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PubMed2005

A possible role for humoral immunity in the pathogenesis of Parkinson's disease.

The pathogenesis of idiopathic Parkinson's disease is unknown, but nigral degeneration and depigmentation are associated with microglial inflammation and anti-inflammatory medications appear to protect against the disease. The possibility that humoral immunity may play a role in initiating or regulating the inflammation has been suggested by experimental studies triggering dopamine cell death using a variety of transfer strategies and the observation of CD8+ T lymphocytes and complement in the nigra in Parkinson's disease. We analysed the association between degeneration and humoral immune markers in brain tissue of patients with idiopathic (n = 13) or genetic (n = 2 with alpha-synuclein and n = 1 with parkin mutations) Parkinson's disease and controls without neurological disease (n = 12) to determine the humoral immune involvement in Parkinson's disease. Formalin-fixed tissue samples from the substantia nigra and primary visual cortex for comparison were stained for alpha-synuclein, major histocompatibility complex II (HLA), immunoglobulin M (IgM), immunoglobulin G (IgG), IgG subclasses 1-4 and IgG receptors FcgammaR I-III. Antigen retrieval and both single immunoperoxidase and double immunofluorescence procedures were employed to determine the cell types involved and their pattern and semiquantitative densities. Significant dopamine neuron loss occurred in all patients with Parkinson's disease, negatively correlating with disease duration (r = -0.76, P = 0.002). Although all patients had increased inflammatory HLA immunopositive microglia, the degree of inflammation was similar throughout the disease (r = 0.08, P = 0.82). All patients with Parkinson's disease had IgG binding on dopamine neurons but not IgM binding. Lewy bodies were strongly immunolabelled with IgG. A mean 30 +/- 12% of dopamine nigral neurons were immunoreactive for IgG in Parkinson's disease with the proportion of IgG immunopositive neurons negatively correlating with the degree of cell loss in the substantia nigra (r = -0.67, P < 0.0001) and positively correlating with the number of HLA immunopositive microglia (r = 0.51, P = 0.01). Most neuronal IgG was the IgG1 subclass with some IgG3 and less IgG2 also found in the damaged substantia nigra. The high affinity activating IgG receptor, FcgammaRI, was expressed on nearby activated microglia. The low affinity activating IgG receptor, FcgammaRIII was expressed on cells morphologically resembling lymphocytes, whereas immunoreactivity for the inhibitory IgG receptor FcgammaRII was absent in all cases. This pattern of humoral immune reactivity is consistent with an immune activation of microglia leading to the targeting of dopamine nigral neurons for destruction in both idiopathic and genetic cases of Parkinson's disease.

Aged↗
PubMed1997

[Inhibition effect of hypoxia on humoral immunity of rats].

To study the effect of hypoxia on humoral immunity function of rat and Ochotona curzoniae (pika), the specific antibody production to novel antigen IgG and immunoresponse to sheep red blood cell (hemolysin forming) were measured. The results show that hypoxia at altitude of 5 km and 7 km for 10 d resulted respectively in 10.3% (P < 0.05) and 21.9% (P < 0.05) decrement in hemolysin formation in rats, as compared with the control group kept at 2.3 km. When the rats were secondarily immunized and kept at the same hypoxia for 10 d, the reduction in hemolysin formation was 4.2% (P < 0.05) and 4.6% (P < 0.05) for the two respective altitudes. These changes, however, were not found in pikas. When rats were immunized two days before hypoxia, 5 km hypoxia for 5 d and 8 d failed to suppress hemolysin formation. Intracerebroventricular (i.c.v.) injection of CRF (1.0 microgram/rat), decreased hemolysin formation and production of IgG by 8.6% (P < 0.05) and 14.0% (P < 0.05) respectively, but intraperitoneal (i.p.) injection of CRF (1.0 microgram/rat) had no effect. On the other hand, i.c.v. injection of CRF receptor antagonist (alpha-helical CRF (9-41), 50 micrograms/rat) prior to 7 km hypoxia caused a hypoxia-induced suppression of IgG production from 24.2% to 12.1% (P < 0.05). Adrenalectomy in rats lowered hemolysin formation by 6.6% (P < 0.05). The above results demonstrate that hypoxia suppresses humoral immunity function and alters initial antigen processing probably through an increase of CRF in the central nervous system.

Altitude↗
PubMed1986

The ontogeny of humoral immunity in rainbow trout, Salmo gairdneri.

