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Results for “Immunity, Cellular”

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At least 343 records · Page 19Linked to original sources

PubMed1988

Experimental Mycoplasma pulmonis infection of rats suppresses humoral but not cellular immune response.

Humoral antibody response to sheep red blood cells and cellular immune response to bovine serum albumin were studied in Mycoplasma pulmonis infected, adult, male Sprague-Dawley rats. The hemagglutinating antibody response to sheep red blood cells was evaluated at 0, 3, 5, 7, 14, 21 and 28 days postinfection. Antibody titers during all days postinfection were depressed significantly (p less than 0.05) in infected rats as compared to noninfected controls. Cellular immune responses were evaluated by a delayed hypersensitivity response. Rats were sensitized at 0, 3, 5, 7, 14, 21 or 28 days postinfection with bovine serum albumin and challenged with heat aggregated bovine serum albumin 7 days later. Cell-mediated immune responses in infected rats were not significantly different at any point from controls. These results indicate that M. pulmonis infection in rats suppresses the humoral antibody response to sheep red blood cells, but not the cellular immune response to bovine serum albumin.

Animals↗

PubMed1999

[Opioid receptor mediated modulation of intrahippocampal enkephalin induced cellular immune function].

In the present work, the effect of intrahippocampal microinjection of opioid receptor antagonist naloxone on the enhancement of cellular immune responses induced by enkephalin was studied in rat. The results showed that (1) the proliferation activity of splenic lymphocytes stimulated by Con A and natural killer (NK) cell activity were decreased with microinjection of 1 microl lipopolysaccharide (LPS,50 ng/microl) into bilateral hippocampus; (2) the decrease of cellular immune responses induced by LPS could be inhibited by a preceding intrahippocampal injection of 1 microl met-enkephalin (10 microg/1 microl); (3) the enhancement of cellular immune responses induced by met-enkephalin could be blocked by an opioid receptor antagonist naloxon (10 microg/microl); and (4) cellular immune responses were also inhibited when naloxon was injected intrahippocampally alone. The above results suggest that the enhancement of cellular immune responses induced by enkephalin was mediated by opioid receptors in hippocampus.

Animals↗

PubMed1977

Clonal priming of human lymphocytes: Specificity and cross-reactivity of cellular immune reactions.

Clonal priming in response to chemical and microbial antigens which defines the specificity of cellular immune reactions, was demonstrated by culture techniques. Human leucocyte cultures stimulated with specific antigens typically show peak levels of D.N.A. synthesis after 5 to 7 days in culture. Such primary leucocyte cultures were incubated for 10-20 days, then the cells were gently centrifuged and resuspended in fresh RPMI 1640 with 20% plasma. These secondary or primed cultures typically showed less than 1000 c.p.m. after 48 hours. However, if the original antigenic stimulant was added, specific accelerated responses were seen by 48 hours in the secondary cultures. Lymphocyte clones in these sceondary cultures primed with dinitrophenylated (D.N.P.) antigens (from subjects sensitised to dinitrochlorobenzene) showed enhanced D.N.A. sythesis in response to the same dinitrophenylated antigens and showed varible accelerated responses to related chemically modified antigens. However, D.N.P.-activated clones in these secondary cultures did not show enhanced responses to microbial antigens even though the lymphocytes had been highly responsive to tetanus toxoid and other microbial antigens in primary cultures. The specificity of this clonal activation was further demonstrated by the enhanced response of secondary cultures of tetanus-toxoid-activated clones to tetanus toxoid but not to dinitrophenylated antigens. The abiltty to detect specificity and cross-reactivity of cellular immune reaction has broad implications for investigations of cellular immunity as well as many potential applications in the diagnosis and understanding the patogenesis of inflammatory and neoplastic diseases in which cellular immune discrimination may be involved.

Antibody Formation↗

PubMed2004

[Cellular immunity in patients with urogenital chlamydiosis].

