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At least 73 records · Page 4Linked to original sources
PubMed1991

Enkephalin-induced stimulation of humoral and cellular immune reactions in aged rats.

Twenty-month-old Wistar rats received intraperitoneal injections of the opioid pentapeptide, methionine-enkephalin (Met-Enk) in periods before and after immunization with cellular and soluble antigens. Animals were treated with 0.2 mg of Met-Enk/kg b.w., a dose previously found to increase immune capacity in young adult rats. Saline-treated 20-month-old, and Met-Enk-treated rats and saline-treated 8-week-old controls were set up for each experimental group. Immune performance was evaluated by plaque-forming cell response, antibody production and various immunoinflammatory reactions. At autopsy, thymus and spleen were weighed and processed for histological examination. The results showed that 0.2 mg dose of Met-Enk produced significant enhancement of both humoral and cellular immune responses in senescent rats. Methionine-enkephalin treatment also induced a significant increase in thymus and spleen weights in these animals. Analysis of the cellular make up of these organs revealed the enlargement of cortical and medullary areas, and pronounced pyroninophilia in the subcortical zone of the thymus and thymus-dependent areas of the spleen. The results suggest that Met-Enk exerts an immunorestorative activity in aged animals, and that changes in the opioid system may play an important role in the maintenance of immune functions during senescence.

Aging↗
PubMed1995

Role of the low zinc bioavailability on cellular immune effectiveness in cystic fibrosis.

An altered cellular immune response as a secondary phenomenon has been suggested to be probably involved in the bronchopulmonary infections by Pseudomonas aeruginosa in cystic fibrosis (CF). The difficulty to eradicate with modern anti-pseudomonal antibiotics the bronchopulmonary infections has led us to further investigate the possible existence of other cellular immune defects and their cause. Alterations in zinc turnover are present in CF. Zinc is relevant for good immune functioning. In particular, zinc is required to confer biological activity to thymulin (ZnFTS), a biochemically defined thymic hormone with a modulating action on cell-mediated immunity. The zinc-unbound form (FTS) is inactive and it can be unmasked by in vitro zinc addition to the plasma samples revealing the total amount of circulating thymulin (active + inactive). Marginal zinc deficiencies may prevent peripheral biological activation of active thymulin. Total zinc-saturable thymulin fractions in CF are similar to those observed in normal subjects, whereas the active quota is strongly reduced associated with concomitant high plasma levels of inactive thymulin compared to the values of healthy children (P < 0.01). A strict correlation exists between zinc and thymic hormone-saturable fraction (r = 0.87, P < 0.01) in CF. These findings suggest that the defect is not due to a thymic failure but to a reduced peripheral saturation of thymulin by zinc ions. This defect might depend on augmented plasma concentration of alpha 2-macroglobulin, which has a higher binding affinity for zinc than thymulin. T cell subsets are normal in CF. Reduced NK cell number and activity are present. Also, plasma IL-2 levels are reduced. The existence of positive correlations between zinc and IL-2 (r = 0.79, P < 0.01) and between zinc or active thymulin and NK activity (r = 0.70, P < 0.01 and r = 0.88, P < 0.01, respectively) suggest a close link among zinc failure, impaired IL-2 activity, low thymulin level, and reduced NK activity in CF patients with both normal and growth retardation. Although the role of NK cells is unknown in CF, a zinc supplementation, in order to induce a complete saturation of thymulin molecules, to correct some cellular immune defects and to improve the growth, may be suggested.

Adolescent↗
PubMed1985

[Heterogenous immune reactivity in brain tumors: results of cellular immunity in relation to brain tissue antigens].

In brain tumors and other neurological diseases cell-mediated immune reactions to fetal brain tissue antigens (FBA), normal tissue antigen of adult brain (NTA) and tumor-associated antigens of different brain tumors (TAA) have been analysed. The detection of sensitized lymphocytes using the MEM-(macrophage-electrophoretic-mobility-) test revealed general tumor-related results applying the FBA, in some extent a cross reactivity and partly no kind of reaction. A phase-specific reactivity to normal brain antigens could not be found, only cases of multiple sclerosis produced restrictive results employing the NTA. By testing tumor-associated brain antigens different reaction types were seen: The common TAA caused a tumor-characteristic reaction; the histo-specific TAA predominantly presented a organotypic form of reaction, confined a histo-specific reaction pattern; in some cases there were found inadequate, non-corresponding reactions as well as unreactivity. With regard to different types of reaction the problems of heterogeneity of the brain tumors and the cellular immune response--i.e. a heterogeneity of 1. or 2. order--were discussed including further factors concerning several special conditions in the nervous system.

