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Results for “Immunity, Cellular”

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PubMed1975

Cellular immunity in cancer: comparison of delayed hypersensitivity skin tests in three common cancers.

Cellular immunity was studied in three homogenous groups of patients with cancer to determine whether the pattern of depression of immune competence varied between solid tumours with different patterns of clinical behaviour. Delayed hypersensitivity skin responses were measured in patients with carcinoma of the breast, stomach, and colon and matched controls. Response to 2,4-dinitrochlorobenzene (DNCB) was used as an indication of primary responses and the Mantoux reaction as an index of recall responses. Responses were diminished in all three cancer groups, but there were significant differences between each type of cancer and even between different control groups. Cellular immunity was lost earliest and to the greatest extent in patients with colonic cancers and tended to be retained until a late stage in breast cancer, with gastric cancer occupying an intermediate position. Thus, while there was some degree of correlation between depressed immunity and prognosis our results gave no evidence that general host immune competence could explain the worse prognosis of gastric than colonic cancer. Paradoxical findings in patients with breast cancer suggested a great complexity in the host tumour interaction. Assessments of immune competence in cancer patients must be related to specific types of neoplasms with appropriate control groups if the results are to be meaningful.

Antibodies, Neoplasm↗

PubMed1977

[State of humoral and cellular immunity in experimental amyloidosis].

On a model of caseine amyloidosis in 52 rabbits it was shown that in the preamyloid phase the humoral immunity was stimulated, but as soon as the first deposits of amyloid appeared, it was inhibited. The cellular immunity was inhibited starting from the 20th day of the experiment. On the 40th day of the experiment the cellular immunity was found to be less inhibited in the animals with initial deposits of amyloid as compared with the animals with no amyloidosis; on the 60--80th day in progressing of amyloidosis differences in the degree of inhibition of the cellular immunity were obliterated. The degree of fixation of IgG in amyloid was directly dependent on its content in the blood serum and on the "age" of amyloid.

Amyloidosis↗

PubMed1997

Humoral and cellular immune reactivity to recombinant M. leprae antigens in HLA-typed leprosy patients and healthy controls.

In our search for Mycobacterium leprae antigens that might specifically induce immunity or immunopathology, we have tested both humoral and cellular immune reactivity against purified recombinant M. leprae antigens in 29 paucibacillary (PB), 26 multibacillary (MB) leprosy patients, and 47 matched healthy contacts. The following M. leprae antigens were tested: 2L-1 (65L-1, GroEl-1), 2L-2 (65L-2, GroEl-2), 4L (SoDA), 43L, 10L (B) and 25L (Sra). The individuals were also typed for HLAD-RB1 and DQB1 in order to see whether leprosy status and/or immune reactivity to these antigens might be associated with certain HLA types. We also tested sera from another 48 patients before, during and after multidrug therapy (MDT) to study the relationship between antibody reactivity to recombinant M. leprae antigens and MDT. Antibody titers to the four recombinant M. leprae antigens tested and to D-BSA were higher in MB patients compared to PB patients and healthy controls, and declined with treatment. From a diagnostic or monitoring point of view none of the recombinant antigens seemed to be an improvement over D-BSA, mainly due to the lower sensitivity. IgG subclasses were measured in positive sera of untreated patients. These were mainly of the IgG1 and IgG3 subclasses, but subclass diversity was also observed and antigen dependent: all four subclasses could be detected against 10L (B), only IgG1 and IgG3 against 43L and only IgG1 against 25L and 2L-1. Cellular immune reactivity against the purified recombinant M. leprae antigens was measured in a lymphocyte stimulation test (LST). As for M. leprae, there was an inverse correlation between antibody and T-cell reactivity. However, the number of LST responders to recombinant antigens was much lower than to M. leprae. The 43L antigen was recognized most often (19%-24% of individuals tested) and more often than the 10L (B) antigen (10%-12%). No clear correlation was observed with leprosy type or protection and, in general, M. leprae nonresponders were also negative with recombinant antigens. Finally, we confirmed that HLA-DRB1*02 is associated with leprosy in this population, and we observed an association between DQB1*0601 and lepromatous leprosy. The number of positive individuals was too small to allow a meaningful analysis of the relationship between HLA type and immune reactivity. Although these data do not allow a conclusion as to one of these purified recombinant antigens being either protection or disease related, the antigen-dependent IgG subclass diversity warrants further study on antigen-specific qualitative differences in immune reactivity that may be relevant for the outcome of an infection with M. leprae.

