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Results for “Humoral immune response”

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PubMed1980

Interactions of glucocorticoids and heparin on the humoral immune response of mice.

Interactions of glucocorticoids and heparin on the humoral immune response of mice to SRBC have been studied. Heparin injected subcutaneously in a depot-form 2 hours before immunization restores the antibody-forming ability of mice immuno-suppressed by hydrocortisone, through pretreatment of mice only with heparin 3 days before immunization decreases the PFC-count in the spleen. Cortisone (ip) and heparin (sc) per se injected at about the time of immunization with suboptimal doses of SRBC resulted only in a slight stimulating or no effect on spleen PFC count and serum antibody level. Cortisone and heparin applied in combination, however, exerted a stimulatory effect on the humoral immune response to SRBC. The route of steroid administration pointed to the significance of macrophages in this phenomenon. As the cooperative effect of heparin + cortisone on the humoral immune response shows a good correlation with their cooperative effect on in vivo (3H)dThd incorporation and thymidine kinase activity of spleen, it was hypothesized that an in vivo mitogenic activity for the spleen cells was responsible for the adjuvant effect observed.

Animals↗
PubMed1990

Cell-mediated and humoral immune response in diabetic patients with periodontitis.

Cell-mediated and humoral immune responses were assessed in 50 patients with type II or non-insulin-dependent diabetes mellitus and 50 nondiabetic patients with periodontitis. The values were compared with those of 50 age and sex-matched control subjects. The cell-mediated immunity assessed by enumerating the total and high-affinity rosette-forming cells of the patient did not show any significant variation from that of the normal control subjects. The humoral immune response was assessed by estimating serum immunoglobulins G, A, M, D, and E by single radial immunodiffusion. Except IgD, all other immunoglobulins were found to be elevated significantly in both diabetic and nondiabetic subjects. The alteration in humoral immune response may be the cause or the effect of periodontitis. The defective host response reported in diabetic patients may be responsible for the increased incidence of periodontitis in diabetic patients as compared to nondiabetic patients.

Adult↗
PubMed1997

Influence of stress on DDT-induced humoral immune responsiveness in mice.

The effects of different durations/intensities of stress on DDT-induced modulation of humoral immune response were evaluated in mice. DDT (20, 50, or 100 ppm x 4 weeks) per se did not influence the primary antibody response to sheep red blood cells (SRBC). However, when DDT-pretreated mice were exposed to single and multiple sessions of restraint stress (RS), the anti-SRBC antibody titers were lower than the control values, the most prominent effects being seen after 50 and 100 ppm DDT exposure in combination with a single intense stressor (24 hr RS) or repeated stress (1 hr RS x 5). In the splenic plaque forming cells (PFC) assay, similar potentiations of DDT-induced immune suppression were seen at 50 and 100 ppm exposure levels in combination with 24 hr RS or 1 hr RS (x5) procedures. In addition, the 20 ppm DDT exposure effect was also potentiated in combination with the multiple RS model. Further, other forms of stress viz. 3 hr cold restraint stress (CRS) or 6 hr RS, which per se did not influence the antibody titer or PFC response, suppressed humoral immune responses, when combined with 100 ppm DDT exposure. These results are discussed in light of the possible interactions between physical/emotional and environmental/xenobiotic stressors in the regulation of humoral immune response.

Animals↗
PubMed1998

Preliminary studies on humoral immune response of sheep to wohlfahrtiosis.

The humoral immune response of sheep to wohlfahrtiosis was studied. An enzyme-linked immunosorbent assay was developed to compare four different types of antigens obtained from the third-stage larvae of Wohlfahrtia magnifica. The antigen prepared from salivary glands detected a humoral response in all 35 infested sheep and was more specific in the ELISA than cuticular, intestinal or whole larval antigens. The level of the humoral response in sheep to wohlfahrtiosis differed according to the location of the wounds.

Animals↗
PubMed1986

The role and mechanism of cobra venom factor-induced suppression of the humoral immune response in guinea pigs.

