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Results for “Immunity, Humoral”

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PubMed1992

The humoral immune response to heat shock proteins.

Humoral immune reactions to heat shock proteins (hsp) from microorganisms are one aspect of microbial infections in humans. The production of antibodies which are specific to epitopes present on procaryotic hsp leads also to the appearance of cross-reactive serum antibodies in the host organism that react with human hsp. This article discusses the consequences of such autoreactive antibodies for the host in context with the development of immune tolerance and autoimmune diseases, especially rheumatoid arthritis (RA), and in experimental animal models for arthritis such as adjuvant arthritis in rats. On the basis of epitope cross-reactivity between hsp and other host proteins, a hypothesis is presented for the development of autoimmune disease following the production of hsp-specific antibodies.

Animals↗

PubMed1991

Intrathecal humoral immune reaction in zoster infections.

Intrathecal humoral immune reaction in 26 patients with a reactivation of varicella-zoster virus was analyzed. 11 suffered from ganglionitis, in 7 cases an additional affection of the lower motor neuron was demonstrable. In 8 patients, meningitis, myelitis or cerebral infarctions by zoster angiitis were diagnosed. Intrathecal immune reaction in ganglionitis was weak whereas an intense IgG synthesis became demonstrable in all meningomyelitis/cerebral infarction cases. As demonstrated by immunoblotting, in early stages of the disease immune reaction in serum and cerebrospinal fluid differed only quantitatively. In the further course, most intrathecally synthesized antibodies were directed against low molecular antigens whereas serum pattern did not change. In some patients, additional antibodies not detectable in serum were demonstrable. Though intensity markedly differed, no qualitative differences between the immune response in ganglionitis and more widespread zoster infections of the CNS were detectable.

Antibodies, Viral↗

PubMed1976

[Humoral immunity in human sarcomas].

Studies on humoral immunity were performed in sarcoma patients before, during and after the treatment. Cytotoxic test was carried on with target cells of human mesenchymoma stable line. The activity of serum and its immunoglobulin fractions in 15 patients with soft tissue sarcoma and in 10 patients with congenital sarcoma was studied. It was found that 19S fraction of patient's blood serum contains cytotoxic antibodies. 7S fraction was permanently inactive. The whole serum was cytoloxic before the treatment in 8 of 12 patients with soft tissue sarcoma. Among 20 healthy donors only 3 were active. There was revealed a possibility of strong specific binding of 19S immunoglobulins (and more rarely of 7S immunoglobulins) with target-cells surface. It evidences the capacity of immunoglobulins to render not only cytotoxic action but also presumably, a blocking effect. Irradiation treatment in doses of 1800-9000 rad fail to diminish the cytotoxic activity of the whole serum and its 19S fraction.

Antibodies, Neoplasm↗

PubMed1980

Humoral immunity in malnutrition.

Malnutrition affects the humoral immune system in diverse fashions. B lymphocyte subpopulations, serum IgG, and IgA levels, and immunoglobulin synthesis and metabolism are usually normal or increased. Hypogammaglobulinemia may occur in very young, severely malnourished infant. Although usually normal, deficient antibody responses to injected antigens are occasionally present, depending on the severity of the malnutrition. Serum IgE levels are usually high in malnutrition, probably due both to the increased incidence of intestinal parasites and to the lack of T cell control of IgE. Despite these high IgE levels, allergy is unusual. Secretory IgA levels in the respiratory and gastrointestinal (GI) fluids are generally decreased, as are secretory IgA antibody responses. This local antibody deficiency may increase GI permeability, stimulate immune complex formation, and result in the formation of IgG food antibodies. Breast milk secretory IgA levels are equivalent in malnourished mothers but because of lessened milk volume, the total amount of secretory IgA delivered to their offspring is diminished. Complement levels are somewhat diminished in the presence of malnutrition with a resultant opsonic deficiency. Although these B cell system aberrations undoubtedly contribute to the enhanced susceptibility to infection of malnourished patients, they are usually less severe than are concomitant T cell deficiencies.

