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 667 records · Page 37Linked to original sources
PubMed2002

The humoral response in TCR alpha-/- mice. Can gammadelta-T cells support the humoral immune response?

An optimal humoral response requires T-cell help; however, it has been questioned if this help comes exclusively from alphabeta-T cells or whether gammadelta-T cells also contribute. We have attempted to answer this question by studying the humoral response in T-cell receptor alpha-chain knockout (alpha-/-) mice, which lack the alphabetaT cell subset. Two model antigens were used to characterize the response: the thymus-independent (TI) antigen native dextran B512 (Dx), and the thymus-dependent (TD) antigen heat shock protein (HSP65) from Mycobacterium tuberculosis. When challenged with Dx, the alpha-/- mice elicited a strong antibody response and formed rudimentary germinal centres (GCs), a T-cell dependent reaction. In contrast, the humoral response to HSP65 was poor. However, alpha-/- mice became primed when challenged with HSP65, because when supplemented with wild-type thymocytes, the antigen-primed animals were able to mount a stronger response than the nonprimed ones when challenged with HSP65. A crucial step seems to be the collaboration between gammadeltaT cells and antigen presenting cells (APCs), as splenocytes from alpha-/- mice were able to respond to HSP65 in an environment containing primed-APCs. Based on these results, we propose a model for B-cell activation in the alpha-/- mice.

Animals↗
PubMed1976

The immune response in cirrhotic rats. Antigen distribution, humoral immunity, cell-mediated immunity and splenic suppressor cell activity.

The immunological disturbances occurring as a result of liver disease have been studied in an animal model of cirrhosis. The mononuclear phagocytic cells of the normal liver phagocytose large amounts of antigen irrespective of whether that antigen is injected directly into the portal or into the systemic circulations. The liver therefore acts as a filter 'in series' and 'in parallel' with the spleen and reduces the immunogenicity of antigens entering the organism by either of these routes. In rats with hepatic cirrhosis, there is a reduction in the capacity of the liver to phagocytose the flagellar antigen of Salmonella adelaide. This results in increased stimulation of splenic lymphoid tissue and in an increased antibody response to this thymus-independent antigen. The increased antigenic stimulus to the spleen may also be responsible for the increased suppressor-cell activity which has been demonstrated in these rats, and may be the mechanism of the diminished cell-mediated immune response both in this animal model of cirrhosis and in the human disease state. These studies suggest that many of the immunological disturbances associated with chronic liver disease may be the result of maldistribution of antigen occurring because of impaired hepatic phagocytic capacity.

Animals↗
PubMed1984

Anti-pancreatic immunity. In vitro studies of cellular and humoral immune reactions directed toward pancreatic islets.

It has been suggested that the immune system may be responsible for the destruction of insulin secreting cells in some types of diabetes. In order to test this hypothesis, we studied the consequences of immune-mediated reactions on the function of pancreatic islet cells in vitro. A model was set up in vitro where mouse pancreatic islet cells are exposed to human lymphocytes or sera + complement then stimulated for the release of insulin or glucagon. A selective inhibition of insulin secretion, but not of glucagon secretion, was observed in the presence of lymphocytes from 37 out of 40 insulin-dependent diabetic (IDD) patients and in the presence of sera (+ complement) from 22 out of 40. Lymphocytes were found inhibitory in almost all patients in both groups, with and without associated autoimmune diseases. In contrast, inhibitory sera were observed almost only in patients with associated autoimmune diseases or recent onset diabetes. The selective inhibition of insulin secretion, but not of glucagon secretion, suggests that lymphocytes or sera may be involved in a destructive process of insulin secreting cells in vivo. This cell-mediated effect depends on direct T lymphocyte cytotoxicity, rather than antibody-dependent cell cytotoxicity, as suggested by the lack of any effect of aggregated immunoglobulins on the reaction. In contrast, when C57BL/6 mice were immunized by mastocytoma cells from a DBA2 strain, their lymphocytes and sera blocked both secretions of insulin and glucagon when incubated in vitro with DBA2 islet cells. This non-selective inhibition may be due to anti-H2 immunity, rather than immunity directed against insulin secreting cells.

