehyde-fixed cells and by immunofluorescence on viable cells. The serum antibody reactivity could be removed by absorption with CEF but not with non-cross-reacting primary tumor cells or a variety of normal tissues. Although sera from normal chickens never showed significant reactivity, a high percentage of sera from chickens that had been injected with DMBA but failed to develop detectable tumors showed antibody activity to a transplantable DMBA-induced tumor and to CEF. On the basis of previously established cross-reactivity patterns in protective immunity to transplantable carcinogen-induced fibrosarcomas, attempts were made to protect against chemical carcinogenesis by prior immunization with selected DMBA-induced transplantable tumors. Tumor-immune chickens showed a significant decrease in the development of tumors during the first 3 mo after injection of DMBA (p = 0.001) or methylcholanthrene (p = 0.033) when compared to controls. This resistance to tumor induction in immune chickens was correlated to the degree of tumor immunity to the immunizing tumor present 1 mo after carcinogen injection (p = 0.046). There was, however, no detectable difference in the incidence of tumors arising later than 3 mo after carcinogen injection. The reduction in tumor incidence in immune as compared to control chickens at 5 mo was therefore less striking than the reduction seen at 3 mo. Immunization with CEF and adjuvants or with adjuvants alone afforded no protection to tumor induction.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1980

Nitrosamine carcinogenicity: a quantitative relationship between molecular structure and organ selectivity for a series of acyclic N-nitroso compounds.

A mathematical model has been developed which describes the selectivity between liver and other target organs for a series of carcinogenic N-nitro-sodialkylamines. The relationship requires structural terms for the parent molecule as well as for the potential metabolites. This suggests that the nitrosamine metabolites are involved in tumor induction and that they participate directly in the mechanisms responsible for selecting the target organ.

Animals↗
PubMed1978

Nitrosamine carcinogenicity: a quantitative Hansch-Taft structure-activity relationship.

Statistically significant correlations have been demonstrated between carcinogenic activity, water-hexane partition coefficients and electronic factors for an extensive series of N-nitroso compounds. Electronic factors were expressed by the Taft sigma* values of substituents on the carbon atoms alpha to the N-nitroso group. Such correlations indicate that transport of the carcinogen to its active site has an important effect on its potency. The correlations also implicate reactivity at the alpha-carbon in the determination of carcinogenic activity and point out various structural types which do not follow the general rule.

Animals↗
PubMedDate not supplied

Primary and secondary wattle swelling response to phytohemagglutinin as a measure of immunocompetence in chickens.

Wattle responses of 2-to-8-week-old chickens to phytohemagglutinins PHA-P and PHA-M were studied. Dilutions of PHA-M that did not induce wattle swelling after one injection did cause readily detectable swelling when injected a second time 1 week later. These responses were absent in birds subjected to thymectomy and gamma-irradiation at hatching and in birds treated with cyclosporin A during the week of sensitization, indicating that these responses are T-cell-dependent. Chickens bearing transplantable fibrosarcomas failed to show responses. It is suggested that reactivity to a second injection of PHA-M may be used as a measure of immunocompetence at the T-cell level in very young chickens.

Animals↗