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Biomedical subjects

J Abb

Publications and source records attributed to J Abb.

At least 55 records · Page 3Linked to original sources
PubMed1981

Retinoid-induced growth inhibition of herpesvirus-transformed marmoset lymphoblastoid cell lines.

The in vitro proliferation of herpesvirus-transformed marmoset lymphoblastoid cell lines (LCL) was inhibited by retinoic acid and retinyl acetate. Both Herpesvirus-ateles-and Herpesvirus-saimiri-transformed LCL with T-cell characteristics and Epstein-Barr-transformed LCL with B-cell markers were more sensitive to retinoic acid than to retinyl acetate. Inhibition of LCL proliferation was dependent on retinoid concentration and became apparent only after 3-4 days of exposure. In vitro assays for marmoset LCL sensitivity to retinoids may indicate the potential usefulness of these compounds in the chemoprevention of virus-induced lymphoma in vivo.

Animals↗
PubMed1980

Retinoids inhibit the mitogenic activity of tumour-promoting phorbol esters on human lymphocytes.

The tumour-promoting agents 12-0-tetradecanoylphorbol-13-acetate (TPA) and phorbol-12, 13-dibutyrate (PDB) I are potent mitogens for human peripheral blood lymphocytes. In contrast, the non-cocarcinogenic substance phorbol lacks lymphocyte-activating properties. Non-toxic levels of retinoic acid (RA) or retinyl acetate (RAt) inhibit the phorbol-ester-stimulated lymphocyte blastogenesis required the near-concurrent addition of retinoids. Differences in the sensitivity of phorbol-ester-stimulated lymphocyte subpopulations to the antagonistic action of RA or RAt, respectively, suggest that the inhibitory effect of retinoids may not be due to a common mode of action. Lymphocyte cultures may provide a useful model system for studies of the mechanisms of action of both phorbol esters and retinoids.

Carrier Proteins↗
PubMed1980

Specific anti-marmoset T-cell globulin: cytotoxic and mitogenic properties.

A virus-transformed marmoset lymphoblastoid cell line (LCL) with T-cell characteristics was used for the production of rabbit anti-marmoset T-cell globulin (RAMTG). Exhaustive absorption of the crude antiserum with kidney-liver homogenate and pooled marmoset B-LCL yielded a T-cell-specific antibody. Specificity of the absorbed RAMTG was evidenced by plateau formation in the cytotoxic activity on marmoset peripheral blood lymphocytes (PBL) and clear discrimination between marmoset T-LCL and B-LCL. Unexpectedly, the absorbed RAMTG was not cytotoxic for human PBL. Assays for mitogenic activity showed that unabsorbed RAMTG exhibited mitogenic activity on marmoset, but not on human or baboon PBL. Unabsorbed rabbit anti-human T-cell globulin (RAHTG) induced cellular proliferation in human and baboon PBL, whereas marmoset or Saimiri sciureus PBL showed no response. Absorbed RAMTG did not stimulate DNA synthesis of marmoset PBL. In conclusion, the specific RAMTG may be useful for studies on the functional role of T-lymphocytes in the marmoset immune response to organ allografts or infectious agents.

Animals↗
PubMed1980

Effects of retinoic acid on the human lymphocyte response to mitogens.

Nontoxic concentrations of retinoic acid enhance DNA synthesis of human peripheral blood lymphocytes in response to phytohemagglutinin or rabbit-antihuman thymocyte globulin, whereas the response to concanavalin A or pokeweed mitogen remained unaffected. Retinoic acid-induced stimulation of lymphocyte reactivity to phytohemagglutinin or antithymocyte globulin was most evident in T cell-enriched subpopulations and required the near-concurrent addition of retinoic acid and mitogens. Retinoic acid-mediated enhancement of lymphocyte proliferation in response to phytohemagglutinin or antithymocyte globulin was paralleled by a concomitant suppression of immune interferon production of lymphocytes stimulated with these mitogens. These findings allow further studies on the immunoregulatory action of retinoids in vitro.

Antilymphocyte Serum↗
PubMed1980

The tumour promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) induces the production of lymphocyte-activating factors (LAP) in human lymphocyte cultures.

The tumour promoting phorbol ester TPA induces the production of lymphocyte-activating factors (LAF) by human peripheral blood lymphocytes. The noncocarcinogenic and nonmitogenic agent phorbol lacks LAF-inducing properties. Production of LAF by TPA-stimulated lymphocytes occurs independent of the presence of macrophages in cultures and shows a correlation to the dose of TPA used for lymphocyte activation. The possible implications of these observations for the in vitro interaction of phorbol esters and cells of the haemopoietic system are discussed.