Antigens, Neoplasm↗
PubMed1978

Humoral and cellular immunity against allogeneic antigens in patients with acute leukaemia.

The humoral and cellular immunity of 12 patients with acute leukaemia (6 AML and 6 ALL) was investigated using several techniques. The study of the humoral response included the screening for allogeneic and autologous lymphocytotoxins, for cytotoxic antibodies against leukaemic blasts, Daudi cells and B lymphocytes and the detection of immune complexes. The cellular immunity was investigated by stimulation of remission lymphocytes by autologous blast cells or allogeneic lymphocytes in mixed cell cultures. Most patients have retained their humoral and cellular immune responsiveness against allogeneic antigens while there seems to be no significant response against leukaemia-associated antigens.

Acute Disease↗
PubMed1989

[Effects of anticonvulsants on cellular immunity].

The effects of anticonvulsants on cellular immunity were examined in murine models. Fresh splenocytes were obtained from mice which had been intraperitoneally given 1 mg of phenytoin, 2 mg of phenobarbital, or 20mg of valproate for 28 days. The serum concentration of phenytoin, phenobarbital and valproate in these animals were 10-20 micrograms/ml, 30-40 micrograms/ml and 50-70 micrograms/ml, respectively. The proliferative response of splenocytes to mitogens was assessed by 3H-thymidine incorporation. The cytotoxic activities of cells such as natural killer (NK) cells, cytotoxic T lymphocytes (CTL), and lymphokine-activated killer (LAK) cells were estimated by a 4 hr-51Cr release assay. Phenytoin suppressed lymphocyte proliferation, NK activity, and CTL activity, but never LAK activity. Phenobarbital suppressed proliferative response to rIL-2 and CTL activity, but did not suppress NK activity nor LAK activity. In turn sodium pyruvate never suppressed any activity on cellular immunity.

Animals↗
PubMed1992

Cellular immune response to the antigen administered as an immune complex in vivo.

Recently, it was shown that 10(2)- to 10(3)-fold lower doses of human serum albumin (HSA) are sufficient for the same T-cell response in vitro, if HSA is administered to the cultures bound in the immune complex rather than in the soluble form. In the present study, we analysed the capacity of HSA in the form of immune complexes to elicit specific cellular immune response in vivo. We found that antigen bound in the immune complex with murine, syngeneic polyclonal antibodies elicited the same T-cell response as fivefold higher doses of free antigen. On the other hand, HSA bound in the immune complexes with xenogeneic, rabbit polyclonal antibodies did not enhance anti-HSA cellular immune response. Our results indicate that binding of antigen in the immune complex could play an important role in enhancing an antigen-specific cellular immune response in vivo.

Animals↗
PubMed1972

Experimental allergic encephalitis. Dissociation of cellular immunity to brain protein and disease production.

The encephalitogenic determinant of brain protein, a nonapeptide having the amino acid sequence Phe-Ser-Trp-Gly-Ala-Glu-Gly-Gln-Lys, has been characterized and synthesized. In a previous study, analogues of this encephalitogenic peptide were synthesized and some were shown to be encephalitogenic while others were not. Guinea pigs were immunized with encephalitogenic peptides having amino acid sequences different from that in the native protein. These guinea pigs did not show cellular immunity in vivo (skin reactivity) or in vitro (lymphocyte stimulation or macrophage migration inhibition) to the encephalitogenic brain protein (EP) although they did show cellular immunity to the immunizing antigenic peptide. Guinea pigs immunized with an encephalitogenic peptide having the same amino acid sequence as the brain protein, or with a nonencephalitogenic peptide having the same amino acid sequence as the native protein but lacking the terminal lysine, did develop cellular immunity to the EP. Animals immunized with EP showed cellular immunity to this protein, but not to the encephalitogenic peptides. Animals immunized with nonencephalitogenic protein (NEP), prepared by altering the tryptophan residue of EP, did not develop disease but did show cellular immunity in vitro and in vivo to the EP. Animals protected from disease by immunization with NEP similarly showed cellular immunity to EP. Thus, the results suggest a dissociation between cellular immunity to EP and the production of experimental allergic encephalitis (EAE). Animals immunized with the encephalitogenic peptides develop EAE, but do not show cellular immunity to EP, and animals immunized with NEP show cellular immunity to EP but do not develop EAE. A fresh approach to the examination of the pathogenesis of EAE is now possible through the use of these well-characterized antigens.

