PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Immunity, Cellular”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1983

Blood transfusions as pretreatment for kidney transplantation: immunization rate and effect on cellular immune response in vitro.

A group of 28 untransfused uremic patients was given five or more units of stored blood as pretreatment for kidney transplantation; 9 patients formed lymphocytotoxic antibodies against B cells and 1 patient developed multispecific antibodies against both B and T cell panels (greater than 80% reactivity). During the same period 22 previously transfused patients received up to five transfusions as pretreatment for kidney transplantation. B cell antibodies were formed by 10 patients, and 4 of these patients also formed T cell antibodies, 2 with broad reactivity. Cellular immune reactivity in vitro was studied on frozen cells from 17 randomly chosen patients. After five blood transfusions no significant changes were seen in blood lymphocyte responses to phytohemagglutinin (PHA), Concanavalin A (Con A), or in mixed lymphocyte cultures (MLC) and cell-mediated lympholysis (CML). After transfusion 3 patients got Non-A, non-B hepatitis and were withdrawn for up to six months from the transplantation list because of increased S-ALAT and S-ASAT. Of the 50 patients, 27 have received kidney grafts, 6 out of 20 who were sensitized, and 21 out of 30 who were nonsensitized. Because of positive crossmatches no patient with multispecific T cell antibodies has received a graft. We conclude that our transfusion regimen for kidney recipients has rendered barely one-third of the patients sensitized (mostly against B cells) and 3 out of 50 hypersensitized. No effect on T cell reactivity could be seen following five planned transfusions. Because fewer patients with antibodies received grafts (30% with antibodies, as compared with 70% without [P less than 0.01]) the blood transfusions seem to have led to a selection effect.

Antibodies↗
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↗
PubMed1979

Cellular immunity in renal diseases.

Cellular immune reactivity was studied in 78 patients with various forms of renal disease by skin testing with four recall antigens and a lymphocyte transformation test with tuberculin PPD and leucoagglutinin. Patients with S-creatine greater than or equal to 230 micromol/l as well as those with chronic pyelonephritis who had S-creatinine values below 230 micromol/l had significantly lower skin reactions than the controls to streptokinase-streptodornase, parotitis and PPD. Glomerulonephritic patients with S-creatinine values below 230 micromol/l had normal skin reactivity. Lymphocyte transformation tests showed decreased reactivity only in patients with S-creatinine level greater than or equal to 230 micromol/l. The results suggest an association of chronic pyelonephritis with a defective efferent, nonspecific arm of cellular immunity.

Adult↗
PubMed1991

[The latent dysfunction of Epstein-Barr virus (EBV)-specific cellular immunity in asymptomatic human immunodeficiency virus (HIV) carriers].

Cellular immunity is known to play a critical role in regulating Epstein-Barr virus (EBV) in the state of latent infection. Activity of EBV-specific cellular immunity decreases as the clinical stages of human immunodeficiency virus (HIV) infection progress, and many complications are induced by reactivated EBV in the late stages of HIV infection. However, in asymptomatic HIV carriers, some show the reduced activity of cellular immunity against EBV, while others still show normal range of the activity even in the presence of abnormality in other immunological parameters. In order to assess early immunological abnormality against EBV in these patients, asymptomatic HIV carriers with normal range of EBV-specific cellular immunity were studied in comparison with that in EBV seropositive healthy controls. 1. All of 4 asymptomatic HIV carriers showed normal range of EBV-specific cellular immunity as seen in healthy controls. 2. Asymptomatic HIV carriers had significantly elevated serum antibody titers to EBV-specific nuclear antigen (EBNA)2, viral capsid antigen(VCA), early antigen(EA), indicative of serological reactivation of EBV. 3. The number and percentage of peripheral CD4 positive lymphocytes, CD4/CD8 ratios were markedly decreased in asymptomatic HIV carriers. 4. In the presence of immunosuppressive agents, 4-deoxy phorbol ester(4-DPE), drastic decrease of EBV-specific cellular immunity was observed in asymptomatic HIV carriers at the concentration which did not affect that of healthy controls. 5. Reduced activity of EBV-specific cellular immunity induced by 4-DPE had no relation with surface marker expression on cytotoxic T cells which serve as cell-to-cell adhesion molecules. Based on these results, it is suggested that there is latent dysfunction of EBV-specific cellular immunity in asymptomatic HIV carriers, who seems to show normal range of immunity in usual assays.

