PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Immunity, Humoral”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 595 records · Page 33Linked to original sources

Cellular and humoral immune responses of mice subclinically infected with Pneumocystis carinii.

Cellular and humoral immune responses to Pneumocystis carinii were investigated. ICR and DDD mice were intranasally infected with 10(4) mouse lung-derived P. carinii, and the delayed-type hypersensitivity (DTH) reaction and antibody titers to P. carinii were measured along with the number of P. carinii cysts in the lungs after infection. The number of P. carinii cysts in the lungs peaked at 2 weeks after infection and then decreased to barely detectable levels by 4 weeks. Serum antibody (immunoglobulin G) titers measured by indirect immunofluorescence increased up to 4 weeks. The DTH footpad reaction was most prominent at 2 weeks postinfection and declined thereafter. Thus, the decline in the number of P. carinii cysts in the lungs corresponded well with the time of the peak of the DTH reaction but not with the serum antibody response. Spleen T cells from infected mice mediated the DTH reaction when transferred intravenously into normal recipients and reduced the number of P. carinii cysts in the lungs when transferred intravenously into P. carinii-infected mice. The results indicated that cellular immunity is important for protection from subclinical P. carinii infections.

Animals↗

The effect of emotional stress on the primary humoral immunity of rats.

The effect of exposure to emotional stress on humoral immune function after injection with ovalbumin, a novel antigen, was studied in adult male Wistar rats. Emotional stress was induced by randomly giving empty water bottles to rats trained to drink water at set times. The results showed that emotional stress induced the decrease in spleen weight and specific immunoglobulin G antibody level to ovalbumin, and increased levels of epinephrine, norepinephrine and corticosterone. A decrease of antibody levels correlated negatively with an increase in plasma norepinephrine levels. These findings suggest that emotional stress can modulate immune function, and that sympathetic nervous system may be involved in this immunomodulation.

Animals↗

[A study of the humoral immunity of mice injected with beryllium chloride].

We studied changes of humoral immunity, such as complement pathway activity, C3 contents and contents of immunoglobulin, in mice injected subcutaneously with BeCl2 or CuCl2 once a week for 12 weeks. Mean body weights of JCL: ICR female mice were approximately 30g in control mice (control group; n = 7), in mice injected with Be (Be group; n = 8) and in mice injected with Cu (Cu group; n = 8). Values of classical complement pathway activity (CH50) were 18.8 +/- 1.4 U per ml, 15.3 +/- 1.8 U per ml and 16.7 +/- 1.3 U per ml in the control group, Be group and Cu group, respectively. The CH50 values of Be and Cu groups were significantly lower than that of the control group (P < 0.01). In contrast, values of alternative complement pathway activity (ACH50) and contents of C3 were almost constant in the three groups. The immunoglobulin content in the Be group tended to increase. The activity of alanine aminotransferase in the Be group was markedly higher than that in the control group (P < 0.05), and the aspartate aminotransferase activity was also high. The CH50 value of mice injected with a small amount of Be once a week over a 12-week period decreased markedly, although either the ACH50 value or C3 content was the same as in the control group. The immunoglobulin content somewhat increased in the Be group. These results suggest the possibility that immune complex is induced by Be.

Animals↗

Contribution of humoral immunity to the therapeutic response in falciparum malaria.

The contribution of humoral immunity to the therapeutic response in acute falciparum malaria was assessed in a case-control study. Forty adult Thai patients with acute falciparum malaria who had subsequent recrudescent infections and 40 patients matched for age, therapeutic regimen, and disease severity who were cured by Day 28 were studied. All cured patients had positive immunoglobulin (Ig) G to ring-infected erythrocyte surface antigen (RESA) in their admission plasma, compared with only 60% of patients who failed to respond to treatment (P < 0.001). The proportion of IgM-positive cases at admission was also higher in the successfully treated group than in the group with failure (70% versus 30%) (P < 0.001). The geometric mean (95% confidence interval) reciprocal IgG titer at admission was significantly higher in cured patients (187.0 [83.5-418.3]) compared with those who experienced treatment failure (11.6 [5.1-26.5]) (P < 0.001). The patients with uncomplicated malaria who were both IgG and IgM positive at admission had significantly shorter fever clearance times and lower admission parasitemia levels compared with those who were negative (P = 0.01 and P = 0.02, respectively). The median (range) in vitro parasite multiplication rate was significantly lower in cultures containing positive anti-RESA antibody plasma compared with those containing normal plasma (0.7 [0.1-3.5] versus 2.6 [0.1-12.1]; P < 0.001). These results suggest that antimalarial antibodies may play an important supportive role in the therapeutic response to antimalarial drugs during acute falciparum malaria.