Amino Acid Sequence↗
PubMed1995

Effect of prolonged use of inhaled steroids on the cellular immunity of children with asthma.

BACKGROUND: Systemic corticosteroids may affect the cellular immunity, but there is no available controlled data on such effects associated with a prolonged use of inhaled corticosteroids. OBJECTIVE: The investigation was designed to study the effect of long-term inhaled beclomethasone dipropionate in daily doses of up to 600 micrograms on cellular immune functions. METHODS: Twenty-four children with asthma treated with inhaled beclomethasone dipropionate for a mean of 22.6 months were compared with 16 children with asthma not treated with an inhaled steroid and with 20 healthy adults. Cellular immune parameters included differential white blood count, T- and B-cell numbers, T helper and suppressor counts, T-cell mitogenic transformation, and interleukin-1 and interleukin-2 secretion. RESULTS: There was no difference in any of the studied cellular immune functions among the three study groups. CONCLUSION: Long-term use of inhaled beclomethasone dipropionate by children with asthma, at daily doses of up to 600 micrograms, has no effect on certain parameters of cellular immunity.

Administration, Inhalation↗
PubMed1997

Inhibitory effects of chronic ethanol consumption on cellular immune responses to hepatitis C virus core protein are reversed by genetic immunizations augmented with cytokine-expressing plasmids.

Chronic hepatitis C viral (HCV) infection is a major clinical problem in alcoholics with liver disease and may result from ethanol effects on the host immune response. To experimentally assess such effects, the DNA-based immunization approach was used to produce humoral and cellular immune responses against the HCV core protein in mice. Mice were fed an ethanol or isocaloric pair-fed control liquid diet followed by immunizations with HCV core DNA-expressing constructs. Chronic ethanol feeding was found to inhibit Th cell and CTL activities and substantially reduced cytokine secretion as well. In addition, a switch from Th1 to Th0 subtype was observed in proliferating CD4+ T cells derived from chronic ethanol-fed mice. These immunosuppressive effects were directly due to ethanol since crossover experiments to an isocaloric control diet restored the defects in cellular immunity. Furthermore, we determined if coadministration of an IL-2 or GM-CSF DNA expression plasmid with a plasmid expressing the HCV core protein (pHCV2-2) would reverse the inhibitory effects of chronic ethanol feeding on cellular immune responses. Coimmunization of chronic ethanol-fed mice with either IL-2 or GM-CSF expression plasmids restored cellular immunity and induced CD4+ inflammatory T cell and CD8+ CTL responses comparable with control mice immunized with pHCV2-2 alone. These studies provide evidence of how chronic ethanol feeding may effect cellular immune responses to a viral structural protein in the context of genetic immunization.

Adjuvants, Immunologic↗
PubMed1987

[Cellular immunity using skin tests in children with malignant diseases at the time of diagnosis and after therapy].

Patients with cancer often have disturbances of cellular immunity. Changes of cellular immunity are frequently associated with tumor progression or an increased risk of a relapse. Cellular immunity is studied with an in vivo test system using 7 different recall antigens. We studied the cutaneous reaction of 80 children with various malignant diseases at time of diagnosis, at the end of the chemotherapy or prior to a relapse of the disease using the multitest Merieux. Before starting treatment patients with systemic diseases showed only a little response to the recall antigens. Patients with solid tumors had normal responses. No prognostic meaning of the multitest results were seen, if it was done before starting the treatment. At time of a relapse, these patients mostly had negative skin reactions using the multitest. It has to be studied if these results show a new systemic disease or if they are expression of an ongoing disturbance of cellular immunity of these patients.