Abnormalities in the cellular immunity chain (CIC) were found in 63.04% of patients with urogenital chlamydiosis (UGC) within a study of cellular immunity in patients with the above pathology. According to the study results, the below listed were the main CIC impairments: a lack or reaction to the inducer of T-helpers (CD3+ and CD4+), and to activated T-lymphocytes (CD3+ and CD25+); higher counts of cytotoxic T-lymphocytes (CD3+ and CD8+), a higher content of B-lymphocytes (CD3+ and CD19+, and lower counts of NK-cells (CD3- and CD56+). However, research of the lymphocyte subpopulation alone is not enough to evaluate adequately the immune system of a patient. In order to choose an adequate scheme for the treatment of UGH patients it is necessary to undertake a study of the immune status that should comprise, apart CIC investigations, the following: humoral immunity, phagocyte function, factors of non-specific body resistance and cytokine status.

Adult↗

PubMedDate not supplied

[The basic indices of cellular immunity in surgery for rheumatic heart defects].

Distinct changes of basic indicators of cellular immunity were diagnosed in 157 patients with rheumatic heart disease which needed surgical correction. A classification of disturbances of cellular immunity is proposed. A definite correlation between the degree of cellular immunity disturbances and basic clinical parameters of the rheumatic heart disease was followed as well as the influence of the immunological changes on the prognosis of operation results and the outcome of the disease.

Adult↗

PubMed1986

[Cellular immunity in dialysis patients using the lymphocyte transformation test (LTT) in comparison to conservatively treated patients with chronic terminal renal failure].

By means of the lymphocyte transformation test (LTT), using the mitogens phytohemagglutinin (PHA), concanavalin A (ConA), lipopolysaccharide (LPS) E. coli and the antigens tuberculin (PPD) and O-streptolysin, a contribution should be made for the judgment of the functional capacity of the immune system--in particular of the cellular immunity--in uraemia patients with and without dialysis therapy. In 33 patients with different duration of the dialysis (0.5 to 130 months) and 15 retention patients who were not yet treated by means of dialysis the LTT was controlled with stimulant agents mentioned above. In these cases was shown that dialysis patients managed metabolically regularly did not show a significant restriction of the cellular immunity in the LTT (PHA-stimulation over 0.55 transformed cells, con-A-stimulation over 0.37 transformed cells). The not dialysed patients with chronic uraemia showed a distinct diminution of the unspecific T-cell transformation by PHA and ConA, whereas the antigen-induced stimulation (PPD, O-streptolysin) was not disturbed in this case as well. In the two cases the B-cell transformation (on LPS) was not significantly disturbed. There was a good concordance with the clinical findings: scarcely general infects, no shunt infections, relatively many organ losses by rejection after transplantation in the dialysis patients. The not yet dialysed retention patients revealed clinically a higher inclination to an infect. There were no own experiences about the course after transplantation without preceding dialysis. It is discussed in how far also immunological investigations may play a role in the establishment of the optimum management of the dialysis, the moment of the beginning with the dialysis and for the "more individual preparation of the transplantation".

Antigens↗

PubMed1987

Prospective study of cellular immunity to hepatitis-B-virus antigens from the early incubation phase of acute hepatitis B.

Cellular immunity to hepatitis-B-virus (HBV) antigens was followed prospectively in five patients who were identified in the early incubation phase of acute HBV infection, between 30 and 70 days before the onset of liver damage. Cellular immunity to pre-S antigens was the first detectable immune response, appearing 30 days before the first rise in serum aminotransferases in every case. T-cell sensitisation to HBcAg followed, with IgM anti-HBc appearing 10 days later. A cellular immune response to HBsAg was the last to appear, 10 days before the onset of liver damage. These cellular immune responses are the earliest host responses to the virus infection and could be critical in initiating and directing the processes of liver damage and viral clearance.

Acute Disease↗

PubMed1984

Lymphoid interstitial pneumonia associated with depressed cellular immunity and polyclonal gammopathy.

