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At least 19 recordsLinked to original sources
PubMed1975

Streptococcal preparation as an activator of host-mediated immune response: cellular immunity and alternate pathway of complement.

Streptococcal preparation, OK-432, was examined for its ability to initiate a host-mediated immune response. Aged individuals with negative skin response to phytohemagglutinin (PHA), as well as reduced in vitro blastoid transformation of lymphocytes, were treated with OK-432, and the response to PHA appeared in two out of three cases. The preparation was also demonstrated to convert C3 proactivator of complement when incubated with fresh human serum, as tested by immunoelectrophoresis, indicating the possibility that OK-432 might activate the alternate pathway of complement.

Aged↗
PubMed1985

Cellular immunity in congestive cardiomyopathy. The normal cellular immune response.

In vivo and in vitro tests of cellular immunity were studied in patients with congestive cardiomyopathy to determine whether these patients have normal or depressed cell mediated immunity to common environmental antigens and mitogens. No abnormality was found, but this does not exclude the possibility that transient depression of cell mediated mechanisms occurs early in the illness before clinical presentation.

Cardiomyopathy, Dilated↗
PubMed1978

The effect of clofibrate and pyridinol carbamate on the circulating immune complexes and cellular immune response in experimental atherosclerosis.

Cholesterol-fed rabbits were treated with clofibrate, pyridinol carbamate and with both drugs simultaneously. The quantity of circulating immune complexes in the sera of the animals was measured weekly and the migration inhibition test was carried out in the 12th week of the experiment. The trend of the changes in the concentration of the immune complexes was rather similar to that of the cellular immune response. Compared with the values obtained in the control animals, in the cholesterol-fed group a markedly higher level of immune complexes and a significant migration inhibition could be detected. The administration of clofibrate or pyridinol carbamate alone had no effect on the concentration of immune complexes. Pyridinol carbamate did not influence the migration inhibition; however, it became similar to the healthy controls in the clofibrate-treated group. Simultaneous treatment with both drugs resulted in a decrease in the quantity of immune complexes and a diminution of the migration inhibition.

Animals↗
PubMed1988

Recombinant HIV structural proteins detect specific cellular immunity in vitro in infected individuals.

Peripheral blood mononuclear cell (PBMC) cultures were established from patients with antibody to human immunodeficiency virus (HIV). Asymptomatically infected patients [5 of 19] had significant lymphocyte transformation responses induced in culture by a purified, recombinant envelope glycoprotein (rgp120) from the virus. A few (4 of 55) subjects with AIDS related complex (ARC) and no subjects with AIDS (0 of 29) had proliferative responses to this protein. These responses correlated directly with circulating levels of helper/inducer lymphocytes (p less than .01) and indirectly with virus antigen in blood (p = .04). Also, these responses occurred significantly less frequently than responses to herpes simplex virus (HSV) or cytomegalovirus (CMV) antigens in seropositive ARC patients (p less than .005). These data indicate that the frequency of immune cellular responses to rgp120 decline in association with disease progression, and become undetectable in frank AIDS. As rgp120-induced proliferation was not observed in cells from 15 seronegative immunocompetent subjects, this response appears immune specific. Immune T-lymphocyte-mediated responses to this HIV envelope glycoprotein may allow the prediction of future clinical events and may be useful in monitoring immune-enhancing therapy in patients with ARC and AIDS.

AIDS-Related Complex↗
PubMed1991

The effects of 13-cis-retinoic acid and beta-carotene on cellular immunity in humans.

Deficiency of vitamin A and/or its precursors has been associated with increased cancer risk in animals and humans. Therapeutic trials of vitamin A and related compounds have demonstrated activity in several cancerous and precancerous conditions. The authors measured the effects of a retinoid, 13-cis-retinoic acid, and a carotenoid, beta-carotene, on the human immune system in vivo in conjunction with their use in ongoing clinical trials. Immune cell subpopulations were analyzed by quantifying the expression of markers using flow cytometric study. Both compounds produced significant effects on immune cell populations. 13-cis-Retinoic acid resulted in an increase in the percentage of peripheral blood lymphoid cells expressing surface markers for T-helper cells with only minimal effect on natural killer cell marker expression. In contrast, beta-carotene produced an increase in the percentage of cells expressing natural killer cell markers with smaller effect on T-helper markers. Modest increases in the percentage of cells expressing Ia antigen, transferrin, and interleukin-2 receptors were produced by both drugs. These results suggest that retinoids and carotenoids can produce major changes in immune cellular marker expression in vivo in humans at doses relevant to their potential clinical use.

Adult↗
PubMed1972

Antigen recognition and the immune response. Humoral and cellular immune responses to small mono- and bifunctional antigen molecules.