The ontogeny of the humoral immune response to a 'thymus dependent' and a 'thymus independent' antigen, human gamma globulin (HGG) and Aeromonas salmonicida (AS) respectively, was investigated in the fry of rainbow trout, Salmo gairdneri, by direct immersion vaccination in the antigens (dose 5 mg/L HGG; 10(8) cells/ml AS; 30 minutes) at known ages/weights from 7 days post hatch, and at 1, 2, 3, and 4 months post hatch. Half the fry in each group were tested for antibodies 4 weeks after vaccination, the remainder were reimmunised and tested again after a further 4 weeks. Appropriate controls to test for tolerance induction and memory responses were included. The results indicate that fry are capable of mounting a humoral immune response very early in ontogeny. There is a period of 'unresponsiveness' which persists for longer against HGG, than against AS, though it was not thought to be tolerance as such. Memory could be detected to HGG in fry given a first immunisation at 2 months. The results are compared with preliminary experiments in which fry were first thymectomised 4 weeks before the first immunisation. In fry thymectomised at 1 month post hatch, and tested for primary and secondary responses at 2 and 3 months, the primary response to HGG is unaltered, but the secondary response is reduced. Both the primary and secondary response to AS is unaltered. When thymectomy is performed later, the effect on the secondary response to HGG is no longer apparent, but the primary response to AS is slightly reduced.

Aeromonas↗
PubMed1996

Interval mapping of quantitative trait loci controlling humoral immunity to exogenous antigens: evidence that non-MHC immune response genes may also influence susceptibility to autoimmunity.

IgG Ab titers elicited to bovine rhodopsin in CFA differ 8- to 10-fold between H2s identical inbred strains A.SW/snJ (high responder) and SJL/snJ (low responder). This variation in IgG Ab titer resulted from a dramatic difference in the rise in Ab titer occurring during the maturation of the T-dependent humoral immune response. To determine the positions of non-MHC genes controlling this quantitative variation in T-dependent humoral immune responsiveness, 206 reciprocal (A.SW/snJ x SJL/snJ)F2 female progeny were immunized and assayed for anti-rhodopsin responsiveness. The genomes of these progeny were screened with 115 polymorphic simple sequence repeat markers covering >90% of the mouse genome. interval mapping analysis localized the positions of these non-MHC immune response genes to genomic intervals on chromosomes 1, 5, and 13. Interestingly, these three intervals coincide exactly with three intervals recently shown to contain genes contributing to susceptibility to systemic lupus erythematosus and/or the production of autoimmune anti-dsDNA Abs. These results suggest that some genes affecting levels of humoral immune responsiveness to exogenous Ag may also play a role in genetic susceptibility to humoral autoimmune diseases. Analyses of the modes of inheritance demonstrated that high responder alleles were inherited from both parental genomes, indicative of epistatic interactions among genes influencing humoral immune responsiveness.

Animals↗
PubMed1980

Humoral immune response in children with iron-deficiency anaemia.

The humoral immune response (as shown by plasma immunoglobulin concentrations and antibody response to diphtheria and tetanus toxoids) was evaluated in 14 children with iron-deficiency anaemia and in 24 normal controls. Mean concentrations of haemoglobin and serum iron and mean transferrin saturation were significantly lower in children with iron-deficiency anaemia than in controls. Serum immunoglobulin concentrations were within the normal range in both groups. Two weeks after immunisation with diphtheria and tetanus toxoids the concentrations of IgG increased significantly in both groups. Antibody titres in iron-deficient children were similar to those of controls before and after immunisation. The mean T-lymphocyte count was significantly lower in iron-deficient children than that in controls, but the mean B-lymphocyte counts were similar in the two groups. These observations suggest that humoral immunity in children is not affected by iron deficiency and that conventional immunisation programmes would be effective in children with iron-deficiency anaemia.

Anemia, Hypochromic↗
PubMed2004

The humoral immune response in viral heart disease: characterization and pathophysiological significance of antibodies.

Several lines of evidence suggest a viral infection as the initiating event for the development of myocarditis (MC). Especially enteroviruses like coxsackie B3 virus have been shown to induce MC in humans and strains of MC-prone mice after an infection. The further course of the disease is, however, determined not only by the viral infection but also by the host's immune system. Both the humoral and the cellular immune system can modify the extent of the damage caused by the disease. The humoral immune system mounts an anti-viral immune response immediately after the infection; however, during the course of the disease, autoantibodies against a variety of different autoantigens emerge. The epitopes recognized by the anti-viral antibodies and those of several autoantibodies have been identified using synthetic peptides. The human disease could be transferred into SCID mice using peripheral blood leukocytes of patients, suggesting a pathophysiological significance of the autoimmune reaction. However, the significance of the humoral immune responses needs to be tested in randomized, prospective studies using immunoadsorption of autoantibodies in patients with inflammatory cardiomyopathy.