This report describes a case of lymphoid interstitial pneumonia (LIP) associated with polyclonal gammopathy and selective depression of cellular immunity. Enhanced humoral immunity is suggested because the patient exhibited increased levels of circulating immunoglobulin (chiefly IgG) and a positive test reaction for rheumatoid factor. When first examined, the patient displayed depressed cellular immunity in that the results of his skin test were negative to dinitrochlorobenzene and phytohemagglutinin (PHA), his peripheral lymphocytes responded suboptimally to PHA, and he had decreased numbers of circulating T cells. When examined 6 yr later, the patient was again hypergammaglobulinemic, but he had regained some of his cellular immune function. Eight years after the patient was initially seen, he showed further improvement in cellular immune function. Analysis of bronchoalveolar lavage cells showed that the patient had a normal proportion of OKT4+ (inducer/helper) cells, but a reduced number of OKT8+ (suppressor/cytotoxic) cells. Thus, his improvement may have been associated with a correction of an imbalance of immunoregulatory T cells. Furthermore, because the disease was active on initial examination but less active after the second evaluation, malfunction of his cellular immune functions may have been involved in the pathogenesis of LIP.

Humans↗

PubMed2001

Deactivation of the innate cellular immune response following endotoxic and surgical injury.

The innate cellular immune (iCMI) system provides for the rapid production of interferon-gamma (IFN gamma) by NK cells in response to microbial threats. In this review, we examine the cellular and cytokine mechanisms of innate cellular immunity as determined in murine endotoxemia. This will be contrasted to the subsequent suppression of these same responses present in the mouse model of endotoxin tolerance, which is characterized by profound deficiency in both IL-12 and IFN gamma synthesis. Transient IFN gamma deficiency due to altered iCMI function has also been described in trauma or burn patients and is termed "clinical immune paralysis." If the common pathogenesis of these entities can be better understood, immune-based interventions might be identified for restoring iCMI function. In addition to the gain in basic immunologic insight, research on this subject may deliver future forms of prophylaxis against infection that do not rely on antibiotics and that will not promote antimicrobial resistance.

Animals↗

PubMed1998

Cellular immune response of Mastomys and gerbils in experimental filariasis.

OBJECTIVE: To determine mitogenic and antigen-specific cellular immune responses of two species of rodents, viz. Meriones unguiculatus and Mastomys coucha to assess the usefulness of the A. viteae/Mastomys model for cellular immune studies in experimental filariasis. METHODS: Lymphocyte blast transformation test (LTT) using spleen cells of normal and A. viteae infected animals. RESULTS: The proliferative response of gerbils was much higher than that of Mastomys to both ConA and filarial antigens. Cells of both species of rodents did not respond to microfilarial (mf) antigen, however, their mitogenic response differed during infection. Some degree of nonspecific suppression was observed in gerbils during prepatent and patent stages of infection, while Mastomys revealed highest proliferation during patent microfilaraemia. Mastomys cells did not respond to adult or mf antigen, while adult-specific proliferation was detected in the case of gerbils. CONCLUSION: The A. viteae/gerbil model shows more similarity to human filarial infection regarding cellular immune response. Markedly low responsiveness of a high percentage of Mastomys and wide variations in the cellular response to nonspecific mitogen limit the usefulness of Mastomys coucha in immunological studies, especially cellular immunity.

Animals↗

PubMed1991

Protracted mononucleosis-like illness associated with acquired cytomegalovirus infection in a previously healthy child: transient cellular immune defects and chronic hepatopathy.

Ordinarily, severe disease due to acquired cytomegalovirus (CMV) infection does not occur in immunocompetent children. We describe a previously healthy boy who acquired primary CMV infection at approximately 2 years of age and experienced a 2-year-long debilitating multisystem illness from which he ultimately recovered. Clinical features of this illness included fatigue, poor weight gain, pallor, unexplained fever, musculoskeletal complaints, drenching night sweats, lymphadenopathy, and massive hepatosplenomegaly. Laboratory abnormalities included elevated erythrocyte sedimentation rate, lymphocytosis, and elevated immune complex levels. Cellular immune function was impaired during the illness but was demonstrably normal during convalescence, and there was no other evidence for a known immunodeficiency state. Immunoblot analysis showed enhanced antibody response to a 66-kd infected cell protein after symptomatic recovery. Despite consistently normal indices of hepatic function, liver enlargement persisted after other symptoms had resolved. Liver biopsy demonstrated a mononuclear cell portal tract infiltrate with fibrosis, but CMV could not be demonstrated directly in this tissue. Primary CMV infection has not been reported previously to cause the persistent symptoms seen in this child.