Antibody Formation↗

PubMed1976

Cellular and humoral immunity in viral hepatitis.

Cellular and humoral immunity combine to determine the outcome following exposure to hepatitis virus and are implicated in the proposed pathogenetic mechanism for acute and chronic hepatitis. Although antibody to HBsAg is found in virtually all following recovery from hepatitis B, a cell-mediated response to HBsAg can be detected in most patients during the acute phase, and it has been suggested that this may cause the acute hepatic damage by an attack on virus-infected cells. Patients who have chronic active hepatitis also frequently have cell-mediated immunity to HBsAg, regardless of whether the antigen can be detected in their sera; thus, previous exposure to hepatitis B may be important in initiating the disease even in antigen-negative cases. Cell-mediated responses to liver-specific lipoprotein, a membrane antigen, occur transiently in many patients who have acute hepatitis and are persistent in virtually all with untreated chronic active hepatitis. The relative importances and precise mechanisms of these immune responses in the pathogenesis of acute and chronic hepatitis remain to be determined.

Acute Disease↗

PubMed2005

Protective effect of bioactive fraction of Sphaeranthus indicus Linn. against cyclophosphamide induced suppression of humoral immunity in mice.

The bioactive fraction of Sphaeranthus indicus produced dose dependent increase in humoral immunity and delayed type hypersensitivity (DTH) response as evidenced by increased antibody production and increase in paw edema. The activity at higher doses, however, declines. Humoral antibody (HA) titre lowered by cyclophosphamide (CP) (p < 0.05) was enhanced by bioactive fraction at doses of 200 (p < 0.05) and 400 mg/kg (p < 0.001). There was dose dependent increase in HA titre in normal as well as immunosuppressed animals indicating that drug is effective in humoral immunity. Animals treated with cyclophosphamide and receiving bioactive fraction showed significant change in DTH response, which directly correlates with cell-mediated immunity, as compared to cyclophosphamide alone. Thus, it can be observed that a bioactive fraction of Sphaeranthus indicus acts as potentiator of DTH. Furthermore, the HPTLC fingerprint profile of the bioactive fraction was established to facilitate its identification and characterization. The results suggest that bioactive fraction influences both humoral and cell-mediated immunity and offers protection against immunosuppression induced by the cytotoxic agent cyclophosphamide.

Animals↗

PubMed2005

Complement component C3d-antigen complexes can either augment or inhibit B lymphocyte activation and humoral immunity in mice depending on the degree of CD21/CD19 complex engagement.

C3d can function as a molecular adjuvant by binding CD21 and thereby enhancing B cell activation and humoral immune responses. However, recent studies suggest both positive and negative roles for C3d and the CD19/CD21 signaling complex in regulating humoral immunity. To address whether signaling through the CD19/CD21 complex can negatively regulate B cell function when engaged by physiological ligands, diphtheria toxin (DT)-C3d fusion protein and C3dg-streptavidin (SA) complexes were used to assess the role of CD21 during BCR-induced activation and in vivo immune responses. Immunization of mice with DT-C3d3 significantly reduced DT-specific Ab responses independently of CD21 expression or signaling. By contrast, SA-C3dg tetramers dramatically enhanced anti-SA responses when used at low doses, whereas 10-fold higher doses did not augment immune responses, except in CD21/35-deficient mice. Likewise, SA-C3dg (1 microg/ml) dramatically enhanced BCR-induced intracellular calcium concentration ([Ca2+]i) responses in vitro, but had no effect or inhibited [Ca2+]i responses when used at 10- to 50-fold higher concentrations. SA-C3dg enhancement of BCR-induced [Ca2+]i responses required CD21 and CD19 expression and resulted in significantly enhanced CD19 and Lyn phosphorylation, with enhanced Lyn/CD19 associations. BCR-induced CD22 phosphorylation and Src homology 2 domain-containing protein tyrosine phosphatase-1/CD22 associations were also reduced, suggesting abrogation of negative regulatory signaling. By contrast, CD19/CD21 ligation using higher concentrations of SA-C3dg significantly inhibited BCR-induced [Ca2+]i responses and inhibited CD19, Lyn, CD22, and Syk phosphorylation. Therefore, C3d may enhance or inhibit Ag-specific humoral immune responses through both CD21-dependent and -independent mechanisms depending on the concentration and nature of the Ag-C3d complexes.