Adolescent↗
PubMed1977

[Modification of immune reactions by antigen-immunosuppressive agent conjugates. V. Studies on antigen-specific activity of 6-mercaptopurine bovine gamma globulin conjugates on the humoral immune response in rabbits].

Rabbits treated daily and for seven consecutive days with 6-mercaptopurine bovine gamma globulin conjugates (MPI--n-BGG; 'I'--characterizes the king of chemical binding and 'n' the number of coupled MP-residues per one mole BGG) show an altered immunological reactivity. A following intradermal immunization with BGG alum adsorbate results in a suppressed anti BGG antibody production on the third day after antigen application (antibody titer 1:320, antibody titer of control animals--pretreated with BGG and uncoupled 6-MP equals 1:5120). Already three days later the antibody titers of the test groups show a significant increase and are two dilution stages higher than the titers of the controls. A suppressive effect on the third day is induced by MPI--13-BGG, MPI--26-BGG, MPI--36-BGG and MPI--46-BGG; the later adjuvant effect can only be seen in the MPI--26-BGG, MPI--36-BGG and MPI--46-BGG but not in the MPI--13-BGG pretreated animal group. While the short time suppression was antigen specific--the humoral immune response against a second unrelated antigen was not reduced--the adjuvans effect was not antigen specific. A pretreatment with the substances mentioned above results in an increased anti BGG and anti HSA serum antibody level. Comparing investigations on the unspecific immunosuppression in rabbits by 6-mercaptopurine shows that application of 10 mg 6-MP/kg/day for seven days at first leads to a suppression but later on to an enhancement of antibody production. Application of 10 mg 6-MP/kg/day for 10 days results in a long lasting suppression without enhancement effect. As a reason for these differences the different catabolism of immunosuppressive agent and antigen is discussed. For the phenomena following antigen specific immunosuppression, similar mechanisms can be responsible.

Agglutination↗
PubMed1987

Humoral immunity in measles infection: a critical factor?

Cell-mediated immunity is generally regarded as the essential factor in recovery from measles infection. In other viral infections humoral immunity has been considered a critical factor when antibody titres were correlated with outcome or when serum therapy proved protective. A review of available studies of severe-to-fatal cases of measles infection having non-neurological symptoms indicate that the antibody response is depressed in virtually all cases. The current view of immune globulin being an ineffective therapeutic agent is based on treatment of measles encephalitis; in fact, the least effect should be expected among encephalitis cases since some already have antibodies from the onset of symptoms. Larger examinations of measles with other than neurological symptoms suggest that immune globulin has a beneficial impact on the clinical course of infection. There are indications that hyperimmune globulin increases the efficacy of this form of treatment. Since measles is still a major cause of hospitalization and mortality, further studies of the therapeutic effect of specific immune globulin are warranted. From our current knowledge, both the humoral and cell-mediated immunity seem to be critical factors in recovery from measles infection.

Antibody Formation↗
PubMed2004

HER2/neu-derived peptides recognized by both cellular and humoral immune systems in HLA-A2+ cancer patients.

HER2/neu is one of the most appropriate target antigens for anti-cancer therapy because of its expression in various types of epithelial cancer. HER2/neu can also be a target for both cellular and humoral immune responses. In this study, we attempted to identify HER2/neu-derived peptides, which are able to be recognized by both humoral and cellular immune systems in HLA-A2+ cancer patients. Among 12 HER2/neu-derived peptides having the HLA-A2 binding motifs, immunoglobulin G reactive to each of 7 HER2/neu peptides was detected in the plasma of >50% of cancer patients. Among these 7 peptides, 3 including HER2/neu 444-452, HER2/neu 466-474, and HER2/neu 484-492, effectively induced peptide-specific and HLA-A2-restricted cytotoxic T lymphocyte activity from peripheral blood mononuclear cells of cancer patients, regardless of different HLA-A2 subtypes. Experiments using blocking antibodies and cold inhibition targets revealed that the cytotoxicity against HER2/neu-expressing HLA-A2+ tumor cells was peptide-specific and CD8+ T cell-dependent. Overall, these results indicate that these 3 HER2/neu-derived peptides are efficiently recognized by both the humoral and cellular immune systems, and therefore could be useful for peptide-based immunotherapy for HLA-A2+ patients with various types of epithelial cancer.