Antibody Formation↗

PubMed1987

Delayed effects of low-dose radiation on cellular immunity in atomic bomb survivors residing in the United States.

Several parameters of cellular immune function were assessed among persons who survived the 1945 atomic bombs in Hiroshima and Nagasaki but who now reside in the United States. The subjects in this study were exposed to various low doses (T65D) of radiation at the time of the bomb. More than half received an estimated 0 Gy (S0 group). Of those exposed to more radiation (S+ group), nearly 90% received less than 0.50 Gy (50 rad). Lymphocytes were isolated from the peripheral blood of these individuals and were assessed for the following parameters of cellular immunity: mitogenic response to phytohemagglutinin, mitogenic response to allogeneic lymphocytes, natural cell-mediated cytotoxicity (NCMC), and interferon production. In every case, the response of the S+ group was greater than that of the S0 group, although only the difference for NCMC was statistically significant. Results of studies presently being performed on A-bomb survivors residing in Hiroshima do not confirm this difference. Therefore, it is difficult to say whether the increase in natural cytotoxicity observed among the American and not the Japanese A-bomb survivors exposed to very low doses of radiation is a hormetic effect which was modulated by post-radiation environmental conditions or a result of selective migration.

Cytotoxicity, Immunologic↗

PubMed1975

Use of transfer factor in patients with depressed cellular immunity and chronic infection.

Two patients with chronic mucocutaneous candidiasis and a defect in cellular immunity received a single injection of dialysable transfer factor from Candida-positive donors in an effort to reconstitute immunologic function. The transfer of cellular hypersensitivity was successful in one of the two patients and was monitored by skin tests and MIF production; however, the effect was temporary and did not change the clinical course of the patient's infection. The other patient did not respond eitherimmunologically or clinically to transfer factor at this time, although she did respond subsequently to repeated doses of transfer factor and amphotericin B therapy (Pabst and Swanson: Brit. med. J. 2:442, 1972). In another instance transfer factor from tuberculin-positive donors was used successfully to eradicate an infection in a patient with progressive primary tuberculosis and an acquired defect in cellular immunity. The patient had not responded clinically or bacteriologically after 7 1/2 months of antituberculous therapy, although the organism was shown to be sensitive in vitro to the drugs she was receiving. She received 6 doses of dialysable transfer factor over a 3-month period and during this time she responded clinically, bacteriologically and roentgenographically.

Adult↗

PubMed2004

Intraspecies variability in the dose-response relationship for Salmonella Enteritidis associated with genetic differences in cellular immune response.

To evaluate the effects of differences in host cellular immunity, we studied the dose-response relationship for infection with Salmonella enterica serovar Enteritidis (SE) in two different rat strains, skewed towards T helper 1 (Th1, Lewis rats) or T helper 2 (Th2, Brown Norway rats) immunoregulation. Rats were exposed orally to different doses of SE after overnight starvation and neutralization of gastric acid. Animals were observed for clinical signs of disease, fecal excretion and SE load in spleen and cecum, histopathology of the cecum, hematology, and cellular and humoral immune responses. Exponential dose-response models were used for binary or continuous outcomes to analyze the experimental data. Cytokine patterns, antibody isotypes, and contact hypersensitivity tests confirmed that Lewis rats are Th1 prone, whereas Brown Norway rats are Th2 prone. The probability of infection per single SE cell was approximately 100 times higher in Brown Norway rats than in Lewis rats. Cellular immune responses were more pronounced in Lewis rats but antibody responses were higher in Brown Norway rats. When infected, colonization levels and inflammation are highest in the intestinal tract of Th2 skewed rats, but systemic infection is more intense in Th1 skewed rats. Successful colonization by only one or two SE clones resulted in a marked increase of neutrophil counts by a factor of two to three in both rat strains.

Administration, Oral↗

PubMed2006

Hepatocyte lesions and cellular immune response in yellow fever infection.