Animals↗

PubMed2001

Humoral immune response to cruzipain and cardiac dysfunction in chronic Chagas disease.

The humoral immune response to epitopes expressed on cruzipain was evaluated in 31 Chagas disease patients (CDP) with different degrees of cardiac dysfunction. We took advantage of the availability of anti-Trypanosoma cruzi microsomal fraction monoclonal antibodies (MoAbs) reactive with epitopes that are recognized (5A9B11) or not recognized (1A10C11) by CDP sera. The 5A9B11- and 1A10C11-like epitopes are expressed on cruzipain. The reactivity of 5A9B11 against cruzipain was completely inhibited by sera of severe cardiopathy patients while a partial inhibition was found with sera from chagasic patients with mild disease. CDP sera did not block cruzipain recognition by 1A10C11. The antigenic determinants recognized by CDP sera appeared to be linear and carbohydrate free. When the overall anti-cruzipain immune response was evaluated, 70% of CDP with severe disease showed cruzipain titers higher than 1/800 while none of them displayed titers lower that 1/400. This report shows for the first time that the humoral immune response against epitopes expressed on cruzipain appeared to be related with the severity of chronic Chagas disease.

Adult↗

PubMed1986

Inhibition of experimental autoimmune tubulointerstitial nephritis in Brown-Norway rats by (15S)-15-methyl prostaglandin E1. Analysis of the effect of prostaglandin E1 on the induction of the humoral immune response and the elicitation of humorally mediated inflammation.

Brown-Norway (BN) rats develop tubulointerstitial nephritis (TIN) after immunization with bovine tubular basement membrane (TBM) and adjuvants. Daily subcutaneous injections (either on Days 0-7 or Days 0-14) of (15S)-15-methyl prostaglandin E1 (M-PGE1) at a dose of 1 mg/kg/day markedly inhibited or completely abrogated the development of both the acute polymorphonuclear (Day 10) and the subsequent mononuclear (Day 14) inflammatory phases of BN rat TIN. Circulating anti-TBM antibody in Days 0-7 M-PGE1-treated rats was moderately diminished on Day 8 after immunization but not on Day 14. Circulating anti-TBM antibody in Days 0-14 M-PGE1-treated rats was only slightly diminished on Day 14. In experiments to test the effect of M-PGE1 on the elicitation phase of humorally mediated inflammation, M-PGE1 inhibited the acute inflammatory response observed 6 hours after intradermal injection of particulate TBM into TBM-sensitized BN rats. The inflammation in these skin tests was demonstrated by passive transfer experiments to be humorally mediated. The inhibition of acute humorally mediated intradermal inflammation was not attributable to neutropenia, because M-PGE1 caused a significant neutrophilia as demonstrated by peripheral blood smears. Although the inhibition of TIN in Days 0-14 M-PGE1-treated rats may have been due, in part, to dysfunction of the elicitation phase of humorally mediated inflammation, the inhibition of TIN in Days 0-7 M-PGE1-treated rats was more likely secondary to the diminished induction of either humoral or cellular immunity.

Alprostadil↗

PubMed1986

Humoral immune response of asymptomatic cats naturally infected with feline leukemia virus.