Antibody Formation↗
PubMed1987

Altered humoral immunity during pregnancy in the guinea pig.

A guinea pig model was developed to determine whether humoral immune responsiveness is altered during pregnancy. Pregnant animals were immunised at mid-gestation with haptenated protein. The humoral response to antigen was measured as numbers of antibody-producing cells in the spleen, the affinity of the antibody produced by spleen cells and the levels of IgG in the serum. The values obtained were compared with those from an age matched non-pregnant control group. Early in the primary response, there was a significant decrease in the number of IgM antibody-producing cells with an associated decrease in serum IgM levels in pregnant animals. Late in the primary response, pregnant and control animals had similar levels of IgM antibody-producing cells. During the later stages of the response, many of the pregnant animals did not respond with IgG antibody-producing cells or IgG in the serum. When IgG-producing cells were detected, the antibody was of lower affinity than that observed with the control group. A selective lack of responsiveness was detected in the primary response of pregnant guinea pigs. The reduced number of IgG antibody-producing cells in gravid animals suggests that an immune switch from IgM to IgG is impaired in pregnancy. The low affinity of antibody produced indicates the immunoglobulin produced in pregnancy may also be functionally limited.

Animals↗
PubMed2000

[The dynamics of the humoral immunity indices and of the beta 2-microglobulin level in children with chronic hepatitis].

Studied in children with chronic hepatitis B (n = 38) were indices for humoral immunity, such as blood serum content of immunoglobulins A, G, M, and beta 2-microglobulin. The revealed increase in the level of the indices under study suggest to us an apparent tension of the humoral link of immunity. The polyenzymic drug preparation wobenzym in the complex of therapeutic measures instituted in the above children was found out to have a positive effect on humoral homeostasis.

Adjuvants, Immunologic↗
PubMed1986

Leishmania donovani: cellular and humoral immune responses after primary and challenge infections in squirrel monkeys, Saimiri sciureus.

Cellular and humoral immune responses were studied in squirrel monkeys after primary and challenge infection with a Khartoum strain (WR 378) of Leishmania donovani. Each of 7 squirrel monkeys, Saimiri sciureus, was inoculated intravenously with 5 X 10(7) amastigotes/kg body weight, and one other monkey (control) was inoculated with uninfected hamster spleen homogenate. Five infected monkeys recovered from visceral leishmaniasis and two infected monkeys died. Three of the five squirrel monkeys which recovered from the primary infection demonstrated acquired resistance when challenged with an intravenous inoculation of 1.0 X 10(8) amastigotes of L. donovani/kg of body weight. Each of these same three monkeys, the two remaining monkeys which recovered from the primary infection and an uninfected control monkey, were challenged subsequently with an intradermal injection of 2.2 X 10(7) promastigotes of L. braziliensis panamensis (WR539) and developed cutaneous lesions. The reactivity of peripheral blood leukocytes from infected squirrel monkeys to phytohemagglutinin was depressed 2 to 10 weeks after infection, and the reactivity to concanavalin A was not affected. Data on responses to pokeweed mitogen were inconclusive. Reactivity to leishmanial antigens was detected at 12 weeks after infection, which coincided with a marked decrease or disappearance of parasites in liver imprints. Two of five surviving squirrel monkeys developed weak delayed skin test responses to leishmanin antigens after 23 weeks; the three remaining monkeys were anergic during the primary infection but developed strong delayed skin test responses to leishmanin antigens at 7 weeks after a challenge with L. donovani. All squirrel monkeys inoculated with L. donovani developed a hyperproteinemia, hypergammaglobulinemia, hypoalbuminemia, and a reversal of the albumin/globulin ratio between 4 to 18 weeks after infection. Plasma IgM and IgG levels were increased between 2 to 18 weeks after infection; much of this increase was due to IgG. Class-specific antileishmanial antibodies, with generally low IgM and high IgG titers, reached a maximum after 14 and 16 weeks, respectively. A correlation was observed between concentration of gamma-globulins and plasma IgM and IgG levels, but not gamma-globulin concentrations and maximum titers of class-specific antileishmanial antibodies. Squirrel monkeys challenged with L. donovani again developed hyperproteinemia, hypergammaglobulinemia, and increased concentrations of plasma IgM and IgG which correlated with high titers of IgG class-specific antileishmanial antibody 4 weeks after reinoculation.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

The humoral immune response of chickens to Mycoplasma gallisepticum and Mycoplasma synoviae studied by immunoblotting.

