Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Immunity, Cellular”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 55 records · Page 3Linked to original sources
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↗
PubMed2006

[Diabetes mellitus and cellular immunity].

Interaction between diabetes mellitus and cellular immunity is reviewed in several aspects. Importance of cellular immunity in the development of type 1 diabetes mellitus is discussed. Experimental mice models of this disease are presented which after the evaluation of similarities of immunologic parameters provide clues to potential mechanisms of the pathogenesis of type 1 diabetes mellitus. In an animal model of spontaneous type 1 diabetes mellitus, the non-obese diabetic mouse develops a spontaneous T cell-mediated insulitis, which is followed by overt diabetes. Disease can be transferred to young non-obese diabetic mice with diabetogenic T cells from older, affected animals. T cells can recognize various islet antigens, including insulin and islet cell enzyme called glutamic acid decarboxylase. Induction of T cell tolerance to these antigens retards the onset of diabetes in mice. Transgenic mouse models of type 1 diabetes mellitus confirm above-mentioned facts. Later alterations of cellular immunity are under the investigation. Disorders of mobilization and chemotaxis, phagocytosis and adherence of polymorphonuclear leukocytes, monocyte function, defects of acquired cellular immunity are thoroughly discussed. Diabetes mellitus, particularly poorly controlled diabetes, impairs different functions and links of cellular immunity. Infections, which are found relatively more frequently in diabetic patients and against which primarily cellular immunity protects, are also reviewed.

Animals↗
PubMed1995

Principle of the bark of Phellodendron amurense to suppress the cellular immune response: effect of phellodendrine on cellular and humoral immune responses.

Previously we have isolated the quaternary base alkaloids, magnoflorine and phellodendrine, from Phellodendri Cortex (cortex of Phellodendron amurense Rupr., Rutaceae) as the biologically active principles to suppress local graft-versus-host (GvH) reactions in mice. In this paper, we focus on phellodendrine. Phellodendrine suppressed local semisyngeneic GvH reactions and systemic allogeneic GvH reactions in X-ray irradiated recipient mice. Phellodendrine also suppressed the induction phase of sheep red blood cell (SRBC)-induced delayed type hypersensitivity in mice and tuberculin-induced delayed type hypersensitivity in guinea pigs, but did not suppress the effector phase of these reactions. Surprisingly, phellodendrine, unlike prednisolone and cyclophosphamide, did not affect antibody production in mice to SRBC. Phellodendrine was expected to be a valuable new type of immunosuppressor against the cellular immune response.

Animals↗
PubMed1981

[Controlled study of unspecific cellular immunity in cancer patients].

Cellular immunity has been studied in 92 patients with solid tumors undergoing surgery, in order to evaluate immunocompetence at the time of diagnosis and to assess the prognostic value of parameters of cellular immunity. The results show that total lymphocyte counts, T-lymphocyte counts and lymphocyte blastogenic responses are moderately depressed at diagnosis in the cancer patients as compared to age matched controls. These parameters of cell mediated immunity "in vitro" seem to be of limited prognostic value, since no correlation was found with the clinical course during the first 6 postoperative months. Depression of delayed hypersensitivity response to cutaneous antigens appeared to be an index of poor prognosis.

Adult↗
PubMed2003

Measurement of cellular immunity in human coccidioidomycosis.

Measurement of cellular immune response in human coccidioidomycosis, a disease of the Western Hemisphere caused by the soil-dwelling fungus Coccidioides, began more than 75 years ago. Numerous studies have shown that measurement of coccidioidal cellular immunity is a useful epidemiologic and clinical tool. The first widely used coccidioidal skin-test reagent, coccidioidin, was derived from a filtrate of cultured mycelia of Coccidioides by Smith and colleagues in the 1940's. It remained the standard until the 1970's, when spherulin, obtained from the spherule form of the fungus, was found to be more sensitive. Both reagents are specific indicators of coccidioidal cellular immunity. Since then, other coccidioidal antigens have been identified and in vitro tests of cellular immunity have been shown to yield comparable results to skin testing. In vitro assays have also begun to open a window on the specific immunologic events of coccidioidal cellular immunity. Persistent expression of coccidioidal cellular immune response appears to augur an improved clinical outcome. Despite this, a study of a coccidioidal vaccine failed to demonstrate efficacy. Current and future studies are focused on modulating the coccidioidal immune response in vitro and in vivo and on developing an improved vaccine.