The study of the in-situ cellular immune response is very important for the understanding of different liver infections. In the present study, 53 liver samples obtained by viscerotomy from patients who died during the course of jungle yellow fever were analyzed. The diagnosis was confirmed by serology, viral isolation and virus-specific immunohistochemistry. The specimens were analyzed by immunohistochemistry using specific antibodies for apoptosis, CD45RO, CD4, CD8, CD20, S100, CD57 and CD68. Quantitative analysis of the labeling pattern showed a clear predominance of the different phenotypes in the portal tract and midzone region of the acini. There was a predominance of T CD4+ lymphocytes, accompanied by the presence of T CD8+ lymphocytes, natural killer cells (CD57), macrophages and antigen-presenting cells (S100). The disproportion between the intensity of inflammation and the degree of hepatic injury was probably due to the intense apoptotic component, which classically does not induce an inflammatory response. The present study demonstrates that, despite the disproportion between injury and inflammation, the cellular immune response plays an important role in the pathogenesis of the hepatocytic injury observed in yellow fever, probably as a result of cytolytic actions through mechanisms involving MHC II and the activation of Fas receptors and granzymes/perforins.

Analysis of Variance↗

PubMed1989

Intracerebroventricular infusion of interleukin 1 rapidly decreases peripheral cellular immune responses.

Low doses (50-200 pg or 3.1-12.4 fmol) of interleukin 1 (IL-1) infused into the brain of rats produced rapid suppression of various cellular immune responses in peripheral lymphocytes of rats. Fifteen minutes after infusion of purified IL-1 beta into the lateral ventricle, natural killer cell activity, response to phytohemagglutinin stimulation, and interleukin 2 production were markedly suppressed in lymphocytes isolated from blood and spleen. These effects were due to infusion of IL-1 into brain since they did not occur when IL-1 was infused into the cisterna magna (essentially posterior to brain) or was injected intraperitoneally. Effects of IL-1 in brain could be blocked by simultaneous infusion of alpha-melanocyte-stimulating hormone, which is known to block the biological actions of IL-1. To stimulate release of endogenous IL-1 in brain, lipopolysaccharide was infused; this produced similar effects as IL-1, and these effects also were blocked by alpha-melanocyte-stimulating hormone. At longer intervals after infusion of IL-1 and lipopolysaccharide (3, 6, and 24 hr), immune responses returned to baseline or remained suppressed; i.e., "rebound" immunopotentiation did not occur. Finally, IL-1 infusion suppressed cellular immune responses in adrenalectomized animals, thereby showing that the effects of central IL-1 on peripheral cellular immune responses were, at least in part, independent of the stimulatory effect of IL-1 on secretion of adrenal hormones. These results indicate a link from brain to peripheral immune responses by means of action of a cytokine acting in the brain.

Animals↗

PubMed2005

[The prognostic value of cellular immunity function in patients with hepatocellular carcinoma].

OBJECTIVES: To study the changes of cellular immunity function in patients with hepatocellular carcinoma (HCC) and its correlation with disease severity. METHODS: T lymphocyte subsets and CD28 co-stimulation molecule in CD8+ T cells in 22 HCC patients were detected using three-color flow cytometry. Serum interleukin-2 (IL-2), transforming growth factor beta 1 (TGFbeta1), and interleukin-6 (IL-6) were determined by ELISA and radioimmunoassay. A group of 30 patients with chronic hepatitis B (CHB), liver cirrhosis (LC), or normal adults (NC) served as controls. RESULTS: Compared with NC, the number of CD8+CD28- T cells increased and CD8+CD28+ T cells decreased in patients with HCC. The number of CD4+ T cells, CD4+/CD8+ ratios, IL-2 level all decreased and CD8+ T cells, IL-6, TGFbeta1 levels all increased in patients with HCC, LC and CHB. The CD4+ T cells, CD4+/CD8+ ratios and IL-2 level in patients with HCC were lower than those with CHB. Serum IL-6 and TGFbeta1 in patients with HCC were higher than those with LC and CHB. The levels of IL-6 and TGFbeta1 correlated with the stages of the tumors. CONCLUSIONS: HCC patients have a cellular immunity dysfunction. Rectifying the imbalanced function could be a potential way for treating HCC. Measurement of these factors would be useful for early diagnosis and evaluating the prognoses of these patients.