L-Tyrosine azobenzene-p-arsonate (RAT) induced cellular immunity without antibody production in guinea pigs. Bifunctional antigens were prepared consisting of one RAT carrier moiety linked either directly to a dinitrophenyl (DNP) haptenic determinant or through one or more 6-amino-caproyl (SAC) spacers. Each SAC unit has an extended span of 8 A. Guinea pigs immunized with these conjugates developed cellular immunity directed against the RAT determinant and antibody specific for the DNP determinant. The anti-DNP response was the same with one or three SAC spacers, but was significantly weaker when the two determinants were joined without a spacer. Animals immunized with either DNP-SAC-TYR or DNP-TYR developed neither cellular nor humoral immunity. Prior immunization with RAT potentiated the secondary anti-hapten response to DNP-SAC-RAT. Modification of RAT at either the arsonate or tyrosine positions showed that other charged groups (sulfonate and trimethylammonium) could substitute for arsonate without loss of immunogenicity. Removal of either the amino or carboxyl group from the side chain of tyrosine did not abolish immunogenicity, but immunogenicity was lost upon removal of both. Immunization with symmetrical bifunctional RAT-(SAC)(n)-RAT and cyclo-(L-RAT-D-RAT) antigens led to cellular immunity but no anti-arsonate antibody, suggesting a barrier to "self-help." These compounds were also ineffective in inducing a secondary anti-arsonate response in animals primed with arsonate-BSA conjugates and RAT.

Animals↗
PubMed1983

Haemodialysis, continuous ambulatory peritoneal dialysis and cellular immunity.

The cellular immunity of haemodialysis and continuous ambulatory peritoneal dialysis (CAPD) patients was studied with regards to T-lymphocyte subsets and to suppressor T-cell function. The two groups of patients showed similar alterations: low proportions of suppressor-cytotoxic T-cells and low suppressive activity. In both groups there is a deterioration of this suppressive activity with time on dialysis.

Aged↗
PubMed1991

RNA-mediated transfer of cellular immunity to a synthetic env antigen of the human immunodeficiency virus (HIV-1).

A sheep was immunized with a synthetic peptide corresponding to amino acid residues 586-606 of the precursor envelope protein GP-160 of the HIV-1 including a conserved epitope region of the GP-41 transmembrane protein in the mature viral particles, referred to as SM 284 HIV-1 [1]. It is demonstrated that immune RNA extracted from the lymphoid organs of the immunized animal (SM 284 HIV-1 I-RNA) was able to transfer immune cellular reactivity to SM 284 HIV-1 in vitro to human and rabbit lymphocytes and in vivo to Cebus apella monkeys. The transfer was detected by the leukocyte adherence inhibition test (LAI) as an indicator of cellular reactivity. One of the most relevant results was the demonstration that SM 284 HIV-1 I-RNA was able to induce cellular immunological memory in vivo in monkeys. These results may be relevant to delineate a new alternative for immunomodulation against HIV infection.

Amino Acid Sequence↗
PubMed1992

Cellular immune reactivity to recombinant OspA and flagellin from Borrelia burgdorferi in patients with Lyme borreliosis. Complexity of humoral and cellular immune responses.

Patients with Lyme borreliosis (LB) usually develop a vigorous T cell response against the causative pathogen Borrelia burgdorferi, but little is known about the antigens recognized in the cellular response. Therefore, T cell reactivities against whole bacteria, recombinant 31-kD (outer surface protein A, [OspA]), and 41-kD proteins (flagellin) from B. burgdorferi were studied in patients with LB, non-LB patients, and healthy donors. In parallel, specific antibodies were determined by Western blot analysis. Virtually all patients with LB exhibited marked cellular responses to whole B. burgdorferi, which were significantly elevated compared with the control groups in both early and late disease stages. However, analyses using the purified antigens OspA and flagellin revealed considerable heterogeneity in the cellular reactivities among individuals as well as variations during the course of infection. T cell responses to OspA were significantly increased in patients with early LB compared with both control groups whereas in late-stage disease responses only exceeded those of non-LB patients and were not different from normal donors. Cellular immune reactivities to flagellin were significantly higher only in early LB compared with both control groups. Reciprocally, several control subjects demonstrated marked cellular responses to OspA and flagellin, suggesting that reactions to these proteins may not always be related to LB. T cell reactivity did not correlate well with the presence of specific antibodies. Almost all seropositive patients in both early and late stage LB had serum antibodies against flagellin, but antibodies to OspA were detectable only in a subset of late LB sera. These data demonstrate the complexity of the humoral and the cellular immune responses to components of B. burgdorferi.

Adolescent↗
PubMed1982

Assays of cellular immunity.

Numerous cellular assays are available to study the response or activities of mononuclear and polymorphonuclear cells in domestic species. When the assays, most developed originally to study rodent or human cells, are adapted to the cells of domestic species, minor or major modifications have been necessary. Furthermore, interpretation of results of the assays with cells from domestic species are not always consistent with those obtained in the original system, and it should not be expected that the assays will always provide results that can be interpreted similarly among species. Application and additional experience with these techniques, as well as new techniques, will provide a foundation for our understanding of the importance of cellular mechanisms in immunity of domestic species.

Animals↗
PubMed1986

Estradiol-induced alteration in the immune system. II. Suppression of cellular immunity in the rat is not the result of direct estrogenic action.