Acute Disease↗

[The dynamics of the humoral immune response to mycobacterial antigens in mice].

The main regularities of humoral immune response to mycobacterial antigens have been studied in experiments on BALB/c mice immunized with live and thermoinactivated Mycobacterium tuberculosis, var. bovis. As shown in this study, the maximum level of serum antibodies to mycobacterial antigen is achieved in two weeks after immunization irrespective of the dose and viability or mycobacteria, then follows a decrease in the antibody level. The absence of uniformity in the dependence of primary immune response and the formation of immunological memory on the dose and viability of mycobacteria has been demonstrated.

Animals↗

[Indicators of cellular and humoral immunity during the process of healing of stomach ulcer].

Cellular and humoral immunity parameters in the process of healing of ulcer were studied in 47 patients with gastric ulcer. Changes in the immune status in these patients depended on the stage of healing of an ulcerous defect (active exacerbation, the beginning of cicatrization, "red" or "white" scar) and were most pronounced at the initial period of ulcer cicatrization. They were manifested by the signs of the immune system activation (primarily by increase in the relative content of theophylline-resistant T-lymphocytes). In patients with more prolonged terms of ulcer healing these changes appear later to indicate one of the factors of slow ulcer cicatrization.

Adult↗

[Effect of ribonucleases on humoral immunity of experimental animals].

The stimulating effect of RNAases on the humoral immune response was observed in experiments with animals. It was shown that the stimulation was mainly mediated by the system of T-lymphocytes. In the T-lymphocyte system positive sensitivity to the enzymes was attributed to the T-helper cell subpopulation.

Animals↗

[Systemic humoral immune response to food antigens following oral immunization or immunization via the respiratory tract].

Differences and similarities of the systemic humoral immune response to cow's milk proteins were investigated after exposure of the gut or of the airways to antigen, both in children and in rabbits. Circulating antibodies were determined by radioimmunoassay (children and rabbits) and by enzyme-linked immunosorbent-assay in a small number of children. An age-dependent reference range was established, reflecting the rapid change of active antibody formation after oral immunization against bovine serum albumin in healthy, non-breastfed children up to the age of 24 months (n = 181). In contrast 16 children with recurrent aspiration due to anatomical disturbances or swallowing difficulties, all had antibody-titers well above this reference range. 7 of 9 children with cow's milk protein intolerance and with failure to thrive (oral immunization) also showed high concentrations of milk antibodies in the circulation. In adult rabbits immunized by oral or inhalational route, the vigorous immune response seen in recurrent aspiration could be mimicked. As investigated by enzyme-linked immunosorbent assay, higher titers of antibodies to bovine serum albumin, alpha-lactalbumin, beta-lactoglobulin, alpha-casein and bovine gammaglobulin could be shown in all isotypes tested (specific anti-IgG, -IgA, and -IgE) both in recurrent aspiration (n = 11) and cow's milk protein intolerance (n = 4) as compared to normal age-matched children (n = 14).

Animals↗

Role of reactive metabolites in suppression of humoral immunity by N-nitrosodimethylamine.

The hypothesis that dimethylnitrosamine (DMN)-induced humoral immune suppression is mediated by reactive intermediates was tested in female B6C3F1 mice using three approaches. First, distribution of reactive species to known target organs (liver and kidney) and to immune organs (peripheral blood components, bone marrow cells, thymus and spleen) was demonstrated by monitoring acid-insoluble radioactivity after single or multiple doses of 6 mg/kg and 2 microCi of [methyl-14C] DMN. Most of the radioactivity resided in acid-insoluble material, which increased with the number of exposures and correlated with suppression of the in vivo antibody response to sheep erythrocytes as determined by enumerating immunoglobulin M antibody-forming cells. Fractionation of spleens from exposed animals into various cell types indicated greater association of acid-insoluble radioactivity with T- and B-lymphocytes as compared to macrophages. Fractionation of spleen cell lysates into protein, DNA and RNA indicated that most radioactivity was associated with the nucleic acid component. Pretreatment of mice with aminoacetonitrile reduced acid-insoluble disintegrations per minute in the spleen. The second approach was to demonstrate the immunosuppressive nature of compounds forming the same toxic intermediate as DMN. The addition of N-nitroso(acetoxymethyl)methylamine to spleen cell cultures resulted in completely suppressed in vitro antibody responses to sheep erythrocytes and dinitrophenylated Ficoll at micromolar concentrations. The third approach involved activating DMN to an immunosuppressive form in vitro. Preincubation of splenocytes with Aroclor-induced mouse hepatocytes resulted in activation of DMN to intermediates capable of markedly suppressing the response of antibody-forming cells to sheep erythrocytes.