The humoral immune response of cats that were naturally infected with the feline leukemia virus (FeLV) was examined after antigenic stimulation with the synthetic antigen poly(L-Tyr, L-Glu)-poly(DL-Ala)-poly(L-Lys). The primary humoral antibody response in FeLV-infected cats was both delayed and greatly reduced, compared with that seen in uninfected control cats. A similar discordance was observed after secondary stimulation with the antigen, in the FeLV-infected cats had both a delayed response and a reduced response, compared with uninfected cats. The levels of total immunoglobulins of the immunoglobulin G and immunoglobulin M classes in the sera of FeLV-infected cats were significantly higher (two- and threefold, respectively) than were those of the uninfected control animals. The presence of an impaired humoral immune response to newly presented antigens in the presence of elevated immunoglobulin levels has been thoroughly documented in the case of people with the acquired immunodeficiency syndrome. This further emphasizes the potential value of FeLV-infected cats as a model for human acquired immunodeficiency syndrome.

Acquired Immunodeficiency Syndrome↗

PubMed1985

Modulation of humoral immune response to influenza vaccines by BCG.

BCG-induced modulation of humoral immune response to influenza vaccines was studied on adult volunteers and laboratory animals. Three influenza vaccine types were used: inactivated whole-virion vaccine prepared by chromatography, chemically split adsorbed vaccine and live allantoic vaccine for intranasal vaccination. According to the indices of humoral immunity against influenza such as seroconversion, frequency and intensity of antibody formation and degree of protection to subsequent administration of the vaccine virus, the BCG vaccine had a marked immunomodulating effect in combination with the adsorbed chemically split vaccine. The effect was slight in the case of the whole-virion vaccine and was absent with the live attenuated vaccine.

Adolescent↗

PubMed1994

Nucleotide actions on humoral immune responses.

Previous studies indicate the importance of dietary nucleotides in maintaining optimal cellular immunity. Our studies using murine spleen cells showed that polynucleotides significantly increase in vitro antibody production in response to T-cell-dependent antigen. They seem to exert actions on T-helper cells at antigen presentation, perhaps during cognitive cell-cell interactions. They do not augment the actions of cloned, antigen-specific, activated T-helper cells, nor do they increase antibody production in response to T-cell-independent antigen or polyclonal B-cell activation. Polynucleotides increase in vitro human immunoglobulin production in response to T-cell-dependent stimuli and antigen. Humoral immune responses to T-cell-dependent antigen were depressed in mice fed a nucleotide-free diet, but were restored by a mononucleotide-nucleoside mixture. Responses to T-cell-independent antigen remained intact in these mice. The mononucleotide-nucleoside mixture had no effect on in vitro antibody production and did not further increase humoral immune responses in mice fed regular lab chow. These results suggest that the in vivo actions of polynucleotides on humoral immune responses may reflect local immune responses, perhaps at the site of inflammation. Mononucleotides and nucleosides may be incorporated into the tissue nucleotide pool fairly rapidly in a state of relative nucleotide deficiency and help restore T-cell-dependent humoral immune responses. Our findings may further support the importance of dietary nucleotides.

Animals↗

PubMed1990

[Study of the phases of development of humoral immune response].

In previously performed investigations to make clinical immunological diagnosis the principle of humoral immune response division into phases was put forward. The phases of humoral immune response were determined with lower content of immunoglobulins.

Antigen-Antibody Complex↗

PubMed1985

The role of porto-systemic shunts in the specific humoral immune response in patients with schistosomal hepatic fibrosis.

The present study was devoted to elucidate the role of collaterals (porto-systemic shunts) in the specific humoral immune response to schistosomal soluble egg antigen (SEA) in patients with schistosomal hepatic fibrosis (SHF). Twenty five patients with SHF with collaterals, ten patients with SHF without collaterals and twenty healthy control subjects constituted the material of this study. In vivo and in vitro tests for humoral immunity to SEA included serum immunoglobulins estimation, immediate intradermal test, indirect haemagglutination test and determination of B lymphocytes count in peripheral blood. Significant differences have been observed between cases without collaterals and those with collaterals; and in the latter group before and after decongestion. These results tend to consolidate the view of the role of collaterals in schistosomal antigenemia and subsequent humoral immune response.

Adult↗

PubMed2005

Impact of pregnancy-related heart failure on humoral immunity: clinical relevance of G3-subclass immunoglobulins in peripartum cardiomyopathy.