Adult↗

PubMed1971

In vitro detection of cytotoxic cellular immunity against tumor-specific antigens by a radioisotopic technique.

[(3)H]Thymidine-labeled tumor cells are used to evaluate the cytotoxic cellular immune response against tumor-specific antigens; the loss of label due to destruction and detachment of target cells from the surface of the culture vessel is measured. Spleen cells from mice immunized against Moloney virus-induced rhabdomyosarcoma specifically destroyed the sarcoma cells, while cells from normal syngeneic mice did not. Peripheral blood lymphocytes from patients with malignant tumors were specifically cytotoxic to autologous tumor cells and to allogeneic tumor cells histopathologically identical to the autologous tumor, but not to autologous nonmalignant fibroblasts, or to allogeneic tumor cells from a histologically dissimilar tumor. Serum from the same patients specifically protected autologous tumor cells from lymphocyte cytotoxicity. This serum-mediated protection of tumor cells against autologous cellular immunocytotoxicity also extended to histologically identical allogeneic tumor cells. Cross-reactivity of anti-tumor cellular immunocytotoxicity in vitro, and its "blocking" by autologous serum, strongly suggest the presence of common tumor antigens. The antagonism demonstrated in vitro between serum and cellular immunity may explain the continued growth of malignant tumors in the face of demonstrable cellular immunity.

Adenocarcinoma↗

PubMed1999

Analysis of cellular immune response in pigs recovered from porcine respiratory and reproductive syndrome infection.

The cellular immune response to a European isolate of porcine reproductive and respiratory syndrome (PRRS) virus in animals recovered from the experimental infection has been studied in vitro. Peripheral blood mononuclear cells (PBMC) from these pigs proliferated specifically when they were stimulated with PRRS virus. This response was not detectable until 4 weeks after inoculation and remained for more than 3 months. Addition of blocking monoclonal antibodies to the cultures showed that this proliferation was mainly dependent on CD4(+) cells with the participation of SLA-class II molecules. T-cell cultures established by stimulating responding cells with PRRS virus and maintained in culture for up to 3 weeks showed an increase of CD8(+) CD4(+) and CD4(-) CD8(+) subsets within activated cells, gated according to their light scatter parameters, whereas CD4(+) CD8(-) cells declined along the time in culture. Within the activated cells, those expressing the TcR gammadelta receptor also increased, being most of them also positive for the CD8 marker. By RT-PCR, T-cells responding to the virus showed a Th1 type cytokine production pattern. During the culture period the cytotoxic activity against K-562 cells increased from 15 to 35% of specific lysis. This cellular immune response may play a relevant role in the clearance of PRRS virus and the recovery of the infection.

Animals↗

PubMed2004

Adoptive transfer of natural antibodies to non-immunized chickens affects subsequent antigen-specific humoral and cellular immune responses.

To determine a regulatory function of natural antibodies in the immune response of chickens, pooled plasma obtained from non-immunized (naïve) 15 months old hens was subjected to keyhole limpet hemocyanin (KLH) antigen-affinity chromatography. Purified KLH-binding antibodies were adoptively transferred intravenously to 5 weeks-old cocks that were subsequently immunized subcutaneously 24 h later with KLH. Control groups consisted of birds that were either adoptively transferred with KLH-binding antibodies purified from plasma of KLH-immunized chickens, or PBS, or a salt precipitated total immunoglobulin fraction obtained from the corresponding pooled nai;ve chicken plasma, respectively.Total, IgM and IgY antibody titers to KLH in the plasma of recipients adoptively transferred with KLH-NAb, but not in the plasma of the groups transferred with salt precipitate or KLH-binding specific antibodies, were significantly enhanced as compared to the non-treated, KLH immunized group. Titers of IgA antibodies binding KLH were decreased in the plasma of the group that received specific KLH-binding antibodies, but not in the plasma of the other groups. Proliferation from peripheral blood leucocytes in whole blood from the KLH-NAb treated group, the group treated with KLH-binding specific antibodies and the group treated with salt precipitate, respectively, to both concanavalin A and KLH were significantly decreased as compared to the group receiving PBS. Our data show that antigen-specific antibodies can be isolated from plasma obtained from non-immunized chickens. Such antibodies that resemble natural antibodies as described in mammals may perform an important role in the enhancement of subsequent antigen-specific antibody responses or the maturation of the immune system, which may differ from the role of specific antibodies.