Animals↗

[Cellular and humoral immunity studies after vaccination against influenza].

The indices of cellular and humoral immunity (the number of leukocytes, lymphocytes, T- and B cells, E- and EAC-RFC, blastogenic reaction of lymphocytes in response to treatment with phytohemagglutinin and influenza virus antigen in vitro, antihemagglutinin and influenza virus antigen in vitro, antihemmagglutinin titres) in humans vaccinated with different types of inactivated influenza vaccines produced in the USSR and the GDR were investigated. The immunogenic potency, general and immunological innocuity of the inactivated influenza vaccines under study and more marked stimulation of the B-system of immunity by them were demonstrated.

Adolescent↗

Humoral immune response of cats to Paragonimus infection.

The time course of humoral immune response to Paragonimus siamensis was studied in 10 cats experimentally infected with either 30 or 60 matacercariae and the antibody produced was detected by enzyme linked immunosorbent assay (ELISA), complement fixation test (CFT), and immunoelectrophoresis (IEP) test. With ELISA and CFT, antibodies was detected as early as 2nd week after infection and the cats remained positive throughout the 12 week period of observation. In contrast, the IEP test was persistently negative. With respect to sensitivity, both ELISA and CFT are equally sensitive but the mean ELISA titer was consistently higher than that of CFT. THe magnitude of the antibody response appeared to be related to duration of the infection but not to the infective dose and the number of worms recovered. There was variability in titers among cats infected with equal numbers of metacercariae. The tests can not be used for differential diagnosis of infections by P. siamensis and P. heterotremus because of the cross-reaction. Such cross-reaction did not not occur against unrelated parasites including hookworm. Toxocara cati and Spirometra mansoni.

Animals↗

Cellular and humoral immune response in pigs given vaccinal and chronic hog cholera viruses.

Humoral immune response (seroneutralization) and cellular immune response (lymphocyte-stimulation test) were analyzed in pigs inoculated with low virulent strains of hog cholera virus or vaccinated with a live-virus vaccine. Vaccinated animals exhibited an intense neutralizing antibody production, but cellular immune response was not detected. Neutralizing antibodies were not found in infected pigs, but a brief cellular immune response (18 days after inoculation) was observed.

Animals↗

Expression and immunologic characterization of recombinant heat shock protein 58 of Leptospira species: a major target antigen of the humoral immune response.

A clone of Leptospira interrogans serovar lai that was isolated by immunoscreening of a genomic lambda library with sera from convalescent patients with leptospirosis directed expression of a unique 62-kDa protein in Escherichia coli. When examined by SDS-PAGE, the protein comigrated with an immunodominant protein present in leptospiral cell lysate. Determination of the nucleotide sequence of the 2.7-kb insert DNA identified two genes homologous to the hsp58 and hsp10 of L. interrogans serovar copenhageni reported previously. The overexpressed recombinant Hsp58 protein was purified and used to immunize a rabbit to produce a polyclonal antibody. Immunoblot analysis using the rabbit anti-Hsp58 G antibodies showed that the 62-kDa protein was commonly present in lysates of other serovars of leptospires, consistent with the strong sequence conservation between the hsp58 genes of the two serovars. Immunoglobulin G antibodies to the Hsp58 were specifically detected by ELISA in 82% of sera (18/22) from patients with leptospirosis. Deletion analysis of the recombinant Hsp58 protein indicated that a strong antigenic determinant for humoral immune response is located between amino acids 360 and 380 (DREKLQERLAKLAGGVAVIHV) of Hsp58, which are highly conserved among the GroEL family. The strong sequence conservation of the Hsp58 among leptospires and its importance as a major target for the humoral immune response warrant further studies of its potential pathogenetic role.

Animals↗

"Sero-switch" adenovirus-mediated in vivo gene transfer: circumvention of anti-adenovirus humoral immune defenses against repeat adenovirus vector administration by changing the adenovirus serotype.

Recombinant, replication-deficient adenovirus (Ad) vectors have been successfully used to transfer and express the normal human cystic fibrosis transmembrane conductance regulator (CFTR) cDNA in vivo in the respiratory epithelium of experimental animals and humans with cystic fibrosis (CF). Since Ad-directed gene expression wanes over time, repeat administration is necessary to achieve an effective treatment for CF. A major hurdle to such a strategy is the possibility that anti-Ad humoral immunity may prevent gene expression in individuals with pre-existing anti-Ad immunity or following repeat administration. One strategy to circumvent such a problem would be alternating the use of Ad vectors belonging to different subgroups. Neutralizing antibodies developed with the administration of one Ad serotype do not cross-react with an Ad belonging to a second serotype in a manner that blocks infection and gene expression. To test this hypothesis, an immunizing dose of wild-type Ad5 (subgroup C), Ad4 (subgroup E), or Ad30 (subgroup D) was administered intratracheally to experimental animals, followed by an intratracheal administration of a replication-deficient subgroup C-derived vector coding for marker genes (chloramphenicol acetyl transferase or beta-galactosidase) or for the normal human CFTR cDNA. As expected, studies with vectors coding for marker genes or for CFTR cDNA demonstrated that airway administration of a vector does not yield efficient gene transfer, if there has been prior recent airway administration of the same Ad subgroup. In contrast, effective expression from the second administration can be achieved with an adenovirus vector belonging to a subgroup different from the first adenovirus administered. These data support the paradigm of alternating Ad vectors derived from different subgroups as strategy to circumvent anti-Ad humoral immunity, thus permitting the use of Ad vectors as a means to treat the respiratory manifestations of CF.