The cobra venom factor (CVF)-mediated suppression of the humoral immune response to bacteriophage phi X 174, a T cell-dependent antigen, was investigated in guinea pigs. The suppression was markedly dependent on the amount of antigen used: decomplementation of animals diminished the humoral immune response when immunizing with low doses of antigen, whereas increasing the antigenic dose resulted in little or no diminution by CVF. In contrast to the results with normal animals, CVF had no influence on the humoral immune response of genetically C2-deficient guinea pigs; i.e., no suppression occurred above that due to the inherited complement deficiency state alone. We therefore postulate that CVF suppresses the humoral immune response by the depletion of C3, with no measurable role for complement split products under these experimental conditions.

Animals↗
PubMedDate not supplied

Cell-mediated and humoral immune response in various vascular diseases.

Cellular and humoral immune reactions were studied in patients with myocardial infarction, arteriosclerosis obliterans and superficial thrombophlebitis. Antigens were prepared from human aortic wall with lipid plaques and from vena cava tissue. Migration of leukocytes was inhibited and both DNA-synthesis and antibody production were increased in all groups of patients. No immune reaction could be observed in the controls. A cross-reactivity between aortic and vascular extracts was detected by the leukocyte migration test and by the passive hemagglutination technique, while the induction of DNA-synthesis proved to be specific. Investigating the time-kinetics of cellular and humoral immune response, cellular immune reactions were found to be still present long after the appearance of humoral antibodies.

Antibody Formation↗
PubMed1990

ABO-incompatible kidney transplantation (A2 to O). Qualitative and semiquantitative studies of the humoral immune response against different blood group A antigens.

The humoral immune response against blood group A antigens with different core saccharide structures has been investigated in four blood group O recipients transplanted with kidneys from two blood group A2 donors. Radioimmunoassay and thin-layer chromatogram binding assay studies showed that different individuals responded differently to the same antigenic stimulus. Antibodies were produced in the recipient that bound to the terminal trisaccharide of the blood group A antigens. In some cases antibodies that bound to a larger antigen epitope, including the fourth and fifth sugar in the polysaccharide core chain, also occurred. Immunoglobulin class-specific, as well as subclass specific, responses were seen. The antibody response in the blood group O recipients receiving an A2 graft seem to be dependent on the antigenic expression in the transplanted kidney. In view of the recent findings of individuality of A antigen expression in kidneys within the A1 and A2 subgroups, an extended typing of A2 donors may be important. The humoral immune response in the recipient may also be dependent on earlier contacts with ABO incompatible pregnancies, vaccinations, or infections. A possible correlation between pre- and posttransplant findings was noted in one case and deserves further notice.

ABO Blood-Group System↗
PubMed1989

The time course of the humoral immune response to rhinovirus infection.

The specific humoral immune response of 17 volunteers to infection with human rhinovirus type 2 (HRV-2) has been measured both by neutralization and by ELISA. Six volunteers who had HRV-2-specific antibodies in either serum or nasal secretions before HRV-2 inoculation were resistant to infection and illness. Of the remaining 11 volunteers who had little pre-existing HRV-2-specific antibody, one was immune but 10 became infected and displayed increases in HRV-2-specific antibodies. These antibodies first increased 1-2 weeks after infection and reached a maximum at 5 weeks. All six resistant volunteers who had high pre-existing antibody and eight of the volunteers who became infected maintained their HRV-2-specific antibody for at least 1 year. At this time they were protected against reinfection. Two volunteers showed decreases in HRV-2-specific antibodies from either serum or nasal secretions. They became infected but not ill after HRV-2 inoculation 1 year later.

Adult↗
PubMed1981

Humoral immune response in vitamin A deficient children.

Humoral immune response was evaluated in children with vitamin A deficiency. The percentage of B lymphocytes and the initial levels of plasma IgA, IgG and IgM were normal. Two weeks after the immunisation with diphtheria and tetanus toxoids, there was a marked increase in the antibody titers. There were no significant differences between the deficient and the normal children. The results indicate that the antibody production is not altered in children with vitamin A deficiency.

Antibody Formation↗
PubMed1998

Analysis of the humoral immune response to Chlamydia outer membrane protein 2.

