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Results for “Immunity, Cellular”

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PubMed1997

The role of cellular immunity both in the induction and effector phases of experimental allergic blepharoconjunctivitis (EAC) in rats.

In allergic conjunctivitis, the early phase reaction has been studied extensively both in humans and animals. Although cellular infiltration is the main feature of the late phase reaction, the role of cellular immunity remains unclear. The purpose of this study was to elucidate the role of cellular immunity both in the induction and effector phases of experimental allergic blepharoconjunctivitis (EAC). To analyse the involvement of cellular immunity in the induction phase, 6-8-week-old male Lewis rats were immunized with ovalbumin (OVA) emulsified with complete Freund's adjuvant (CFA), incomplete Freund's adjuvant (IFA), TiterMaxR (TM), aluminum hydroxide [Al(OH)3], or without any adjuvant. Three weeks after immunization, the rats were challenged with OVA by eye drops, and 24 hr later they were euthanized and their eyes, including the lids, blood, and lymph nodes were harvested for analysis of disease and immune responses. The results indicated that adjuvants were necessary to induce disease as well as both cellular and humoral immunity. Al(OH)3, CFA and TM induced stronger disease and cellular immunity than IFA. The intensity of disease correlated with that of cellular immunity. To further investigate the involvement of cellular immunity in EAC, lymph node cells collected from immunized rats were adoptively transferred into naive syngeneic recipients that were challenged 4 days later with OVA. EAC developed in the recipients of lymph node cells that were also stimulated in culture with OVA. These recipient rats developed cellular infiltration in the lid and conjunctiva, in a dose-dependent manner. These results suggest that cellular immunity played a major role in the development of EAC, both in the induction and effector phases.

Adjuvants, Immunologic↗

PubMed1996

Impaired specific cellular immunity to the varicella-zoster virus in patients with herpes zoster oticus.

The possible involvement of depression on cellular immunity in reactivation of varicella-zoster virus (VZV) in herpes zoster oticus was investigated. The subjects comprised 59 cases of herpes zoster oticus, 33 cases of herpes zoster sine herpete (ZSH) with facial paralysis, and 205 cases of Bell's palsy. The transformation rate of lymphocytes to phytohaemagglutinin in herpes zoster oticus tended to be lower than that in Bell's palsy. In skin tests with purified protein derivatives of tuberculin, the positivity rate in herpes zoster oticus was significantly lower than that in Bell's palsy (p < 0.015). In skin tests using VZV antigen the positivity rate in herpes zoster oticus and ZSH were significantly lower than that of Bell's palsy (p < 0.001 and p < 0.015, respectively). Thus, it was noted that cellular immunity, especially specific cellular immunity against VZV, was significantly depressed in herpes zoster oticus and ZSH. We consider that depression of specific cellular immunity plays an important role in triggering reactivation of VZV and onset of these diseases.

Adolescent↗

PubMed1997

Protective cellular immunity: cytotoxic T-lymphocyte responses against dominant and recessive epitopes of influenza virus nucleoprotein induced by DNA immunization.

DNA immunization offers a novel means to induce cellular immunity in a population with a heterogeneous genetic background. An immunorecessive cytotoxic T-lymphocyte (CTL) epitope in influenza virus nucleoprotein (NP), residues 218 to 226, was identified when mice were immunized with a plasmid DNA encoding a full-length mutant NP in which the anchor residues for the immunodominant NP147-155 epitope were altered. Mice immunized with wild-type or mutant NP DNA were protected from lethal cross-strain virus challenge, and the protection could be adoptively transferred by immune splenocytes, indicating the role of cell-mediated immunity in the protection. DNA immunization is capable of eliciting protective cellular immunity against both immunodominant and immunorecessive CTL epitopes in the hierarchy seen with virus infection.

Animals↗

PubMed1975

Cellular immunity in malnourished mice.

The effects of malnutrition on the cellular immune response were studied in mice. Cellular immunity, measured by contact sensitivity to 2,4-dinitrochlorobenzene, was found to be impaired in protein energy deficient animals.