Adenoviruses, Human↗

[Local cellular and humoral immunity in patients with acute bronchitis].

Complex investigation of some factors of local immunity in acute bronchitis (AB) was conducted in order to determine the mechanisms of formation of immunodeficient states in respiratory system and their influence on disease course. Study of cellular link of pulmonary local defense (PLD) included investigation of total number of cells in bronchoalveolar lavage fluid (BALF), their viability, alveolar macrophages (AM), neutrophils, lymphocytes (T- and B- lymphocytes), phagocytic index and phagocytic number of AM and neutrophils, receptor system of AM and neutrophils. Examination of PLD humoral factors in BALF in the patients with AB consisted of determination of IgA, IgM, IgG and lysocin contents. The data obtained shows the dependence of state of local cellular and humoral immunity on AB clinical-and-etiologic form. The most expressed degree of cellular and humoral immunodeficiency is caused by staphylococcal infection. The role of dysfunction of cellular and humoral link of pulmonary immune defense in bronchoobstructive syndrome genesis was established. Restoration of cellular and humoral immunity indices in convalescents with AB lags behind the time of clinical recovery. The significant degree of immunodeficiency in the patients with AB lingering form can be a pathogenetic factor in chronization of inflammatory process in lungs.

Acute Disease↗

Nephritogenic glycoprotein. XI. Comparison of humoral immune responses in rats injected with nephritogenoside and those given Heymann antigen.

A single footpad injection of a triglycosyl glycopeptide (nephritogenoside, NG) isolated from rat glomerular basement membrane can induce proliferative glomerulonephritis (PGN) in homologous animals, resulting in contracted kidney. On the other hand, it is well known that administration of rat tubular brush border antigen (Fx1A) causes a membranous glomerulonephritis (MG) in homologous animals. When a partially purified NG (crude NG, cNG) is injected in rats, a mixed lesion of PGN and MG resulted. To investigate the correlation between renal glomerular lesions and humoral immune responses in animals given NG and cNG, levels of antibodies to cNG and Fx1A, and those of immune complexes (ICs) are measured in sera from animals of these experimental groups using enzyme-linked immunosorbent assay. Significant levels of antibodies to cNG and Fx1A and those of ICs are detected in all groups of rats injected with cNG, Fx1A and pronase-digested Fx1A. It was revealed that antibodies to cNG in sera from rats injected with cNG, Fx1A and pronase-digested Fx1A recognize the common epitopes shared with Fx1A. On the other hand, neither antibodies nor ICs are detected in rats injected with NG, suggesting that humoral immune mechanisms may not play a leading role in the pathogenesis of NG-induced glomerulonephritis.

Animals↗

Neonatally induced inactivation of the vascular cell adhesion molecule 1 gene impairs B cell localization and T cell-dependent humoral immune response.

Vascular cellular adhesion molecule (VCAM)-1 is a membrane-bound cellular adhesion molecule that mediates adhesive interactions between hematopoietic progenitor cells and stromal cells in the bone marrow (BM) and between leukocytes and endothelial as well as dendritic cells. Since VCAM-1-deficient mice die embryonically, conditional VCAM-1 mutant mice were generated to analyze the in vivo function of this adhesion molecule. Here we show that interferon-induced Cre-loxP-mediated deletion of the VCAM-1 gene after birth efficiently ablates expression of VCAM-1 in most tissues like, for example, BM, lymphoid organs, and lung, but not in brain. Induced VCAM-1 deficiency leads to a reduction of immature B cells in the BM and to an increase of these cells in peripheral blood but not in lymphoid organs. Mature recirculating B cells are reduced in the BM. In a migration assay, the number of mature B cells that appears in the BM after intravenous injection is decreased. In addition, the humoral immune response to a T cell-dependent antigen is impaired. VCAM-1 serves an important role for B cell localization and the T cell-dependent humoral immune response.

Animals↗