Amino Acid Sequence↗
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↗
PubMed2004

Humoral immunity to HIV-1: kinetics of antibody responses in chronic infection reflects capacity of immune system to improve viral set point.

We analyzed the humoral immune response in 46 patients following structured treatment interruption (STI) to investigate the general potential of therapeutic vaccination in chronic HIV-1 infection. Evoked antibody titer increases to glycoprotein 120 (gp120) and p24 were low during 4 short-term STIs and only reached significance during a fifth long-term interruption. Although induction of binding antibodies to viral antigens was not associated with potent suppression of viremia, we observed that individuals with a rapid and high response to p24, and to a lesser extent also to gp120, lowered their viral set points significantly. Of note, the increase of the anti-p24 response correlated with specific CD4 T helper frequency to this antigen. Despite induction of binding antibody responses, which correlated with improved viral control, the increase in neutralizing activity was marginal and did not lead to this enhanced viral suppression. However, a subgroup of patients who potently suppressed viremia independently of STI had significantly higher pre-existing neutralization titers, suggesting a role of humoral immunity in conferring potent protection. In summary, measuring the kinetics of antibody responses provided a marker to validate the responsiveness and capacities of the immune system of HIV-1-infected individuals and reflected the patients' ability to decrease viral set points.

Adult↗
PubMed1993

Gene complementation in biological crosses for humoral immune response to glutamic acid-alanine-tyrosine.

Level of humoral immune response to GAT has been associated with the MHC of chickens. Matings between two unrelated lines of chickens with low antibody response to GAT (G-B1 and S1 Line B19L) resulted in progeny that were higher responders to GAT challenge (P < .05) than either of the parental lines. Progeny of matings between two related sublines that are low responders to GAT (S1 Lines B19L and B1L) had antibody responses to GAT that were not higher than the parental lines. Progeny of the between-line cross were backcrossed to S1 B19L and G-B1 (B13) parental lines, as well as mated inter se. These matings produced F2 progeny whose GAT response was significantly associated (P < .05) with their MHC (Ea-B) type. The progeny were of three MHC types (B19B19, B19B13, and B13B13) that bound 66.6, 71.9, and 4.6%, respectively, of the GAT in a radioimmunoassay. The results from these matings suggest that MHC or MHC-linked genes, as well as genes not linked to the MHC, contribute to control of humoral immune response to GAT in the lines of chicken tested.

Amino Acid Sequence↗
PubMed1984

Humoral immune dysfunction as a result of prenatal exposure to diphenylhydantoin: correlation with the occurrence of physical defects.

The effect of prenatal exposure to diphenylhydantoin (DPH) on postnatal immune function of offspring was studied using a longitudinal experimental design and in vivo immunoassays. Maternal Balb/c mice were dosed by gavage on gestation days 9 through 18 with 0, 20, 40, or 60 mg/kg DPH. Humoral immune function was assessed by measuring the serum antibody levels to type III pneumococcal polysaccharide 5 days after immunization by radioimmunoassay. Cell-mediated immune function was assessed by measuring the delayed-type hypersensitivity response to the contact allergen oxazolone using a micrometer method. A dose-related suppression of humoral immune function was observed in male and female offspring at 25 days but not at 15 weeks of age. Cell-mediated immunity was not affected by prenatal DPH exposure at 25 days or 15 weeks of age. Offspring developed purulent eye exudates at 12 days of age; the incidence and persistence was related to DPH dose. The immunosuppressive effect of DPH on humoral immune function was significantly greater in offspring born with open eye defect than in similarly treated but physically normal offspring. The results suggest that prenatal exposure to DPH may adversely affect the normal development and expression of humoral immune function, particularly in those offspring with other manifestations of DPH's developmental toxicology.

Abnormalities, Drug-Induced↗
PubMed1992

Conserved natural humoral immunity to thyroglobulin in patients with multiple myeloma.