Antigens, Neoplasm↗
PubMed1975

Humoral and cellular immunity in asthma.

Parameters of humoral and cellular immunity have been measured in 91 asthmatic patients. Mean serum levels of IgG and IgE were raised. IgG levels were higher in those with a family history of asthma. IgE levels were higher in those with a past history of atopic eczema, but intrinsic and extrinsic asthma could not be differentiated on the basis of IgE levels. Thirteen of 74 patients failed to respond to tetanus immunization, while only 1 failed to respond to Salmonella typhi H antigen. Tetanus nonresponders had a raised mean serum IgA level, reduced spontaneous lymphocyte tritiated thymidine uptake, and reduced thymidine uptake in fetal calf serum. Eight of 87 patients failed to mount delayed hypersensitivity reactions to a battery of five intradermal antigens. The tritiated thymidine uptake of lymphocytes stimulated with phytohemagglutinin was normal in autologous serum, but reduced in fetal calf serum. The data support the hypothesis that asthma may be associated with immunodeficiency states.

Adolescent↗
PubMedDate not supplied

Longitudinal studies of cellular immunity of patients with osteogenic sarcoma during chemoimmunotherapy.

The cellular immune reactivity of 24 patients with osteogenic sarcoma was studied longitudinally during surgical treatment and subsequent adjuvant chemoimmunotherapy. Cellular immune function was studied using in vitro assays of lymphocyte reactivity to mitogens and nonspecific allogenic antigens. Circulating cells were characterized by the total lymphocyte and wbc counts, determination of E-rosetting populations, and percent of polymorphonuclear leukocytes. Both fresh and cryopreserved lymphocytes were utilized and compared. The preoperative values from these studies offered no useful indication of those patients likely to have disease recurrence. Likewise, longitudinal studies during the course of adjuvant treatment did not predict relapse before other routine clinical studies could identify it. There was no difference in the studied lymphocyte functions and hematologic tests between the group receiving BCG immunotherapy and those not receiving BCG. Our studies indicate that current measures of cellular immune function are of little value in the monitoring of patients with osteogenic sarcoma.

Antineoplastic Agents↗
PubMedDate not supplied

Immunologic study of carcinoma of the digestive tract. Effects of the tumor stage. I. Cellular immunity in the preoperative period.

We studied the behavior of the cellular immune system in two types of carcinoma of frequent clinical occurrence: large bowel and gastric cancers. We contrasted both types of neoplasia with respect to the behavior of cellular immunity in the preoperative period, according to the evolutive stage of the tumor. Two hundred and nine subjects were studied: 86 with gastric adenocarcinoma, 63 with adenocarcinoma of colon-rectum and 60 healthy controls. Total lymphocytes were quantitated, as were B and T cell subpopulations, and T cell function by measuring the response to PHA. Summarizing the results, a clear depression in cellular immunity was observed in stage III of gastric cancer. In large bowel cancer the repression of cellular immunity is of lesser magnitude than in gastric cancer.

Adenocarcinoma↗
PubMed1974

Relationship of antimicrobial cellular immunity to delayed hypersensitivity in Listeriosis.

The relationship of antimicrobial cellular immunity to delayed hypersensitivity (DH) was studied in mice antigenically stimulated by living Listeria monocytogenes confined to diffusion chambers in peritoneal cavities or by subcutaneous inoculation of sublethal doses of the organism. Mice showed DH reactions when tested 6 days after inoculation, and reactions were positive for at least 90 days in some mice. DH also became established when the mice were stimulated by antigens diffusing from peritoneal chambers containing viable Listeria. Mice were categorized as DH positive or DH negative if they developed more or less than a 5% increase in foot volume 24 h after the injection of Listeria antigen. Some antigenically stimulated mice did not elicit the DH reaction. Consequently, the animals were arranged as immunized groups (DH positive and DH negative) and Listeria chamber implant groups (DH positive and DH negative). When challenged with L. monocytogenes, all four groups were significantly resistant as compared with controls. Thus, the in vivo tests for immunity and DH did not show direct correlation. The results suggested that antimicrobial cellular immunity can occur as a phenomenon independent of DH. Evidence for antimicrobial cellular immunity as the principle mechanism of resistance in murine listeriosis is discussed with consideration for possible heterogeneity of function by thymus-derived lymphocytes.