The humoral immune response to Chlamydia outer membrane protein 2 (Omp2) was studied. Omp2 is a highly genus-conserved structural protein of all Chlamydia species, containing a variable N-terminal fragment. To analyze where the immunogenic parts were localized, seven highly purified truncated fusion proteins constituting different regions of the protein were produced (Chlamydia pneumoniae-Omp2aa23-aa93, Chlamydia psittaci-Omp2aa23-aa94, and Chlamydia trachomatis-Omp2aa23-aa84, aa87-aa547, aa23-aa182, aa167-aa434, aa420-aa547). By an enzyme-linked immunosorbent assay with serologically defined patient sera, Omp2 was found to be a major immunogen of both C. pneumoniae and C. trachomatis infections (P < 0.0001). The humoral immune responses were not confined to any particular region of the Omp2 protein, and no species-specific anti-Omp2 immunoglobulins were detected.

Antibodies, Bacterial↗
PubMed2006

A comparison of regional and systemic humoral immune responses to a nematode infection.

The kinetics of humoral immune response against Trichinella spiralis (TS) was characterized with immunofluorescence assay. The mesenteric lymph nodes (MLN) and the spleen of infected rats were examined for concurrent expression of multiple antibody (Ab) isotypes from day 1 to day 15 after infection. The tissues were processed and stained with either a pan-B cell marker (OX33) conjugated with rhodamine (XRITC) or combinations of dual monoclonal Ab probes plus A secondary Ab conjugated with XRITC or fluorescein (FITC). As compared to the uninfected controls, the spleen and the MLN showed significant proliferation of dual-Ab expressing B cells (Debc) on days 5 and 7, respectively. During the immune response, only minimal numbers of B cells expressed single Ab isotype while most B cells expressed more than one isotypes of Ab. When combining all the numbers of Debc within each tissue for each respective days, and comparing those numbers with the total numbers of B cells that were OX33+ in the serial sections of the same tissue specimens, the combined Debc in the spleen were > 6 times higher than the OX33 labeled B cells on day 10, and the Debc in MLN were > 3 times higher than the OX33+ B cells on day 10. Our results thus indicate that the Debc most likely expressed more than two Ab isotypes during the peak days of the humoral immune response to the parasite and this phenomenon occurred in both regional and systemic lymphoid tissues.

Analysis of Variance↗
PubMed1994

Specific and nonspecific aspects of humoral immune response in leprosy.

1. We have studied some generic and specific aspects of the humoral immune response in 96 patients with leprosy (29 paucibacillary and 67 multibacillary individuals). We determined serum immunoglobulins (IgM, IgG and IgA), CH50, C1q, C3 and C4, circulating immune complexes (CIC), C-reactive protein (CRP), rheumatoid factor (RF) and antinuclear antibodies. No specific pattern of general humoral immune changes could be observed. 2. The specific immune response was studied by the detection of specific IgM anti-M. leprae antibodies. An immunoradiometric assay (IRMA) and an ELISA were compared for clinical effectiveness. IRMA showed greater sensitivity for the serodiagnosis of leprosy as compared to ELISA (88.1% vs 58.2% for multibacillary patients and 20.7% vs 10.3% for paucibacillary leprosy patients). Specificity was 96% for IRMA and 97% for ELISA. 3. Our results indicate that nonspecific changes in the humoral immune response are of little value in assessing leprosy patients and that immune assays for the detection of specific anti-M. leprae antibodies may be of value in the diagnosis, study and follow-up of these patients.

Adolescent↗
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↗
PubMed1985

Influence of genetically inherited complement deficiencies on humoral immune response in guinea pigs.