Biopsy↗

PubMed1975

Cellular immunity in neoplasia. Antigen and mitogen responses in patients with bronchiogenic carcinoma.

Cellular immune responses of patients with histologically confirmed lung carcinoma were assessed in vivo using cutaneous response and in vitro with a microlymphocyte blastogenic transformation (LBT) assay. In addition, correlation of the cutaneous response with the migration inhibitory factor (MIF) assay and LBT response was examined. The results indicated that cutaneous responses seen in patients with cancer of the lung were consistently lower than similar responses in normal controls (p less than 0.001). Similarily, the percentage of positive cutaneous responses seen with patients included in this study was lower than the frequencies reported by others. Stimulation of cells from lung cancer patients by PHA-M was also depressed when compared to similar lymphocytic responses in normal volunteers (p less than 0.001). The correlation between cutaneous response to tuberculin and the in vitro assays was high. The few instances of disparity demonstrate the need to utilize more than one assay in evaluating cellular immune functions. These data would support the work of others that indicate a depression of cellular immunity in advanced malignancy.

Antigens, Neoplasm↗

PubMed1983

Effects of acute nitrogen dioxide exposure on cellular immunity after lung immunization.

The effects of acute NO2 exposure on antigen-specific cell-mediated lung immunity in Fischer 344 rats were evaluated. Animals were exposed for 24 hr to either room air or 5, 10, or 26 ppm NO2 before intratracheal immunization with 10(8) sheep red blood cells (SRBC). Cellular immunity was evaluated by antigen-specific lymphocyte stimulation assays of pooled lymphoid cell suspensions from either the thoracic lymph nodes or spleens. Elevated cellular immunity was observed after exposure to NO2. The ability of the 26 ppm NO2 exposure to increase cellular immunity seemed to parallel, and in some cases even exceed, that seen in control animals immunized with SRBC mixed with 2 X 10(7) heat-killed Bacillus Calmette-Guerin. These results support the theory that lung damage, and/or alterations of regulatory populations of immune cells, induced by agents such as NO2 can be responsible for the production of abnormally elevated immune responses to antigens deposited in the damaged lung.

Animals↗

PubMed1990

Suppression of cellular immunity in obstructive jaundice is caused by endotoxins: a study with germ-free rats.

The increased susceptibility to infections after surgery in jaundiced patients is considered to be caused by an impairment of cellular immunity and/or nutritional status. Endotoxins are suggested to play a role in the pathogenesis. However, the mechanism of action is unknown. Germ-free rats were used to study the effect of biliary obstruction in a model with negligible amounts of endotoxin. Cellular immunity, production of tumor necrosis factor (as a mediator of endotoxin toxicity) by peritoneal macrophages, and the nutritional status were assessed. Significant suppression of cellular immunity was found in conventional rats with obstructive jaundice. In contrast, cellular immunity was not suppressed in jaundiced germ-free rats. Large amounts of tumor necrosis factor were spontaneously secreted by peritoneal macrophages of jaundiced conventional rats, whereas macrophages from jaundiced germ-free rats did not. Moreover macrophage activation (expressed in tumor necrosis factor production) was significantly related to suppression of cellular immunity. Weight changes and depression of albumin levels were not different in germ-free and conventional rats after bile duct ligation. The data presented indicate that suppression of cellular immunity in obstructive jaundice is caused by endotoxins, whereas the impaired nutritional status seems to not be affected by the presence of endotoxins.

Animals↗

PubMed2006

[Preliminary study on determination of specific cellular immunity of patients with hepatitis B].