Estradiol has been reported to suppress numerous cellular immune response. What is not known is how estradiol exerts this effect. In vivo administration of estradiol to male rats caused time-related immunomodulatory effects leading to enhancement of lymphocyte transformation while suppressing a mixed lymphocyte reaction (MLR) response. The suppression of the MLR response was not due to alterations in the ratio of helper and suppressor T cells, nor was it due to alterations in either cell viability or the number of cells in culture. Lymphocytes cultured in vitro with estradiol, however, fail to show any alteration in the responsiveness in either MLR or lymphocyte transformation assays. The suppressive effects of estradiol cannot be transferred from a primary MLR culture to a second MLR culture using the supernatants from the primary MLR culture. Lymphocytes from animals given estradiol in vivo show no alteration in the production of interleukin 2: added in vitro to primary MLR cultures, Interleukin 2 failed to restore full responsiveness to lymphocytes from animals treated in vivo with estradiol. These results suggest that estradiol acts indirectly to cause an alteration in the responsiveness of the regulatory cells of the cellular immune system.

Animals↗
PubMed1975

Immune mechanisms in leukemia: suppression of cellular immunity by drugs and x-irradiation.

The relative suppressive effects of x-irradiation (XR), cyclophosphamide (CY), prednisolone (PRD), and methotrexate (MTX) on the primary and secondary cellular immune response of C58/wm mice to syngeneic line Ib transplantable leukemia (Ib cells) were quantified. An LD10 dose of each agent was used for immunosuppression. XR, CY, and PRD were markedly suppressive for the primary immune response if given 24 hr before mice were immunized to Ib cells but less immunosuppressive if given 24 hr later. MTX was only slightly immunosuppressive XR, CY, and PRD also suppressed the secondary immune response if given before but not after antigen. The immunosuppressive effect of these agents was evaluated by defining their median immunosuppressive dose or the median time in days required for mice to recover from graded doses of each immunosuppressive agent. For example, the median recovery time from an LD10 of XR, CY, and PRD was 29.3, 19.7, and 3.7 days, respectively. Immunologic competence remaining after XR or drug treatment was quantified in terms of the LD50 dose of Ib cells required to kill recipient mice. For XR, CY, PRD, and MTX it was 10(6.16), 10(2.15), 10(6.90) and greater than 10(7.0) viable Ib cells, respectively. The overall results provided evidence that the primary and secondary cellular immune responses to a weak syngeneic tumor antigen were resistant to immunosuppression once they were initiated. There was a good correlation between the relative immunosuppressive effect of the test agents and the amount that they reduced the number of immune spleen cells. The agents also impaired the immunocompetence of individual spleen cells. Mechanisms by which XR or drugs might exert their immunosuppressive effects were discussed.

Animals↗
PubMed1975

Immune mechanisms in leukemia: suppression of cellular immunity by starvation.

The effects of starvation on the cellular immune response of C58/Wm mice to syngeneic malignant lymphoid cells (1b cells) were studied. Mice were starved 1-3 days before or after immunization. The capacity of starved animals to survive immunization was used to quantify immunosuppression. When starvation bracketed immunization by -1 to +1 days, only 2 of 23 mice survived primary immunization, compared with 100% survival for nonstarved controls. A 2-day period of starvation +1 to +7 days after primary immunization reduced survival about 30%. For a test of the effect of starvation on the secondary immune response, mice were immunized, starved 2 days, and then challenged with viable lb cells. When mice were starved from -3 to +1 days before or after challenge, there was a 25-45% decrease in survival. Starvation caused a disproportionate depletion of lymphoid tissue elements. The proportional loss in the weight of the spleen and thymus was essentially twice as great as the loss in total body weight. The peripheral blood leukocyte count was reduced by about 20% when mice were starved 1 day and by approximately 50% when they were starved 2 days. When mice were starved 1-2 days, the differential leukocyte count did not shift and there was no significant change in the number of blood erythrocytes or in the hematocrit. Starvation for 2 days caused a 65-70% reduction in the number of viable mononuclear spleen cells. Starvation for 3 days caused about 90% reduction. Adoptive cell transfer experiments showed that the immunocompetence of individual spleen immunocytes was not reduced by starvation.

Animals↗
PubMed1991

Bestatin administration and the change in cellular immunity.

The change in cellular immunity by Bestatin (ubenimex) treatment--30 mg/day orally--was investigated in 23 gastrointestinal cancer patients for: 1), functional T cell subsets; 2), IL-2 receptor; 3), PHA-induced blastogenesis; and 4), PPD skin reaction. The absolute number of helper T cells (Th) and cytotoxic T cells (Tc) increased in 74 and 79% of cases, respectively, compared with pretreatment values. On the other hand, the absolute number of suppressor T cells (Ts) decreased in 79% of cases. IL-2 receptor increased in 56% of patients, PHA blastogenesis increased in 67% of patients and PPD skin reaction was elevated in 75% of cases comparing to pretreatment values. These results suggest that Bestatin could increase cellular immunity in cancer patients.

Antibiotics, Antineoplastic↗