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Results for “Humoral immune response”

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At least 19 recordsLinked to original sources

PubMed1976

Immune responses of the bovine fetus and neonate to Escherichia coli: quantitation and qualitation of the humoral immune response.

The humoral immune responses of fetuses and neonates of Escherichia coli O:26:K60:NM were studied in 26 Angus-Hereford crossbred calves. Bacterin (5.0 X 10(10) organism) was injected in utero directly into the amniotic fluid of seventeen 7- to 8.5-month-old fetuses (principals). Saline solution was injected in the same manner into 9 control fetuses. Colostrum-deprived neonates were allotted to 10 groups and either were euthanatized at birth or were subjected to oral revaccination, challenge inoculation with the homologous organism, or both. The resistance to challenge exposure was a function of previous in utero injection of bacterin, age when challenged, and dose of challenge organisms used. Control calves were susceptible to only a large challenge dose, whereas almost all of the prinicipal calves were resistant. Revaccination of principal calves with bacterin at birth, exposure to the large challenge dose, or both, caused a marked increase in anti-O26 passive hemagglutination titers. Results of quantitative and qualitative radioimunossay indicated that the immune response to the O26 antigen was mainly of the immunoglobulin M (IgM) class, although there were also demonstrable changes in immunoglobulins (Ig) G1 and G2. The actively acquired immune responses were serotype specific, and there was no cross reactivity with 4 other E coli serotypes. An unidentified immunoprecipitate band was observed in immunoelectrophoretograms of whole bovine serum which may represent another class of Ig or which may be a subclass of IgG1 or IgG2.

Animals↗

PubMed1978

The effect of ubiquinone-7 and its metabolites on the immune response. IV. Chemical structure-adjuvant activity relationship of quinonyl derivatives on humoral immune response.

The effects of the emulsion of quinonyl acids (QS-n, ES-n, KS-n) and related compounds (QSA-n) in Freund's incomplete adjuvant on the humoral immune response to bacterial alpha-amylase were assayed, and their structure-adjuvant activity relationships were discussed. All the quinonyl acids tested (500 microgram/mouse) enhanced the humoral immune response two to seven times as much as that of the control group, five weeks after immunization. 3'-Methyl and 2', 3'-double bond in the carboxy side chains of ubiquinone metabolites (Q acid-I, -II) were not essential for the adjuvant activity. The conversion of methoxyls on the quinone ring into methyls, and that of benzoquinone into phenol also did not affect the activity, but the activity seemed to depend on the carbon number of the carboxy side chain, and the prominent adjuvant activity was observed in the carboxylates having the carboxyalkyl chain of five to seven carbons. High doses (1 or 5 mg/mouse) of ubiquinone-7 and -2 enhanced the humoral immune response two to three times as much as that of the control group, and quinonyl alcohols (QSA-n) enhanced that with low dose (500 microgram/mouse).

Adjuvants, Immunologic↗

PubMed1979

Augmentation of the in vitro humoral immune response by pharmacologic agents. I: An explanation for the differential enhancement of humoral immunity via agents that elevate cAMP.

Agents that elevate intracellular concentrations of cAMP in cultured spleen cells can augment the in vitro 19s humoral immune response to SRBC. DBcAMP and 8BrcAMP were more effective than MIX, CT, PGE1, or ISO in producing the enhanced PFC response, when they were present only during an early stage of immune induction. The thesis is presented that the differential ability of these agents to augment humoral immunity results from their relative ability to maintain elevated concentrations of intracellular cAMP. Studies on the cellular mechanism by which cAMP elevation produces immune enhancement reveal that DBcAMP effects are on a T-cell-deficient population of murine spleen cells (predominantly B cells and macrophages). In addition, we showed that DBcAMP cannot replace the need for helper T cells in the induction of the PFC response to SRBC. Taken collectively, these results suggest that cAMP may be an important immunoregulatory signal, and that a variety of pharmacologic agents that modulate the induction of the humoral immune response may operate via this as a final common biochemical pathway.