Adolescent↗
PubMed1979

[Cellular immunity factors in dysentery].

Cellular immune response was studied in 89 adult patients suffering from various clinical forms of acute dysentery, with the use of the lymphocyte blast-cell transformation reaction under the action of a specific antigen (dysenterin) and a nonspecific mitogen (phitohemagglutinin). Functional value of T-lymphocytes proved to be retained in patients with acute dysentery; there was also lymphocyte stimulation by a specific antigen in patients with moderately severe and severe forms of dysentery during the first week of the disease. Specificity of blast-cell transformation of sensitized lymphocytes under the action of dysenterin was shown. Patients with a high percentage of the lymphocyte blast forms displayed a more rapid positive progress of the main clinical indices at the height of the disease than analogous patients with a low blast percentage in the blood. The expediency of using the blast-cell transformation reaction for differential diagnosis and prognosis of moderately severe and severe forms of acute dysentery is discussed.

Acute Disease↗
PubMed1989

[The nature of the factors in immune lymph nodes that stimulate humoral and cellular immune reactions].

In the early period after antigen action, cells of the lymph node draining area of antigen injection produce a factor, which after its administration to intact mice, promotes intensified migration of myelopeptide producers in the bone marrow and increases bone marrow suppressor activity. Factor administration produced 2-3-fold increase in macrophage, peritoneal and lymph node count as compared with control, and 2-4-fold increase in humoral and cellular immune response. The factor consists of three easily identifiable components: Ig, MHC class II determinants and antigen determinants, that form unique complex similar to, or identical with the complexes detected in vivo within 3-6 hours after immunization in serum by other authors.

Animals↗
PubMed1972

Infection-immunity in tularemia: specificity of cellular immunity.

The relationship between hypersensitivity and cellular resistance to infection with facultative intracellular parasites was studied in mice by using infection-immunity in tularemia as a model system. Delayed hypersensitivity to antigenic fractions of Francisella tularensis was first detected 6 to 7 days after immunization with viable F. tularensis vaccine, at which time immunity against challenge infection developed. Both immunity and delayed-type sensitivity reached maximal levels by 9 to 10 days. Immediate hypersensitivity occurred after immunization with both viable and nonviable tularemia vaccines but could not be correlated with resistance since nonviable antigens were not protective. Attempts to relate resistance to F. tularensis with nonspecific immunity factors were unsuccessful. Immunization of mice with BCG vaccine stimulated protection against infection with F. novicida and Salmonella typhimurium but provided no protection against infection with F. tularensis. Moreover, viable tularemia vaccine, while inducing marked protection against challenge with specific organisms, afforded no protection against infection with S. typhimurium or S. enteritidis. It is concluded that cellular immunity in tularemia involves an immunologically specific component.

Animals↗
PubMed1978

Cellular immunity in rheumatic heart disease.

Cellular immunity to non-specific antigens (PPD, Candida albicans, and streptococcal antigens) and mitogen (PHA) was investigated in patients with valvular heart disease of rheumatic origin. The result disclosed that lowered response in cellular immunity exists in these patients. The possible significance of this finding in occurrence of rheumatic activity was discussed.

Adult↗
PubMed1991

Cellular immunity in current active pulmonary tuberculosis.