Animals↗

PubMed1984

In vitro studies on the cell-mediated immune response to human brain tumors. II. Leukocyte-induced coats of glycosaminoglycan increase the resistance of glioma cells to cellular immune attack.

We have examined the ability of cultured human glioma cells to elicit allogeneic cytolytic lymphocyte responses in vitro in order to delineate properties of glioma cells that may contribute to their ability to escape cellular immune attack. When glioma cells were cultured together with allogeneic peripheral blood mononuclear cells (PBMC) in mixed lymphocyte-tumor cultures (MLTC), it was observed that cells from eight of 12 glioma lines were surrounded by clear pericellular "halos," which appeared to impede contact between PBMC and the glioma cells. Enzymatic, histochemical, and immunochemical studies indicated that these halos represented glycosaminoglycan (GAG) coats that contained hyaluronic acid (HA) as a major constituent. Electron microscopic studies demonstrated the presence of many thin microvillous processes spanning the width of the halos. The presence of GAG coats around glioma cells in MLTC reduced the generation of cytolytic T lymphocytes specific for antigens on the glioma cells. Likewise, these cell coats decreased the lysis of glioma cells by cytolytic lymphocytes, once generated. The production of thick coats of GAG by glioma cells was induced by interaction of glioma cells with a nondialyzable factor produced by PBMC in culture. This factor did not cause glioma cells to release increased amounts of HA into the medium, but rather increased the production of HA that remained associated with the glioma cell surface. The formation of thick, protective GAG coats by glioma cells as a result of their interaction with the PBMC-derived factor constitutes a nonspecific suppressor mechanism that may contribute to the ability of this class of human solid tumors to evade cellular immune attack.

Brain Neoplasms↗

PubMed1998

Activation and suppression of natural cellular immune functions by Pneumocystis carinii.

The regulatory role of soluble cytokines in innate cellular immune responses induced by Pneumocystis carinii was assessed in vitro in direct comparison to induction by Listeria monocytogenes. This report shows that P. carinii organisms, as well as L. monocytogenes, stimulated in whole spleen cell cultures of SCID mice the release of IFN-gamma, TNF-alpha/beta, IL-10, IL-12, and iNO. This response was independent of functional T cells. Both macrophages (M phi) and natural killer (NK) cells were necessary for either microorganism to induce release of these cytokines. Cocultures of purified M phi--including alveolar M phi--and purified NK cells indicated that no other cell population was necessarily involved. Microbial induction of NK cell-derived IFN-gamma has been reported to be mediated by the combined effects of TNF-alpha and IL-12 released by M phi upon adequate microbial stimulation. Interestingly, only L. monocytogenes, but not P. carinii organisms could directly induce detectable amounts of TNF-alpha/beta, IL-12, or iNO in purified M phi cultures. In dose-response experiments, release of IFN-gamma, TNF-alpha/beta, and iNO was reduced at high relative concentrations of either microorganism. This high-dose suppression was at least partially controlled by M phi-produced IL-10. Our data show that, P. carinii potently induces activating and inhibitory innate cellular immune response mechanisms and indicate that the initial step of macrophage-mediated NK cell activation might also involve other pathways than those described to date.

Animals↗

PubMed2006

Dopamine affects cellular immune functions during polymicrobial sepsis.