Animals↗
PubMed1981

Effects of Corynebacterium parvum on cellular immunity of cancer patients, assayed sequentially over 63 days.

The immunologic effects of Corynebacterium parvum (2 mg/M2) infused at three-week intervals were determined by 19 sequential assays in each of nine patients with metastatic malignancy. Peripheral blood immunologic profiles were followed for 63 days. No statistical significant changes (P greater than 0.05) occurred in total white cell, lymphocyte, or monocyte counts. Subpopulation assays demonstrated significant increases in E rosetting cells but not in sIg-bearing cells; there was a corresponding significant decrease in null-cell proportions. Killer cell lymphocytotoxicity was measured by 51Cr release from Chang target cells. Significant increases were observed one week after immunization and were maintained on subsequent immunizations. NK- and K-cell cytotoxicity were particularly augmented; T-cell cytotoxicity expressed as lytic units/ml was significantly increased on fewer assay occasions. Killer cell function has a possible in vivo antitumor role and methods of boosting and maintaining the activity deserve consideration. A three-week immunization schedule with C. parvum is supported by the current work and is the basis of a randomized adjuvant immunotherapy study of patients with malignant melanoma.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1975

Cellular immune reactivity in vitro and tumor rejection provided by tumor-associated antigens of friend-virus-induced leukemia.

Cell-mediated immunity (CMI) and tumor rejection were studied in the Friend virus leukemia system of C57Bl/6 mice. Mice were immunized with Friend leukemia virus (FLV) or X-irradiated FBL-3 leukemic cells and studied temporally for the development of CMI reactivity by assays of 51Cr release lymphocyte cytotoxicity, lymphocyte transformation, migration inhibition, Winn tumor cell neutralization and transplantation rejection. High levels of specific lymphocyte cytotoxicity were observed by day 7 f0llowing FLV infection; this reactivity reached a peak between 17 and 21 days, and returned to background levels by day 36. Further, positive Winn assays were obtained with spleen cells from mice immunized with FLV at times when the mice resisted live FBL-3 tumor challenge. Positive lymphocyte transformation was obtained with spleen cells from mice immunized with FLV or FBL-3, but not with cells from normal mice or mice immune to a syngeneic methycholanthrene-induced tumor, when cultured with papain-soluble FBL-3 or RBL-5 tumor-cell extracts or mitomycin-C (MMC)-treated FBL-3 or RBL-5 cells. Positive reactivity in the lymphocyte transformation assay occurred after reactivity had peaked in the lymphocyte cytotoxicity test. Similar positive macrophage migration inhibition patterns were also obtained with peritoneal exudate cells (PEC) from FLV-immunized mice using papain-solubilized tumor-associated antigen (TAA) from FBL-3 cells. These data suggest that sequential development and modulation of CMI reactivity occurs as observed in different assays following immunization in this system.

Animals↗
PubMed1977

Detection of cellular immunity to tumor-associated antigen(s) in mice by the macrophage spreading inhibition test.

Soluble preparations of antigens from a methylcholanthrene-induced fibrosarcoma of C57BI mice were prepared by homogenization of tumor tissue and high-speed centrifugation of the homogenate. These preparations were able to sensitize syngeneic mice to tumor-associated antigens (TAA) of the fibrosarcoma, and to provoke a delayed hypersensitivity reaction when injected into the footpad of sensitized mice. Furthermore, the same soluble preparations could inhibit in vitro the spreading of peritoneal macrophages from mice sensitized to TAA. A similar inhibition of macrophage spreading was obtained when peritoneal cells from C57BI mice, bearing transplants of the fibrosarcoma, were incubated with the preparations. We conclude that the macrophage spreading inhibition test, like other in vitro assays, can detect cell-mediated immunity to tumor-associated antigens.

Animals↗