The humoral immune response over time of White Leghorn chickens experimentally infected with Mycoplasma gallisepticum or M. synoviae by an aerosol inoculation or a contact exposure were compared by immunoblotting. The response of chickens infected with M. gallisepticum were similar with respect to proteins recognized and intensity of response, regardless of mode of infection. On the other hand, chickens infected by aerosolization of M. synoviae responded to more proteins and with greater intensity than did M. synoviae contact-exposed birds. Chickens infected with M. gallisepticum responded with antibodies to over 20 proteins, while chickens infected with M. synoviae responded with antibodies to 12 proteins. Field sera from chickens naturally infected on commercial poultry farms with M. gallisepticum or M. synoviae were analyzed by immunoblotting and were found to react with a number of mycoplasma proteins. However, no correlation was seen when comparing intensity of immunoblot staining and hemagglutination-inhibition titer of the field sera. The experimental antisera were used to identify species-specific proteins of M. gallisepticum and M. synoviae. Six immunogenic species-specific proteins of M. gallisepticum with relative molecular masses of 82 (p82), 65-63 (p64), 56 (p56), 35 (p35), 26 (p26), and 24 (p24) kilodaltons (kDa) were identified. Two species-specific proteins of M. synoviae with relative molecular masses of 53 (p53) and 22 (p22) kDa were identified. Additionally, a highly immunogenic 41 (p41) kDa protein of M. synoviae was identified. Species-specific proteins identified in these mycoplasmas and the 41 kDa protein of M. synoviae were purified by preparative SDS-PAGE in amounts sufficient for further characterization and for use in serodiagnostic tests.

Aerosols↗
PubMed1997

Humoral immune response of chicks to different clinical isolates of avian adenovirus type-1.

The humoral immune response of 7-day-old chicks to different strains of avian adenovirus (AAV) type-1 was determined by counter immunoelectrophoresis (CIE) and enzyme-linked immunosorbent assay (ELISA). In CIE antibody was detected 14 days post-infection (PI) whereas in ELISA antibody was detected 7 days PI. The ELISA titre reached its peak at 21 days PI in all groups. The pattern of immune response among the groups was found to be similar.

Adenoviridae Infections↗
PubMed1997

Humoral immune response within the lung in HIV-1 infection.

In order to study the humoral immune defences in the respiratory tract during HIV-1 infection, we measured the levels, local productions and anti-HIV and antibacterial activities of IgG and IgA in the bronchoalveolar lavage fluid (BALF) and serum of 61 adult patients with severe HIV infection and of 56 HIV- controls. Albumin was used as the serum transudation factor. The increase of immunoglobulin levels in the serum of HIV-infected patients was confirmed. The IgG level was also increased in epithelial lining fluid (ELF), whereas the total IgA level was unchanged and secretory IgA (SIgA) level was decreased. The ELF/serum immunoglobulin ratios suggested that the IgG present in ELF resulted mainly from transudation, in contrast to SIgA, which was synthesized locally in controls but greatly diminished in HIV-infected patients. IgG to HIV-1 could be detected in BALF of all the patients, but IgA to HIV-1 only in 30% of patients. BAL IgG reacted more consistently and with a broader array of HIV-1 antigens than did IgA. BAL IgA, when present in samples, reacted primarily with viral envelope antigens. Because IgA specificities to some HIV-1 antigens were detected more intensively by BAL than by serum immunoglobulins, we conclude that the mucosal immune response is distinct from that in serum. IgG antibody activity to Streptococcus pneumoniae was decreased in HIV-infected patients' sera, and IgA antibody activities to S. pneumoniae and to Pseudomonas aeruginosa were decreased in ELF in HIV-infected patients.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Humoral immune response of humans to lipooligosaccharide and outer membrane proteins of Haemophilus ducreyi.