Animals↗

PubMed1986

Cellular immunity to vaccinations and herpesvirus infections after bone marrow transplantation.

The cellular immune response to herpesviruses was studied in 46 recipients of marrow grafts (23 autologous, 23 allogeneic). That study was performed in vitro by evaluating the degree of lymphocyte proliferative responses to herpes simplex virus (HSV), cytomegalovirus (CMV), and varicella zoster virus (VZV). No primary infections with any of those viruses were noted after bone marrow transplantation (BMT). The incidence of active infection in seropositive patients was significantly lower after autologous BMT than after allogeneic BMT (HSV, 2/22 vs. 11/22 patients, respectively, P = 0.007; CMV, 4/12 vs. 9/10 patients, respectively, P = 0.02; VZV, 3/23 vs. 11/23 patients, respectively, P = 0.02). After autologous BMT, the restoration of cellular immunity to the three viruses occurred at a clearly faster rate than after allogeneic BMT. That pattern may have contributed to the low incidence of active infections with those viruses after autologous BMT. Recipients of allogeneic marrow from donors with a positive lymphocyte proliferation test to HSV had a significantly increased incidence of active HSV infection post-BMT (8/9 patients) than those who received marrow from donors with a negative test (3/13 patients; P = 0.008). Acute or chronic graft-versus-host disease (GVHD) decreased the cellular immune response to the three herpes viruses, but not significantly. Our program of vaccinations with diphtheria and tetanus toxoids started in the fourth month post BMT. Chronic GVHD patients who were vaccinated had a clearly impaired cellular immune response to both toxoids as compared with those without chronic GVHD.

Bone Marrow Transplantation↗

PubMed1972

Cellular immunity to nuclear antigens in systemic lupus erythematosus.

Cellular immune repsonses were determined by skin testing and mitogen- and antigen-induced blastic transformation of peripheral blood lymphocyte cultures in 24 patients with systemic lupus erythematosus (SLE) and 24 normal subjects. The incidence of positive skin tests with Candida albicans, PPD (tuberculin-purified protein derivative) intermediate strength, Trichophyton and histoplasmin was not significantly different in the two groups nor was lymphocyte stimulation by the mitogen phytohemagglutinin-M (PHA-M), implying that cellular immunity is normal in SLE. However, the SLE patients had a significantly increased incidence of positive skin tests and stimulated lymphocyte cultures to a number of nuclear antigens compared with normal subjects. No correlation could be made between the test results and the activity of the SLE at the time of study except for a significant association between lymphocyte culture stimulation by rabbit thymus native DNA and active SLE nephritis. Patients with a membranous antinuclear factor (ANF) pattern had positive skin tests with rabbit thymus native DNA and usually had active disease.

Adolescent↗

PubMed1982

[Evaluation of cellular immunity in drug addicts].

The cellular immunity was evaluated in 52 drug addicts, as well as in a non-addict group of 30 healthy soldiers. For this purpose, intradermal test with protein purified derivative, dinitrochlorobenzene, test of migration inhibitory factor with protein purified derivative and candidin antigens and cutaneous window were performed. Results were different: The results obtained indicated a depressed cellular response in the drug addicts.

Adolescent↗

PubMed1982

Pyoderma gangrenosum. Occurrence with altered cellular immunity and a circulating serum factor.

Aberrations of cellular immune functions in pyoderma gangrenosum (PG) may lead to nonspecific activation of inflammatory cells or to an imbalance of suppression leading to autoaggression (chronic ulceration). A patient with severe unremitting PG had anergy to a battery of seven skin test antigens. Mixed lymphocyte reactions, autologous mixed lymphocyte reactions, lymphocyte proliferative responses to antigens, and the production of leukocyte inhibitory factor were substantially suppressed, while the lymphocyte responses to mitogens were unaffected. Quantitative immunoglobulin and complement levels were normal. The inhibition of cellular immune functions was mediated by a factor in the patient's serum. This factor also inhibited lymphocyte functions of normal unrelated control subjects. Preliminary studies demonstrated that the factor is nondialyzable, heat stable, and not adsorbed by Staphylococcus A protein. Pulse therapy with large doses of corticosteroids resulted in dramatic clinical improvement.