1-Methyl-3-isobutylxanthine↗

PubMed1976

Cellular and humoral immune response analysis of bone-allografted rats.

Long-term cellular and humoral immune responses were studied in inbred rats in which bone was allografted. Transplants were made across major histocompatibility barriers. Mixed lymphocyte culture tests and humoral cytotoxicity assays were performed in order to determine degrees of cellular and humoral immunity. Grafts of complete bone and of bone free of marrow elicited both types of immune response and it is proposed that transplantation antigens for both types of reaction exist in the bone tissue itself. A gene-dose effect was found. Allogeneic bone grafts gave a stronger reaction than semiallogeneic grafts, and second-set grafts triggered a hypersensitivity type of humoral immune response. This study suggests that until the host-bone graft immunological relationship is better understood, the graft tissue should be matched to the host for major transplantation antigens to help prevent unexpected failures in massive bone allotransplantation.

Animals↗

PubMedDate not supplied

Immunological studies with aortic and venous tissue antigens. III. Examination of cell-mediated and humoral immune response induced by human vascular antigens.

The effects of human vascular antigens on the cell-mediated and the humoral immune response were studied in guinea pigs. In animals immunized with buffer extracts of aortic and venous wall a well measurable cell-mediated and humoral immune response were developed. Between the two kinds of vascular extracts in the skin tests, migration inhibition tests and antibody-production tests a cross-reactivity was observed, whereas the induction of desoxyribonucleic acid-synthesis proved to be specific. No cellular or humoral immune response to vascular extracts was detectable in the control animals. Analysing the time-kinetics of the cell-mediated and humoral immune response it was found, that with the increased production of antibodies the cellular immune reactions did not cease until the ninth week.

Animals↗

PubMedDate not supplied

Use of an adsorption enzyme immunoassay to evaluate the Haemophilus ducreyi specific and cross-reactive humoral immune response of humans.

Serodiagnosis of chancroid is limited by the cross-reactivity of Haemophilus ducreyi with Haemophilus influenzae and Haemophilus parainfluenzae. This research describes an adsorption enzyme immunoassay (EIA) that assesses the humoral immune response of North Americans and Africans to H. ducreyi. Adsorption effectively removed anti-H. influenzae and anti-H. parainfluenzae antibodies, revealing that North American control sera had no residual anti-H. ducreyi reactivity. However, African control sera still had a residual anti-H. ducreyi response. Assessment of the duration of the humoral immune response in sera from African patients with chancroid showed that the humoral antibodies persisted for up to 8 months after the diagnosis. This may explain the lack of specificity of the adsorption EIA in areas where chancroid is endemic. The detection of the humoral immune response was affected by the strain of H. ducreyi used, with indigent strains being most useful. Using H. ducreyi 35000 for Canadian sera, the sensitivity of the adsorption EIA was 100% and the specificity was 88%. For African sera, H. ducreyi strain R018 was used, and the adsorption EIA had a sensitivity of 81% and a specificity of only 23%. These data reveal that the existing humoral response in a country where chancroid is endemic differs from that in a country where it is not, and that care must be used interpreting unadsorbed humoral immune responses. The adsorption EIA approach may prove useful as an epidemiologic tool for definition of existing (past and present) levels of exposure to H. ducreyi.

Adolescent↗

PubMedDate not supplied

[Humoral immune response in hepatic and intestinal amebiasis in children].

The various classes of immunoglobulins with antibody function against E. histolytica were studied in 8 children with amebic liver abscess and in 7 with acute intestinal amebiasis. The predominant fraction was IgG in 7 patients from the first group and in 1 from the second; this suggests a secondary type humoral immune response which implies a previous experience with E. histolytica antigens. A definitive predominance of IgM was shown in a patient with amebic liver abscess, the same as in primary humoral immune response. Humoral antibodies did not develop in the remaining 6 patients with acute intestinal amebiasis. The disparateness of the humoral immune response found in these cases make it difficult to speculate on the role of immunoglobulins in the pathogenesis or in immunologic protection in amebiasis. Possibly, the most important is the participation of cellular immunity.