We studied humoral immunity to human thyroglobulin (hTg) during the course of multiple myeloma (MM). In this report, we describe the anti-hTg antibody activity in the sera of patients with MM. Among 63 sera tested, 28 (44%) had IgG anti-hTg autoantibodies (aAb), 16 (25%) exhibited IgM aAb, and six (9%) had IgA anti-hTg aAb. For the majority of sera the anti-hTg autoantibody activity was associated with more than one immunoglobulin class. IgG anti-hTg antibodies were observed in 9/11 patients with IgA MM and in 19/40 patients with IgG MM. The IgM anti-hTG antibody activity was found in the sera of 11 patients with IgG MM. These results show that the anti-hTg activity in these patients is associated with residual polyclonal immunoglobulins. However, in the serum of one patient presenting a double monoclonal gammopathy (IgG and IgA lambda MM), the anti-hTg activity was carried by both the IgG lambda and the IgA lambda molecules, suggesting that in this case the activity was due to the monoclonal immunoglobulin itself. We also studied the epitopic specificity pattern of all these anti-hTg aAb. Only three sera recognized one antigenic region on hTg, suggesting that the majority of the anti-hTg aAb in MM patients were directed against antigenic regions other than those recognized by our panel of murine mAb. In conclusion, our results demonstrated that humoral immunity to hTg is maintained in MM patients. These data contrast with the well-documented suppression of immunity to foreign, especially bacterial, antigens described in MM.

Adult↗
PubMed1981

Murine defense mechanism against Candida albicans infection. I. Collaboration of cell-mediated and humoral immunities in protection against systemic C. albicans infection.

Mice immunized with viable C. albicans cells demonstrated a high incidence of cell-mediated and a low incidence of humoral immune response. There was good agreement between the final survival rate of C. albicans infected mice and the rate of simultaneous cell-mediated and humoral immune response acquisition. Immunized mice with positive delayed hypersensitivity (DTH) against C. albicans crude antigen showed significant protection against intravenous challenge with C. albicans. Furthermore, the transfer of immunoglobulins from rabbit anti-C. albicans serum to DTH-positive mice enhanced protection, while it did not protect control mice against a subsequent challenge with C. albicans. These results suggest that cell-mediated immunity plays a major role and humoral immunity a side role in the defense mechanism(s) of C. albicans infected mice.

Adult↗
PubMedDate not supplied

[Modulation of the humoral immune response in rats by antibodies from the maternal milk].

The influence of specific antibodies of mother's milk on the parameters of humoral immune response and the degree of sensitization to ovalbumin in the progeny was studied in experiments on non-suckling rats. On the second postnatal day lactating rats were immunized subcutaneously with ovalbumin in a dose of 200 micrograms with aluminium hydroxide (10 mg) as adjuvant. On day 22 after birth the young rats which were fed by immunized (test) or intact (control) mothers, received intraperitoneal injections of 100 micrograms ovalbumin. After 8 days the humoral immune response in the young rats was estimated by the number of antibody-forming cells in the spleen, by the count of rosette-forming cells and by the humoral antibody titer. The sensitization degree was evaluated by the titers of reagin antibodies in the passive skin anaphylactic reaction. The number of antibody-forming cells in the spleen of young rats in the test group was 20 times lower as compared to those in the control group. In the test group the humoral antibody titers were suppressed and the sensitization degree was decreased. It has been concluded that the mother's milk antibodies induce immunosuppressive effect on the parameters of the humoral immune response of the progeny and on the degree of their sensitization.

Animals↗
PubMed1986

Humoral immune responses in murine pregnancy. V. Relationship to the differential immunogenicity of placental and fetal tissues.

The nature of the humoral immune response induced in virgin female mice by injections of F1 placental and fetal tissues has been examined and compared to that induced by immunization with F1 adult spleen cells and by multiple allogeneic pregnancy. In a 'responder' strain mouse, as defined by the ability of multiple allogeneic pregnancy to elicit an anti-paternal humoral immune response, both F1 placental and fetal tissues induced the formation of alloantibodies primarily of the IgG1 sub-class, similar to those induced by allogeneic pregnancy, but different from those elicited by adult spleen cells. However, only the placental tissues induced alloantibodies possessing all the characteristics of those appearing in multiparous allogeneic pregnancy. In contrast, the alloantibodies induced by the injected fetal tissue possessed complement-dependent cytotoxic activity, indicating that the inability of pregnancy-induced alloantibodies to mediate cytotoxicity may not be related to their restriction to the IgG1 sub-class. In a 'non-responder' mouse strain, where multiple allogeneic pregnancy does not lead to a maternal alloantibody response, F1 placental tissues, in contrast to fetal and adult tissues, failed to induce a humoral immune response. Injection of F1 placental tissue therefore elicits responses that mimic both the properties and the strain-dependent distribution of the alloantibodies identified in normal murine pregnancy. This implies that the immunogenic stimulus in pregnancy emanates from the placental rather than the fetal compartment of the allogeneic conceptus.