Adult↗

PubMed1977

Transfer factor and cellular immune response in urinary tract infections in children.

Cellular immune responses in vivo and in vitro were studied in 20 children with chronic or relapsing urinary tract infections. Skin tests revealed decreased immune responses to PPD in cases with chronic or recurrent pyelonephritis and to OM, in these cases and in cases of lower urinary tract infections. Blast transformation responses to PPD, OM and PHA were at least as high as in controls. Administration of chromatographically purified fraction from human leucocyte transfer factor resulted in a positive skin reaction with antigen concentration, which before TF administration had caused a negative reaction. The results suggest that the action of the transfer factor component used in this study is based on an immunologically nonspecific stimulation of the cellular immune response.

Adolescent↗

PubMed1999

Emerging principles for T cell receptor recognition of antigen in cellular immunity.

The structural basis of antigen recognition in cellular immunity has been elucidated through the determination of crystal structures of major histocompatibility complex (MHC) molecules bound to antigenic peptides, T cell receptors (TCR), CD8 and CD4 co-receptors and, most recently, TCRs in complex with peptide-MHC (pMHC). The mechanisms that generate the diversity of the immune response to invading microorganisms were first realized at a genetic level and are necessary in order to cope with the enormous number of potential antigens. This diversity is manifested in the protein products of the genes which code for the components of the TCR signalling complex. The structure of the TCR reveals both striking similarities with and fundamental differences from its functional counterpart, the antibody, in the humoral immune system. The conserved manner in which the TCR recognizes and interacts with its peptide-MHC ligand allows the TCR great latitude in its potential to form productive interactions with antigen-presenting cells that bear numerous ligands to which the TCR has not been previously exposed. This phenomenon of cross-, or alloreactivity arises from a combination of conserved structural features across all MHC molecules, both self and foreign, and some degree of molecular mimicry. Non-classical MHC ligands presenting either modified or specialized peptides, lipids, carbohydrates, or no ligand at all, are now thought to play increasingly important roles in cellular immunity. We review some of the recent structural results and our current state of knowledge about TCR structure, and how this relates to its function.

Animals↗

PubMed1998

Aging and the immune response to tetanus toxoid: diminished frequency and level of cellular immune reactivity to antigenic stimulation.

The period of efficacious immune reactivity afforded by tetanus immunization and the need for continuing some forms of tetanus vaccination programs have been the subjects of recent debates. Our studies demonstrate that the level of antitetanus immunity based on immunological memory (i.e., cellular immune responsiveness) varies dramatically as a function of age, with older individuals constituting a population which is increasingly susceptible to tetanus infection.

Adolescent↗

PubMed2006

Prostaglandin E1 attenuates impairment of cellular immunity after cardiopulmonary bypass.

OBJECTIVE: It is well documented that cardiopulmonary bypass (CPB) severely impairs cellular immunity. The objective of this study was to investigate the effect of prostaglandin E1 (PGE1) on cellular immunity after CPB. METHODS: Patients who underwent elective cardiac surgery were randomly divided into the PGE1 group (n=12) and the control group (n=12). In the PGE1 group, PGE1 was administered at 20 ng/kg/min from just after the induction of anesthesia to the end of surgery. Peripheral blood mononuclear cells (PBMCs) were taken before anesthesia and on postoperative days 1, 3 and 7 (POD 1, POD 3 and POD 7). Proliferation responses of T cells to phytohemagglutinin (PHA) and pure protein derivative (PPD) antigen were measured as indicators of cellular immunity. RESULTS: PGE1 significantly attenuated the impairment of both PHA and PPD response after cardiac surgery on POD 1 (PHA response, 30 +/- 21% vs. 53 +/- 32%, control vs. PGE, p=0.048; PPD response, 18 +/- 21% vs. 39 +/- 27%, control vs. PGE, p=0.046). The reduced glutathione content of PBMCs in the control group was significantly decreased on POD 1. CONCLUSION: PGE1 attenuated the impairment of cellular immunity after cardiac surgery with CPB by reducing oxidative stress on PBMCs.