Cells, Cultured↗
PubMed1979

Lymphocyte activation by the tumor-promoting agent 12-O-tetradecanoylphorbol-13-acetate (TPA).

TPA, a highly active tumor-promoting agent, is an effective mitogen for primate peripheral blood lymphocytes. Optimal stimulation of human lymphocytes was obtained 4 days after the addition of TPA at a concentration of 7.5 ng/ml. Lymphocyte fractionation experiments demonstrated that both T and B cells incorporated 3H-thymidine significantly in response to TPA. Lymphocyte blastogenesis was not due to the reactivation of latent herpesviruses by the tumor promoter, since similar responses to TPA were obtained with virus-genome positive or negative cells. Increased levels of DNA synthesis were observed when TPA was added to marmoset, baboon, rhesus monkey, or chimpanzee peripheral blood lymphocytes. Canine peripheral blood lymphocytes and spleen cells from guinea pigs, rats, and mice were not stimulated by TPA. These observations suggest that TPA-induced lymphocyte blastogenesis may be useful for studies of lymphocyte activation and of the molecular mechanisms of action of tumor-promoting phorbol esters.

Animals↗
PubMed1978

Matching for DLA-A, DLA-B and DLA-D antigens and skin allograft survival in unrelated beagle dogs.

The effect of matching for immunogenetic markers on the survival of skin allografts in unrelated dogs has been studied. Skin grafts in recipients differing from donors for either DLA-A or DLA-B antigens, or both, had mean survival times (MST) of 9.3, 9.7 and 8.5 days, respectively. Differences between these groups were not significant. Prolonged survival of skin grafts, however, was found in SK-LD-indentical (MST: 12.4 days) or SD-identical/LD-different (MST: 12.5 days) donor-recipient combinations. We conclude that dkin allograft survival in dogs appears to be controlled by DLA-A and DLA-B, but not by DLA-D determinants.

Animals↗
PubMed1978

Cell-mediated immunity in canine marrow graft recipients given cyclophosphamide.

The cellular immune status of 48 canine chimeras was studied between 15 days and 3 years after a lethal dose of cyclophosphamide (CY) and an allogeneic marrow graft. Marrow graft recipients were given no further immuno-suppressive treatment. Recovery of total white blood cell counts was complete by day 20 after grafting. Peripheral blood lymphocyte counts did not reach the normal range until day 100. Short-term chimeras (less than 100 days postgrafting) showed marked impairment of cell-mediated immunity as indicated by the inability to respond adequately to nonspecific mitogenic (PHA, ConA, PWM) and specific antigenic (allogeneic lymphocytes, PPD) stimulation in vitro. Skin test reactivity to PPD after immunization with BCG was also significantly depressed. Long-term chimeras (more than 100 days postgrafting) had normal in vitro response to mitogens; lymphocyte blastogenesis to specific antigens however remained decreased for prolonged periods postgrafting. The survival time at first set allogeneic skin grafts showed no significant difference between chimeras and normal control dogs. Lymphocyte transformation in response to stimulation with specific antigens may prove a useful parameter for the in vitro evaluation of defects in cellular immune reactivity following allogeneic marrow transplantation.

Animals↗
PubMed1978

Autologous bone marrow grafts in dogs treated with lethal doses of 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea.

Hematological and immunosuppressive effects of various single doses of 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU) were evaluated in the preclinical canine model. Immune function appeared not to be impaired by treatment with CCNU, but severe myelotoxicity contributed to the death of 3 of 4 dogs given 10 mg CCNU per kg and 5 of 5 dogs given 15 mg CCNU per kg within 10 days after drug administration. Infusions of autologous bone marrow protected 6 of 6 dogs receiving 15 mg CCNU per kg and 6 of 6 dogs receiving 20 mg CCNU per kg from lethal marrow failure. Dogs given 30 mg CCNU per kg and autologous marrow died within 7 days from severe gastrointestinal toxicity. We conclude that autologous bone marrow support may allow the use of high-dose CCNU regimens and thereby increase its therapeutic efficacy in the treatment of advanced cancer.

Animals↗
PubMed1977

Hematologic and immunologic studies in dogs given nitrogen mustard (hn3).