BACKGROUND: To evaluate an enzyme linked immunospot (ELISPOT) method for testing the specific cellular immunity of patients with hepatitis B and preliminarily investigate into the difference of cellular immunity in patients with various types of hepatitis B. METHODS: The patients with acute hepatitis B, chronic hepatitis B liver cirrhosis, healthy persons with HBV vaccine immunization, healthy persons with past HBV infection and HBV naive persons were enrolled in this study. Their peripheral blood mononuclear cells were tested by ELISPOT to determine the number of gamma-interferon secreting cells. RESULTS: The number of gamma-interferon secreting cells was significantly different between the patients with acute hepatitis B and those with chronic hepatitis B, and between the patients with acute hepatitis B and those with liver cirrhosis (P=0.0209 and P=0.0211). CONCLUSION: The specific cellular immunity in the patients with hepatitis B could be evaluated by determining the number of gamma-interferon secreting cells with the method of testing their peripheral blood mononuclear cells by ELISPOT. The specific cellular immunity was stronger in the patients with acute hepatitis B than in those with chronic hepatitis B and liver cirrhosis.

Enzyme-Linked Immunosorbent Assay↗

PubMed1989

Humoral and cellular immune responses to lens protein in patients with congenital cataract.

In order to understand the immune responses to lens protein in patients with congenital cataract, the passive hemagglutination assay for humoral immunity and the leukocyte migration test for cellular immunity to lens protein were performed on 43 patients with congenital cataract and 30 healthy persons served as control. The results showed that there was no significant difference in the incidence of humoral immune responses to lens protein between patients with congenital cataract and the controls (P greater than 0.05), but the incidence of cellular immune responses to lens protein in patients with congenital cataract was higher than that of the controls (P less than 0.005). The results of this study suggested that during the development of congenital cataract, lens protein leaked into the aqueous humour and entered the systemic circulation, sensitizing lymphocytes and producing cellular mediated immune responses. Further investigation is necessary to determine whether there is any relationship between the immune responses to lens protein and the formation of congenital cataract.

Adolescent↗

PubMed1975

Induction and in Vitro demonstration of cellular immunity to DNA and RNA viruses in guinea-pigs.

Guinea-pigs were immunized with different cells infected with vaccinia virus, herpes simplex virus type 1, herpesvirus saimiri, and the virus of vesicular stomatitis. Development of cellular immunity against these viruses was observed with transformation of blood and spleen lymphocytes and with the migration inhibition test using peritoneal exudate cells. Cellular immunity against vaccinia virus was first seen 6 days after the inoculation of cell-bound vaccinia virus by lymphocyte transformation. The avtivation of the vaccinia virus specific cellular immune response could be induced with tissue culturrus. Since infectious virus particles are not synthesized within this time period, it is likely that virus-induced antigens in the cell surface are active in production of cellular immunity. Vaccines from heterologous host cells were more effective inducers of an immune response than syngeneic cell cultures. For in vitro testing of cellular immunity to viruses, viral antigens could be used in both infective and inactivated form. Delayed hypersensitivity to viral antigens was always accompanied by immune reactions to the host cells used for virus propagation.

Animals↗

PubMed1986

Sex-dependent local cellular immunity to alloantigens.

A local component of cellular immunity was detected in mice that had been immunized against histocompatibility antigens. The status of this local immunity was determined using a node-onto-kidney (NOK) assay in which lymph nodes draining the site of immunization as well as distant (nondraining) lymph nodes of the immunized mice were grafted onto the kidneys of mice of the immunizing strain. In this assay, the weight gained by each node piece was taken as a measure of its immunological responsiveness. The responsiveness of a draining lymph node was directly compared with that of a distant node after both had been grafted onto the same host kidney. We consistently found that the draining lymph nodes of immunized male mice were more responsive than their distant nodes, whereas the draining lymph nodes of immunized female mice were less responsive than their distant nodes. Male mice were converted to the female pattern of hyporesponsiveness in the draining nodes by performing bilateral orchidectomy, suggesting that the male pattern depends upon the presence of testicular hormones. Additional studies showed there was a significant reduction in the reactivity of uterine draining lymph nodes during both syngeneic and allogeneic pregnancy, raising the possibility that the female pattern of hyporesponsiveness facilitates fetal survival by reducing the maternal immune response to fetal antigens and alloantigens during pregnancy.

Animals↗