OBJECTIVE: To determine whether infusion of dopamine modulates cellular immune functions and survival during systemic inflammation. DESIGN AND SETTING: Randomized animal study, university research laboratory, Level I trauma center. SUBJECTS: Male NMRI mice. INTERVENTIONS: Mice were subjected to laparotomy (sham intervention, LAP) or polymicrobial sepsis induced by cecal ligation and puncture (CLP). Mice in each of these conditions received either an intraperitoneal infusion of 0.9% saline (CLP/saline; LAP/saline) or an intraperitoneal infusion of dopamine (1.0 microg/kg/min i.p., CLP/DOP; LAP/DOP). Metabolic data and survival were monitored 24 h and 48 h after onset of sepsis, and animals were terminated 48 h after induction of sepsis to determine splenocyte apoptosis (Annexin V binding capacity), splenocyte proliferation (3H-Thymidine incorporation assay), splenocyte IL-2, IL-6 and IFN-gamma release (ELISA) and leukocyte distribution (WBC; CD3, CD4, CD8, B220, F4/80, NK1.1). MEASUREMENTS AND RESULTS: Infusion of dopamine in septic mice increased splenocyte apoptosis and decreased splenocyte proliferation and IL-2 release of septic mice. Furthermore, an inhibitory effect of dopamine infusion on splenocyte proliferation and the release of the TH1-cytokines IL-2 and IFN-gamma was observed in sham operated control mice. These effects were paralleled by a decreased survival of dopamine-treated septic animals (47% vs. 67%). Treatment with DOP did not affect sepsis-induced changes of leukocyte distribution. CONCLUSIONS: We conclude that dopamine is capable of modulating cellular immune functions in a murine model of sepsis.

Animals↗

PubMed1981

Dissociation between humoral and cellular immune responses to lens antigens.

Rabbits immunized against lens extracts from various other (xenogeneic) species reacted well with the immunizing lens extracts by immunological assays measuring either humoral or cellular immune responses. A dissociation was observed, however, between the humoral and cellular immune responses when lenses from rabbit (allogeneic) or from nonimmunizing species were tested. Antibodies from these rabbits cross-reacted with lenses from rabbit or all other tested species, with levels similar to those obtained with the immunizing lens extracts. The antibodies were determined by both serological tests and the Arthus skin reaction. On the other hand, these rabbits failed to cross-react with rabbit or nonimmunizing animal lens extracts by the cell-mediated delayed skin reaction, and their lymphocytes reacted poorly in culture with the nonimmunizing lenses. A similar dissociation between the humoral and cellular responses was found in rabbits immunized against allogeneic lens. Most of these rabbits produced moderate levels of lens antibodies demonstrated by the serological tests and the Arthus skin reaction but failed to exhibit delayed-type hypersensitivity, and their lymphocyte cultures reacted poorly or not at all to the rabbit or other lenses. The results are discussed in view of their relevance to the hypotheses concerning the pathogenesis of phacogenic uveitis.

Animals↗

PubMed1990

Effect of acute or daily cocaine administration on cellular immune response and virus infection in mice.

The effects of in vivo cocaine administrations on cellular cytotoxicity were studied. Cocaine induced a dose-related immunosuppression of natural killer cell activity, with maximal depression at 1-5 mg/kg. In addition, the degree of inhibition following a single intraperitoneal (i.p.) or intravenous cocaine dose (acute treatment, 1 mg/kg) was similar to that after repeated administration (subchronic treatment: 1 mg/kg/day i.p. for 7 consecutive days or subcutaneous administration by Alzet 2001 osmotic minipumps). T cells from cocaine-treated mice failed to generate cytotoxic T lymphocytes (CTL) in mixed lymphocyte cultures and acute or subchronic cocaine treatment also inhibited CTL generation in vivo. On the other hand, acute administration induced a very rapid (24-hour) inhibition of natural cytotoxicity, with a return to normal within 72 h after treatment. By contrast, repeated doses led to more protracted immunologic consequences and a delayed recovery (144 h). The effect of cocaine on susceptibility to influenza virus (PR8) infection was also investigated. Both acute and subchronic treatment significantly decreased resistance to PR8 infection. The results clearly indicate that cocaine has a potent suppressive effect on cellular immunity and that abuse can adversely affect the outcome of infectious diseases.

Animals↗

PubMed2004

Developmental immunology and vaccines: cellular immune development and future vaccine strategies.

This section deals with how new knowledge of the development of cellular immunity in the neonatal period informs vaccine development and reviews the immune responses of the most vulnerable group of newborns, those born prematurely, to vaccines. It describes how the development of future vaccine strategies relies on a detailed understanding of immune ontogeny and the potential consequences of intervention on developing cellular immune responses.

Dendritic Cells↗