Hematologic and immunosuppressive effects of single doses of nitrogen mustard (HN3) were evaluated in 20 dogs. HN3 caused profound depression of peripheral blood counts in all animals. Recovery of total white blood cell counts in dogs surviving the acute gastrointestinal toxicity of HN3 was complete by day 15. Recovery of platelet and lymphocyte counts to initial levels took a more prolonged course. Granulopoietic progenitor cells (CFU-C) in the bone marrow were assayed by an in vitro culture system. Concentrations of CFU-C were markedly decreased one day after HN3-treatment, but showed at near-lethal doses rapid restoration to normal values within 4 to 7 days. Cellular immune function of HN3-treated dogs was impaired for prolonged periods as indicated by the reduced capacity of canine lymphocytes to proliferate in vitro in response to stimulation with mitogens. Humoral immune function was similarly affected as determined by the depressed and delayed antibody formation against an intravenous challenge with sheep red blood cell. In conclusion, our results suggest a different effect of HN3 on lymphoid and myeloid precursor cells.

Animals↗
PubMed1977

Effects of busulfan (BU) on hemopoiesis and immune reactivity in dogs.

Hematologic and immunosuppressive effects of BU were evaluated in 21 dogs. Twenty to 30 mg BU/kg produced severe but in most cases reversible myelotoxicity. All animals given 40 mg BU/kg died of marrow failure which was consistently reversed by the infusion of autologous marrow. Granulocytic progenitor cells (CFU-C) in the bone marrow of BU-treated dogs were severely depressed by day 7 after drug administration and in surviving animals showed only slow recovery to normal values. Cell-mediated immunity as determined by the in vitro reactivity of lymphocytes was normal after stimulation with T-cell mitogens (PHA, ConA), but impaired after stimulation with B-cell mitogens (PWM, SpA). Antibody formation against sheep red blood cells was not suppressed by BU-treatment.

Animals↗
PubMed1977

In vitro and in vivo immune response to specific antigens in canine marrow graft recipients.

Cellular and humoral immune reactivity to primary and secondary challenge with tetanus toxoid, diphtheria toxoid and keyhole limpet hemocyanin was studied in normal dogs and canine bone marrow chimeras prepared for marrow grafting by lethal doses of cyclophosphamide. Short-term chimeras (less than 100 days postgrafting) showed general impairment of immune function as indicated by marked depression of skin test reactivity, lymphocyte blastogenesis in vitro and antibody formation. Long-term chimeras (more than 100 days post-grafting) demonstrated gradual improvement of immunologic capacity related to the stage of postgrafting. Prolonged immunoincompetence was suggested by decreased lymphocyte proliferation in vitro in response to stimulation with tetanus and diphtheria toxoids and by incomplete conversion from 19S to 7S antibody synthesis. Lymphocyte blastogenesis to specific antigens may prove a useful parameter for the in vitro evaluation of defects in cell-mediated immunity following allogeneic bone marrow transplantation. Our findings of prolonged immunodeficiency in the preclinical canine model point out the necessity for vigilance in early detection and treatment of infection and underline the importance of approaches aimed at accelerating immunologic reconstitution.

Animals↗
PubMedDate not supplied

Interferon production in male homosexuals with the acquired immune deficiency syndrome (AIDS) or generalized lymphadenopathy.

We measured serum interferon (IFN) levels and leukocyte IFN production in vitro in homosexual men with AIDS or generalized lymphadenopathy and in asymptomatic homosexual or heterosexual men. Acid-labile interferon alpha was detected in the serum of two patients with AIDS and in three out of nine patients with lymphadenopathy, but not in the sera of healthy homosexual or heterosexual controls. The presence of serum interferon in patients with AIDS or lymphadenopathy was correlated with a marked deficiency of their leukocytes to synthesize interferon alpha in response to viruses or tumor cells, but did not significantly interfere with the production of interferon gamma in response to lectin or bacterial enterotoxin. Our results suggest an inverse correlation between serum interferon alpha and the amount of interferon alpha produced in leukocyte cultures in male homosexuals with AIDS or generalized lymphadenopathy.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

HIV antigen, HIV antibody and serum interferon in a patient with encephalopathy.

Acute encephalopathy was associated with the presence of human immunodeficiency virus type I (HIV I) antigen and seroconversion to anti-HIV I in a 27-year-old homosexual man. Examination of consecutive sera from the patient revealed circulating interferon (IFN) alpha which became detectable with the appearance of HIV I antigen but before development of anti-HIV I. Serum IFN was present for only a limited time and was not demonstrable after neurological symptoms resolved. It may be speculated that circulating antiviral activity contributed to the clinical manifestations of acute HIV I infection.

Acquired Immunodeficiency Syndrome↗