Aged↗

PubMed2002

Expression of tegument protein pp65 of human cytomegalovirus (CMV) and its application to the analysis of viral-specific cellular immunity in CMV-infected individuals.

Investigations into human cytomegalovirus (CMV)-specific cellular immunity are important to better understand and manage CMV infections. CMV phosphoprotein pp65 is thought to be a major antigen for CMV-specific cellular immunity. We newly synthesized protein pp65 with a baculovirus expression system and purified it via metal affinity chromatography in a soluble form. The recombinant protein pp65 was antigenic in an enzyme immuno-linked assay for pp65-specific IgG in sera from 196 children. Traditional lymphoproliferation assays have shown that pp65 protein promotes specific lymphoproliferation in CMV-seropositive donors. Using an intracellular cytokine detection system, we showed that this recombinant protein stimulated CD4-positive T cells to express interferon-gamma. The results of these assays using protein pp65 were comparable with the use of CMV whole antigen. pp65- and CMV-specific cellular immunity, and CMV DNA load were also compared in four recipients of unrelated cord blood transplantation. The delay in re-constitution in CMV-specific cellular immunity was associated with reactivation of CMV. These results indicated that the recombinant protein pp65 can be used to study specific immunity in CMV infections.

Adolescent↗

PubMed1975

Comparison of specificities of humoral and cellular immune response to haptens.

In this study we induced humoral and cellular immunity to three isomers of aminosulfanilic and aminobenzoic acids and compared their respective specificities. These studies were facilated by using a new method for preferentially inducing a cellular immune response to haptens: the haptens were covalently coupled to mycobacteria and injected into animals in incomplete Freund's adjuvant. Humoral antibody was induced by coupling the same isomers to bovine serum albumin and injecting them into animals in complete Freund's adjuvant. Both groups of animals were examined for hapten-specific cellular immunity (migration inhibition factor, delayed skin tests) and for antibody response (passive hemolysin test). The results show that although both cell-mediated and humoral responses can discriminate the para, meta and ortho isomeric forms of the haptens used, the antibody response demonstrated much less cross-reactivity. The relevance of this finding to different requirement for B and T cells in antigenic recognition is discussed.

Aminobenzoates↗

PubMed2006

Effect of astragalus injection on serious abdominal traumatic patients' cellular immunity.

OBJECTIVE: To explore the change of serious abdominal traumatic patients' cellular immunity and the effect of Astragalus Injection (AI) on it. METHODS: Sixty-three serious abdominal traumatic patients were randomly assigned into two groups, the conventional group and the treated group, patients in the conventional group were given conventional treatment, while others in the treated group were given conventional treatment as the basis, with AI 20 ml was added into 250 ml of 5% glucose solution given through intravenous dripping, and then on the first day and 14th day, their T cell activated antigens as well as that of 10 healthy subjects were monitored. RESULTS: On the first day, in the conventional group and treated group, the levels of CD(3)(+), CD(4)(+), CD(4)(+)/CD(8)(+), CD(16)(+), CD(69)(+) and CD(3)(+)/homologous leucocytic antigen-DR (HLA-DR(+)) were apparently lower than those in the healthy group (P < 0.05), while the CD(8)(+) was significantly higher than that in the healthy group (P < 0.05), and there was no significant difference between the conventional group and the treated group (P > 0.05); on the 14th days, the levels of CD(3)(+), CD(4)(+), CD(4)(+)/CD(8)(+), CD(16)(+), CD(69)(+) and CD(3)(+)/HLA-DR(+) of the treated group got closed to healthy subject value, and got even higher than those of conventional group (P < 0.05); CD(8)(+) got close to that of healthy subjects, while obviously lower than that of conventional group (P < 0.05). CONCLUSION: After serious abdominal trauma, cellular immunity lowered, auxiliary use of AI was beneficial to the restoration of cellular immunity.