Animals↗
PubMed2001

Characterization of the cellular and humoral immune response to outer surface protein C and outer surface protein 17 in children with early disseminated Lyme borreliosis.

OspC and Osp17 are immunodominant proteins of Borrelia burgdorferi eliciting a clear humoral immune response in adult patients with systemic Lyme disease. In this study, the cellular immune response to B. burgdorferi and the major outer surface proteins OspC and Osp17 was investigated in children during the course of early disseminated B. burgdorferi infection. Lymphoproliferative responses to recombinant proteins were compared to the protein-specific humoral immune reaction. OspC induced a clear antibody response but elicited an even stronger cellular immune response. In contrast, a cellular as well as humoral immune reaction to Osp17 was only rarely detected. Follow-up examinations demonstrated that the lymphoproliferative response to B. burgdorferi and OspC persisted for several months after antibiotic therapy. Here, we show that in early disseminated Lyme disease of childhood, OspC is a potent antigen influencing both the humoral and cellular immunity, while Osp17 plays only a minor role in immune activation.

Adolescent↗
PubMed2000

Humoral immunity against the proline-rich peptide epitope of the IgA1 hinge region in IgA nephropathy.

BACKGROUND: The human IgA1 hinge region is a unique mucin-like O-linked proline-rich glycopeptide, and its core peptide was found to be exposed aberrantly by the underglycosylation in IgA nephropathy (IgAN). We describe here the presence of humoral immunity against the IgA1 hinge peptide epitope in IgAN and evaluate the relationship between the underglycosylation of the IgA1 hinge region and humoral immunity. METHOD: The serum anti-IgA1 hinge peptide antibody (anti-alpha1HP ab) titre was measured and compared between the IgAN (n=37) and control groups (n=34) by enzyme-linked immunosorbent assay (ELISA) using a synthetic peptide corresponding to the human IgA1 hinge region, PVPSTPPTPSPSTPPTPSPS, as an antigen. Next, to evaluate the relationship between the underglycosylation of the IgA1 hinge region and the humoral immunity, the reactivity of the serum IgG from the patients with IgAN against monoclonal IgA1 which had been digested enzymatically to remove the carbohydrates from the IgA1 hinge region was measured by ELISA. RESULTS: The anti-alpha1HP ab titre was significantly higher in the IgAN group than in the control group (OD value: IgG class, 0.564+/-0.344 vs 0. 331+/-0.154, P=0.0014; IgM class, 0.272+/-0.148 vs 0.141+/-0.072, P<0.0001) and it was positive in approximately 40% of the patients with IgAN. In addition, the reactivity of the serum IgG from the IgAN patients against the monoclonal IgA1 was found to be increased as the carbohydrates were enzymatically removed from the IgA1 hinge region (when native=100; asialo, 122+/-9.5; agalacto, 167+/-11.5; naked, 188+/-3.9). CONCLUSION: These results suggested that the peptide epitope of the IgA1 hinge region which was aberrantly exposed by underglycosylation could induce the humoral immune response in IgAN.

Adolescent↗
PubMed2001

Changes in subgingival microflora and humoral immune response following periodontal therapy.

OBJECTIVES: To investigate the effect of scaling and root planing (SRP) on the microflora and humoral immune response in adult periodontitis. MATERIALS & METHODS: Clinical measurements, subgingival plaque samples, gingival crevicular fluid and sera were taken from 4 sites in 28 adult periodontitis patients before and after SRP. Polymerase chain reaction was used to determine the presence of A. actinomycetemcomitans, P. gingivalis, B. forsythus, P. intermedia, and T. denticola. ELISA was used to investigate the systemic and local antibody titres to these organisms, and thiocyanate dissociation for the determination of serum antibody avidity. RESULTS: SRP produced a good clinical improvement. On a subject basis there was little significant change in the microflora. However, on a site basis, there were significant reductions in P. intermedia, B. forsythus and T. denticola. There was little change in systemic and local antibody titres following SRP, although there was a significant reduction in antibody avidity to P. gingivalis and P. intermedia CONCLUSION: Post-therapy clinical improvement was associated with a reduction in bacterial prevalence, but statistical significance was only reached at a site level and this microbial reduction was not significant for all organisms. No significant post-therapy effects on the humoral immune response were noted other than a reduced antibody avidity to P. gingivalis and P. intermedia. The lack of a clear pattern in the humoral immune response may reflect a failure of the host response to produce adequate levels of biologically functional antibodies, and complex interactions between the subgingival flora and the host response.

Adult↗