A group of 10 patients with recently diagnosed pulmonary TB were studied and compared to 10 bacillus Calmette-Guérin (BCG) immunized healthy individuals. Cellular immune mechanisms were explored in vitro utilizing fresh and precultured peripheral blood mononuclear cells exposed to PHA, PPD, and recall antigens (SK/SD and CA). Proliferative assays were also carried out in the presence of either each patient's serum (autologous serum) or cocultured with CD3(+)-depleted adherent cells. Serum measurements of soluble interleukin-2 (IL-2) receptor and synthesis of IL-2 generated by mononuclear cells stimulated with PPD and SK/SD were also performed. Patient sera were able to inhibit autologous as well as allogeneic cell responses, and a significant adherent cell suppressive effect was observed. As a whole the group of patients showed decreased blast transformation to PPD, preserved proliferative responses to other recall antigens, and a low PPD-induced generation of IL-2. Furthermore, as possible evidence of preactivated T cells, these patients demonstrated high soluble IL-2 receptor serum levels. Early compromise of specific cell-mediated immunity, including IL-2 abnormalities, may be of significance in newly diagnosed pulmonary TB.

Adult↗
PubMed1976

[Cellular immunity in newborn infants with hyperbilirubinemia].

In order to identify the possibility of prenatal or perinatal bacterial contact with immunization of the cellular immunity system as underlying cause of the "idiopathic" newborn icterus (without blood group incompatibility) the lymphocyte transformation test with addition of streptolysin O or E. coli antigen was carried out in 68 newborns with a birth weight ranging between 1260 and 4200 g. The sensitization rate identified among the newborns with hyperbilirubinaemia did not differ significantly from those of the control group. Thus an ensured connection between a prenatal streptococcus or E. coli contact and the appearance of an idiopathic newborn hyperbilirubinaemia could not be established.

Antibodies, Bacterial↗
PubMedDate not supplied

[Effects of levamisole in the treatment of a group of patients with atopic asthma and depression cellular immunity].

We investigated the possibility of decreased cellular immunity (C.I.) in a substantial group of atopic asthmatic patients with respiratory tract infections during autumn and winter. Two-hundred and ten atopic asthmatic patients were selected, and the following tests for cellular immunity were performed. Skin tests with 11 bacterial and fungal antigens. Normal average value of the skin reactions is 2.5 mm. E rosettes with sheep erythrocytes. Normal value for patients of this age is 60 +/- 8%. Immunoglobulins A, G and M and complement fractions C3 and C4 were determined by radial immunodiffusion. IgE was determined using PRIST (Phadebas, Pharmacia). IgE was elevated in all except two of the patients. IgG, IgA and IgM, C3 and C4 were normal. Twenty five of the 85 patients had some depression in cellular immunity (decreased E rosettes and/or decreased skin reactions). Patients with depressed cellular immunity were given 2.5 mg Levamisol three times a week for three months. Their progress was evaluated clinically and immunologically and a positive correlation was found between clinical improvement and increased C.I. in 18 of the 25 patients. We consider Levamisol to be useful in approximately 8.5% of all asthmatic patients.

Adolescent↗
PubMed1977

Cellular immunity in chronic Chagas' disease.

The cellular immune response was assessed in 20 patients with chronic Chagas' disease (American trypanosomiasis). Thymus-derived lymphocyte function was determined in vivo by cutaneous reactivity to several antigens including a soluble preparation derived from Trypanosoma cruzi and sensitization to 2,4-dinitrochlorobenzene. The in vitro T-cell reactivity was investigated by the proliferative response to phytohemagglutinin and to T. cruzi antigen and by inhibition of leukocyte migration with the specific antigen. In addition, the proportion and absolute numbers of peripheral blood T and B-lymphocytes were determined by rosette formation. This research indicates that the general and specific cellular immune response, evaluated by the tests herein mentioned, is well preserved in patients, with Chagas' disease. We conclude that chronic Chagas' disease is not associated with deficiency in cellular immunity, nor does it lead to it. Conceivably, the active participation of delayed hypersensitivity may play an important role in the expression of the human chagasic lesions.

Adult↗