To assess the role of complement in the induction of the humoral immune response, we studied the antibody response of guinea pigs genetically deficient in the second component of the classical complement pathway (C2D-GP) to bacteriophage phi X 174--a T cell-dependent antigen--in comparison with normal guinea pigs and C4D-GP, for which a disturbance in induction of antibody response has been described. We were able to establish a clear dose-response relationship: with low doses of antigen (1 X 10(9) PFU/kg), the antibody response of both complement-deficient strains was grossly impaired as compared with normal guinea pigs. After primary immunization, the peak antibody titer was diminished (1 log10) and declined rapidly; after secondary immunization, the diminution became even more distinct. Both complement-deficient strains had unusual secondary antibody responses almost identical to their primary ones, and amplification of antibody titer, as well as regular isotype switch from IgM to IgG, was absent. By increasing the antigen dose (2 X 10(9) PFU/kg), the antibody responses of the complement-deficient guinea pigs tend to normalize, and when high doses of antigen (1 X 10(10) PFU/kg) were used, the behavior of the complement-deficient animals was nearly indistinguishable from that of normal animals. Partial restoration of the immune response was seen when substituting the genetic complement deficiency by giving serum as source of the missing complement component. The important contribution of the C2 deficiency is given by the now compelling evidence that it is not the missing individual component itself, but rather the common block in sequential activation of C3 via the classical pathway in both complement deficiencies, that is responsible for the impaired humoral immune response, especially at low antigen doses. We therefore postulate that an intact classical pathway contributes to reaching a normal humoral immune response.

Animals↗
PubMed1995

Principle of the bark of Phellodendron amurense to suppress the cellular immune response: effect of phellodendrine on cellular and humoral immune responses.

Previously we have isolated the quaternary base alkaloids, magnoflorine and phellodendrine, from Phellodendri Cortex (cortex of Phellodendron amurense Rupr., Rutaceae) as the biologically active principles to suppress local graft-versus-host (GvH) reactions in mice. In this paper, we focus on phellodendrine. Phellodendrine suppressed local semisyngeneic GvH reactions and systemic allogeneic GvH reactions in X-ray irradiated recipient mice. Phellodendrine also suppressed the induction phase of sheep red blood cell (SRBC)-induced delayed type hypersensitivity in mice and tuberculin-induced delayed type hypersensitivity in guinea pigs, but did not suppress the effector phase of these reactions. Surprisingly, phellodendrine, unlike prednisolone and cyclophosphamide, did not affect antibody production in mice to SRBC. Phellodendrine was expected to be a valuable new type of immunosuppressor against the cellular immune response.

Animals↗
PubMed1998

Humoral immune response to p53 in malignant glioma.

p53 immunoreactivity and humoral immune response to p53 were examined in 14 patients with malignant glioma, including 4 patients with leptomeningeal glioma cell dissemination. Twelve patients expressed p53 protein within the tumour tissue. p53 antibodies were detected in the serum in 2 of 14 patients but never in the cerebrospinal fluid (CSF). Soluble p53 protein was detected neither in serum nor in CSF of the glioma patients. CSF levels of the immunosuppressive cytokine, transforming growth factor (TGF)-beta, were elevated in the glioma patients, including those with a humoral response to p53. These preliminary findings raise the possibility of systemic humoral immune responses to antigens, including mutant p53, expressed by glioma cells in the central nervous system.

Adult↗
PubMed1987

Humoral immune response of foals to experimental infection with Rhodococcus equi.

Humoral immune response to Rhodococcus equi in experimentally infected foals was studied with the enzyme-linked immunosorbent assay (ELISA) method. Class-specific antibodies were measured by ELISA in the sera of foals after intratracheal or oral inoculation with R. equi ATCC 6939 or T 48 and in the lung washings of a foal after intratracheal inoculation or of normal horses. After intratracheal or oral inoculation with R. equi, serum antibodies were first detected in immunoglobulin G (IgG) followed by IgM and IgA classes, but significant levels of IgM and IgA developed only in the foal infected intratracheally with R. equi T 48. Only the foal infected intratracheally with T 48 developed pneumonia. Anti-R. equi IgG and IgA antibodies appeared in lung washings of the intratracheally infected foal. There were differences in the antibody response to R. equi among the intratracheally infected foals, the orally infected foal and the naturally infected foal. These results suggest that the humoral immune response to R. equi may be affected by the type of R. equi strain and the route and extent of R. equi exposure.

Actinomycetales Infections↗