Child↗

PubMed1977

Schistosomiasis mansoni in the hamster: cellular and humoral immune responses to soluble egg antigens (SEA).

Cellular and humoral immune responses to soluble egg antigens (SEA) were studied in the course of Schistosoma mansoni infection in the hamster. No immune response to SEA could be detected before the parasite had started oviposition. The liver granuloma size reached a maximum 6 weeks after infection and decreased rapidly thereafter. The in vitro cell-mediated immune response to SEA (lymphocyte blast transformation) showed a maximum reaction 12 to 16 weeks after infection (depending on the infection rate) and also declined later. Parallel to the lowered reactivity of the lymphocytes to SEA in vitro, responsiveness to the nonspecific T-cell mitogen, phytohemagglutinin M, was also reduced in chronic infections. Humoral anti-SEA antibodies could be detected in increasing amounts up to 10 weeks after exposure.

Animals↗

PubMed1992

[Effects of substance P in rat spinal cord on the humoral immune response to SRBC].

The effects of substance P (SP) in rat spinal cord on the humoral immune response to sheep red blood cells (SRBC) were investigated by the hemolytic plaque-forming cell (PFC) technique. Radioimmunoassay was used for assessing SP content. Catecholamines contents were measured by high performance liquid chromatography (HPLC) with electrochemical-detection. The results suggest that SP in the spinal dorsal horn, but not in the lateral horn, could inhibit the thymus-dependent humoral immune response to SRBC, and this inhibitory effect might be related to the influence of dorsal horn SP on thymic activity. Increased SP content in the spinal dorsal horn at the peak of a humoral immune response might suppress the immune response and play a negative feedback role, preventing excessive immune response.

Animals↗

PubMed1975

Effect on reserpine on humoral immune responsiveness in young chickens.

The role of reserpine in modifying a primary humoral immune response was evaluated in three experiments with young chickens. It was found that chickens injected with reserpine prior to an intravenous antigenic challenge with sheep red blood cells exhibited an enhanced primary humoral immune response. The enhanced response occurred concomitant with an elevation in adrenal cortical activity as evidenced by the significant elevation of serum corticosterone in the reserpine-treated chickens. These data suggest that both the adrenal cortex and medulla may influence immune responsiveness in the chicken.

Animals↗

PubMed1978

Role of bacterial products in periodontitis: humoral immune response to Eikenella corrodens.

Eikenella corrodens can induce periodontitis-like disease in gnotobiotic rats. Some components of this bacterial cell elicit measurable humoral immune response during the development of the disease, but in this system endotoxin is not among the efficient immunogens. Because no humoral immune response could be seen to the endotoxin of Eikenella corrodens it is assumed that this endotoxin can act uncontrolled in monoinfected rats. Accordingly, the lack of protective humoral immune response to pathogenic components of Eikenella corrodens may be the major factor permitting the development of the disease described here. The possibility that both cell-mediated immunity and uncontrolled endotoxic action are parts of the pathomechanism of the disease is supported by our observations.

Animals↗

PubMed1975

Effect of the antitumor antibiotic chromomycin A3 on the humoral immune response in rats.

Chromomycin A3 (250 mug/kg) suppressed the humoral immune response in rats against sheep erythrocytes when administered 48 h or later after antigenic stimulus. The antibiotic at this dose enhanced immunity when given along with or before antigen administration. The natural heterohemagglutinin levels in rabbits and guinea pigs were not affected by the antibiotic (10 mug/kg per day x 7).

Animals↗

PubMed1992

Humoral immune response to the antigen administered as an immune complex.

Antigen (HSA) bound in immune complexes at equivalence with syngeneic anti-HSA antibodies elicit much stronger humoral immune response then soluble HSA. On the other hand, administration of immune complexes formed with xenogeneic (rabbit) anti-HSA antibodies suppressed humoral immune response against HSA, but not against rabbit IgG in mice. We suggest that immunization with antigen bound in immune complex might represent a powerful tool in enhancing humoral immune responses.