Coccidioides↗
PubMed2005

Cellular immune responses against hepatitis C virus.

Cellular immune responses are typically important in recovery from acute infections, and studies of acute hepatitis C confirm that broadly directed CD4+ and CD8+ T cell responses are associated with spontaneous clearance of infection. However, a major unanswered question is what role the cellular immune response plays in progression of liver disease during chronic infection. Classic models of hepatitis C suggest that cellular immune responses promote liver injury, either by causing direct cytolysis of infected cells or by promoting inflammation. However, clinical evidence suggests that persons with cellular immune dysfunction, such as that due to with human immunodeficiency virus (HIV) infection, have more-rapid disease progression. Recent data suggest that cellular immune responses do serve to limit the progression of liver disease, even if they are ineffective at clearance of virus. There is limited information on the effect of HIV coinfection on the cellular immune response to hepatitis C virus, but further study of this issue might shed light on the pathogenesis of liver disease in both immunocompromised and nonimmunocompromised hosts.

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↗
PubMed2005

A non-living nasal influenza vaccine can induce major humoral and cellular immune responses in humans without the need for adjuvants.

Twenty-eight healthy adult volunteers were immunized intranasally with an inactivated whole-virus influenza vaccine based on the strain A/New Caledonia/20/99 (H1N1), either in saline or mixed with formaldehyde-inactivated Bordetella pertussis as a mucosal adjuvant, or in a thixotropic vehicle with mucoadhesive properties. After four doses, all groups of vaccinees developed significant IgG- and IgA-antibody responses, measured by ELISA, in respectively serum and nasal secretions. None of the volunteers had demonstrable hemagglutination inhibition (HAI) antibodies in serum before being immunized, whereas more than 80% of them reached HAI titers>or=40, considered protective, after immunizations. In addition, cellular immune responses, measured as significant increases in CD4+ T-cell proliferation and granzyme B-producing cytotoxic T-cells, were detected against the vaccine strain as well as against heterologous virus strains (H3N2). However, no additive effect on these responses could be demonstrated with use of B. pertussis or the thixotropic substance in the present vaccines. It appeared, actually, that the mucoadhesive vehicle containing the thixotropic substance was less efficient than were the two other formulations. An influenza vaccine made as a simple particulate formulation of inactivated virus, and given repeatedly onto the nasal mucosa, may thus be an attractive alternative to currently available vaccines.

Adjuvants, Immunologic↗
PubMed1982

Cellular immunity in burns.

Evaluation of cellular immunity in burns was undertaken using the following parameters: T-cell count; blastoid transformation and macrophage migration inhibition factor index (MIF). Their influence upon bactericidal index was also measured as T-cell count per mm3 and in percentage was found to be depressed in parallel, probably due to some cellular immune in parallel, probably due to some cellular immune functions active at the burned site. Blastoid transformation and MIF index were found to be depressed in parallel especially in major burns, i.e. above 25 per cent. These parameters had a significant influence upon the bactericidal index thus enhancing its activity to a considerable extent when values of the former were approaching near normal limits.

Burns↗
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↗
PubMed1996

Prenatal endocrine activation alters postnatal cellular immunity in infant monkeys.

Cellular immune responses were evaluated in 35 infant rhesus monkeys generated from two types of pregnancy conditions. Pregnant females were administered either saline or adrenocorticotropic hormone (ACTH) for 2 weeks between Days 120 and 133 postconception, approximately 1 month before parturition. After birth, lymphocytes obtained from infants in the ACTH condition failed to respond as readily to allogeneic cells in mixed lymphocyte cultures, proliferated less to Con A, exhibited lower suppressor function following stimulation with Con A, and showed lower cytolytic activity against target cells. For some measures, the prenatal effect was observed more consistently in male infants. Differences were evident with these in vitro immune assays through 6 months of age, indicating that acute disturbance during the prenatal period can have lingering effects on postnatal immunity.

Adrenocorticotropic Hormone↗
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↗