Abdominal Injuries↗

PubMedDate not supplied

[Cellular immune response detected in blast transformation test with lymphocytes from rabbits immunized with nucleocapsid of herpes simplex type 2 virus].

A preparation of herpes simplex virus type 2 (HSV-2) nucleocapsid (NC) was obtained after treatment of intracellular virus with detergents followed by centrifugation in linear sucrose density gradient. Electron microscopic analysis revealed polymorphism of HSV-2 NC population. Three main types of capsid structures were found: empty capsids, NC containing various amounts of nucleoid material, and NC with complete nucleoid. Morphological heterogeneity correlated with heterogenous sedimentation profile of the total NC preparation of labeled virus represented by light, intermediate, and heavy structures. Specific blasttranformation tests with lymphocytes from rabbits immunized with HSV-2 NC demonstrated differences in the primary and secondary cellular immune responses. The secondary cellular immune response was characterized by a more rapid and strong increase in BTT values than the primary immune response.

Animals↗

PubMedDate not supplied

Changes of the cellular immunity tests during the evolution of Hodgkin's disease.

To detect the changes of cellular immunity which occur at the same time as the pathological process and to find out the possible biologic indicators with prognostic value, a study was carried out on 140 patients with Hodgkin's disease (HD) in different clinical periods: onset, under therapy (cytostatics and/or irradiations), remission, after splenectomy and under immunotherapy. The study of cellular immunity included the determination of lymphocytes subpopulations by the rosette tests and their functional estimation by tests of blastic transformation to mitogens and antigens. Though the values obtained presented a wide dispersion, the rosette tests showed variations in correlation with the clinical stage, therefore with the severity of disease. It was observed that therapy and splenectomy change the cellular immunity tests. The only test with a certain prognostic value was found to be the in vitro lymphocyte response to PPD which became positive after therapy, particularly in the group of patients who showed good response to treatment. A dynamic follow-up of the cellular immunity tests might give an indication on the mechanisms of production of the immune deficit in HD.

Hodgkin Disease↗

PubMed2002

HIV-1 protein Vpr suppresses IL-12 production from human monocytes by enhancing glucocorticoid action: potential implications of Vpr coactivator activity for the innate and cellular immunity deficits observed in HIV-1 infection.

The HIV-1 protein Vpr has glucocorticoid receptor coactivator activity, potently increasing the sensitivity of glucocorticoid target tissues to cortisol. Patients with AIDS and normal cortisol secretion have manifestations compatible with glucocorticoid hypersensitivity of the immune system, such as suppression of innate and cellular immunities. The latter can be explained by glucocorticoid-induced inhibition of cytokine networks regulating innate and Th1-driven cellular immunity. We demonstrated that extracellularly administered Vpr protein dose-dependently potentiated glucocorticoid-induced suppression of both mRNA expression and secretion of IL-12 subunit p35 and IL-12 holo-protein, but not IL-12 subunit p40 or IL-10, by human monocytes/macrophages stimulated with LPS or heat-killed, formalin-fixed Staphylococcus aureus (Cowan strain 1). This effect was inhibited by the glucocorticoid receptor antagonist RU 486. Also, Vpr changed the expression of an additional five glucocorticoid-responsive genes in the same direction as dexamethasone and was active in potentiating the trans-activation, but not the trans-repression, properties of the glucocorticoid receptor on nuclear factor kappaB- or activating protein 1-regulated simple promoters. Thus, extracellular Vpr enhances the suppressive actions of the ligand-activated glucocorticoid receptor on IL-12 secretion by human monocytes/macrophages. Through this effect, Vpr may contribute to the suppression of innate and cellular immunities of HIV-1-infected individuals and AIDS patients.

Base Sequence↗