The humoral immune response to purified lipooligosaccharide (LOS) and outer membrane proteins (OMP) of Haemophilus ducreyi was evaluated. Sera from chancroid-endemic (Uganda, Kenya) and -nonendemic (Canada) countries were tested by an ELISA. The response to OMPs was cross-reactive with other Haemophilus species, and elevated levels of antibody were detected in patients that did not have chancroid. The LOS component stimulated an H. ducreyi-specific immune response that was detected only in patients with chancroid. The sensitivity of the LOS ELISA was 96% (95% confidence interval, 89.9%-100%) and the specificity was 97% (95% confidence interval, 95.8%-98.2%). Thus, the anti-H. ducreyi LOS immune response is a significant diagnostic and epidemiologic indicator.

Adolescent↗
PubMed2006

Status of cellular rather than humoral immunity is correlated with clinical outcome of enterovirus 71.

We valuated specific cellular and humoral immune response of cases of enterovirus 71 (EV71) infection and correlated immune response with clinical outcome. After obtaining informed consent, we enrolled 30 EV71 cases including 7 cases with brainstem encephalitis plus pulmonary edema, 12 cases of CNS (CNS) involvement and 11 uncomplicated cases. We measured antibodies specific to EV71, lymphocyte proliferation response and EV71-stimulated cellular response of Th1/Th2 cytokines and chemokines. The 7 EV71 cases involving brainstem encephalitis plus pulmonary edema had a significantly lower phytohemagglutinin stimulation index than other cases (p = 0.04). After EV71 stimulation of peripheral mononuclear cells, there was a significant increase in cellular Th1 cytokine (gamma-interferon) and proinflammatroy cytokines. However, cases with pulmonary edema had significantly lower cellular gamma-interferon (p = 0.04), lower cellular IL-1beta (p = 0.04), lower cellular IL-6 (p = 0.04), lower cellular tumor necrosis factor-alpha response (p = 0.04), and lower cellular macrophage inflammatory protein-1alpha (p = 0.04) response compared with other cases. Their titers of EV71 neutralizing antibodies demonstrated no difference among cases. These results suggest lower EV71-specific cellular response may be associated with immunopathogenesis of EV71-related pulmonary edema.

Antibodies, Viral↗
PubMed1991

[Effects of anti-ulcer drugs on humoral immunity].

The effect of cholinolytics in combination with antacids, belomet, solcoseryl and enterodes on humoral immunity was evaluated in 134 ulcer patients. Elevated levels of salivary secretory IgA and blood IgG, IgA, lowered blood IgD exhibited in ulcer exacerbation. Antibodies to oligopeptides isolated from the serum of ulcer patients occurred in 80.6% of the patients. Whatever the drug used, after-treatment levels of secretory salivary IgA and blood IgA dropped, blood IgD rose. Belomet treatment gave rise to higher titres of antibodies to oligopeptides. Solcoseryl, cholinolytics with antacids led to increased blood levels of IgM and reduced levels of IgG. Recovery of the indices occurred in patients on enterodes. It is stated that changes in immunity depend both on ulcer healing and direct action of antiulcer drugs.

Adolescent↗
PubMed1989

[Study of general principles of humoral immune response in viral infection by sample analysis of the properties of specific immunoglobulins].

Humoral immunity in murine experimental influenza was specified using experimental mathematical modelling intended for further systemic analysis of dynamics of immunological processes. The methodology of the proposed approach was based on the choice of affinity as an indicator of the function of specific antibodies, and on the concept of discrete functional structure of the immune system. The data were obtained by calculating affinity and antibody heterogeneity indices and by evaluating the distribution of functions by affinity. The successions of active antibody subpopulations with affinities varying in the course of infection and the presence in the plasma of protein fractions capable of low-affinity binding with influenza virus in non-infected animals were demonstrated. The relationship between the detected plasma protein populations and corresponding antibody-producing cells was confirmed. The mathematical modelling results were verified by physicochemical and immunochemical methods. The mechanisms by which the observed phenomena may be realized were considered from the viewpoint of the current theory of immunity.

Animals↗