Animals↗

PubMed1978

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↗

PubMed1975

The humoral immune response to allografts of foetal small intestine in mice.

The influence of the presence of "passenger leucocytes" on the production of anti-H2 antibodies has been studied in mice receiving allografts of foetal small intestine, adult skin or intradermally injected spleen cells. It was found that the humoral immune response to foetal intestine (a tissue without passenger leucocytes) was identical temporarily to that elicited by skin allografts and these responses differed from that following injection of allogeneic spleen cells in that antibodies to solid grafts took longer to appear. The humoral immune response to small intestine grafts was not evident until several days after the onset of graft rejection as assessed morphologicallymanti H2 antibody production was not observed in thymus deprived recipients of foetal small intestine allografts or allogeneic spleen cells, and this suggests that the humoral immune response to transplantation antigens is thymus dependent.

Animals↗

PubMedDate not supplied

Primary humoral immune response against tumor membrane antigens and foreign antigens by plasma cell tumor bearer mice.

The MOPC-460 plasma cell tumor possesses tumor specific antigens. It nevertheless grows and kills its syngeneic host. The possible impairment of immune responsiveness in tumor bearing mice was investigated by measuring their ability to mount a humoral immune response against foreign antigens, such as sheep red blood cells or bacteriophage T4. No significant decrease in the response to either antigen was found until the tumor mass exceeded 10-15% of the host's body weight. Moreover, circulating anti-tumor antibodies were detected in the serum throughout the initial period of tumor growth. The possible interference of these antibodies with cell-mediated defence mechanism was ruled out by experiments where the humoral response was selectively suppressed from birth by repeated administrations of anti-immunoglobulin heavy chain antiserum. In a "suppressed" mice, tumors took, grew and developed more rapidly than in controls. It is concluded that, at least in the model studied, the humoral immune response operates as a defence mechanism against expansion of the tumor clone.

Animals↗

PubMed1976

[Modification of the immune reaction by antigen-immunosuppressive-agent conjugates. IV. Studies on the specific suppression of humoral immune response in guinea pigs by antigen-immunosuppressive-agent conjugates].

Bovine gamma globulin (BGG) antigens were modified by the binding of 6-mercaptopurine and toluyl residues, and their influence on the humoral immune response in guinea pigs was investigated. The antigen-immunosuppressive agent-conjugates (AIC) were different, depending on the method used for their preparation and the number of coupled residues per one molecule of BGG. Conjugates denoted as MPI-n-BGG were prepared by special chemical binding of corresponding thioisocyanates. MPII-n-BGG were synthetized by acetylation, and MPIII-n-BGG conjugates, by reductive alkylation. Pretreatment of guinea pigs with MPIII-19-BGG, MPII-16-BGG resulted in a stimulatory effect on the subsequent humoral immune response induced by BGG application. A significant suppressive influence was detectable if the animals had been pretreated with MPII-6-BGG and MPI-26-BGG. MPI-13-BGG and MPI-36-BGG had no effect on the later induced anti-BGG antibody formation. The immune response against a second antigen (human serum albumin) was not influenced by this kind of pretreatment of the animals. Therefore it seems justified to conclude that both stimulatory and suppressive effects seen here were antigen specific and that both the method for chemical modification and the number of coupled 6-MP residues are very important for their effectivity.

Agglutination↗

PubMed1976

Analysis of the humoral immune response to influenza virus in vitro.

The induction of in vitro primary and secondary humoral immune responses to influenza virus in murine splenic explant culture is described. Anti-influenza antibody synthesized in vitro was detected and quantitated by a radioimmunoassay which utilized influenza coupled to bromoacetylcellulose. Both in vitro primary and secondary responses could be stimulated over a large range of virus doses. In vitro secondary responses were maximal when spleen donors had been immunized by the parenteral route although secondary type responses could be demonstrated as well after primary immunization by pulmonary infection. In vitro stimulation with influenza virus was relatively insensitive to inhibition at high antigen doses. The results are discussed in terms of the response of other antigens in spleen fragment culture.

Animals↗