BACKGROUND: The impact and clinical relevance of pregnancy-related heart failure (HF) on humoral immunity are not known. Heart failure is often characterized by immunoglobulins (Ig) that differ in subclass profile with etiology. Subclass immunoglobulins differ in the biologic information they confer in disease. Therefore, given that progressive gestation is associated with immunologic incompetence, we sought to study the relative impact of pregnancy-related onset of HF on humoral immunity. METHODS: Immunoglobulins (class G and subclasses G1, G2, G3) against cardiac myosin were evaluated in 47 patients with peripartum cardiomyopathy (PPCM) from different global regions: South Africa (n = 15), Mozambique (n = 9), and Haiti (n = 23) and compared with healthy mothers and patients with idiopathic dilated cardiomyopathy (DCM). C-reactive protein, tumor necrosis factor-alpha, and Fas-Apo-1 were also studied in PPCMs. RESULTS: All PPCM groups were similar in Ig profiles. The immunoglobulins, frequencies and reactivities, were markedly and nonselectively raised in PPCM patients compared with DCM. Immunoglobulin frequencies in PPCMs, Haiti: G1 58%, G2 66%, G3 54%; Mozambique: G1 77%, G2 66%, G3 66%; and South Africa: G1 47%, G2 53%, G3 53%, were higher compared with DCMs from South Africa (n = 24): G1 8%, G2 8%, G3 21%, or the United Kingdom (n = 68): G1 10%, G2 8.8%, G3 22% (P < .0001). Hence, unlike the selective up-regulation of immunoglobulins of the G3 subclass (IgG3s) in DCM, class G and all subclass immunoglobulins were raised in PPCM. Of the serological variables, IgG3s (immunoglobulins with proinflammatory characteristics) discriminated NYHA functional status at diagnosis. IgG3-positive patients were in a higher NYHA class at initial presentation (P < .05). CONCLUSIONS: Immunoglobulin subclass profiles in patients with HF differ with etiology. Unlike DCM, the impact of pregnancy-related HF on humoral immunity is not subclass-restricted. However, raised levels of IgG3s may be of prognostic value in clinical PPCM.

Adult↗

PubMed2004

Incomplete humoral immunity against hepatitis C virus is linked with distinct recognition of putative multiple receptors by E2 envelope glycoprotein.

Little is known about the role of the humoral immune response to hepatitis C virus (HCV). This study provides molecular evidence for the mechanism by which neutralizing Abs from the sera of chronic HCV patients have lower inhibitory activities against the binding of HCV E2 envelope protein to human hepatoma cell lines than to a lymphoma cell line. E2 binds to several putative receptors, specifically human CD81; human scavenger receptor, class B, type 1; and heparan sulfate. We have shown that E2 binds to target cells via these receptors in a noncompetitive manner. Thus, incomplete inhibition of one of the receptors leads to only a partial E2 blockade and, possibly, evasion of the host immune response. We demonstrated that the difference in and reduction of inhibition was closely related to impaired blockade of E2 binding to scavenger receptor, class B, type 1, and heparan sulfate. We have also shown that soluble E2 protein binds to multiple soluble receptors via separate binding domains on E2, providing further evidence for the distinct recognition of multiple cellular receptors by E2. This report suggests a novel finding that biased humoral immune responses to HCV E2 might provide an alternative mechanism for viral escape without the involvement of mutation. Additionally, our data give crucial consideration to the development of HCV vaccines that stimulate protective humoral immune responses.

Antigens, CD↗

PubMedDate not supplied

Effect of beta carotene on disease protection and humoral immunity in chickens.

The effect of beta carotene on disease protection and humoral immunity in chickens was investigated in comparison with the effect of other lipid-soluble antioxidant vitamins, vitamin E and A, which are both proven immunoenhancers and contributors to disease protection. Beta carotene alone was not as effective as either vitamin in protecting chickens from Escherichia coli infection, nor did it significantly enhance humoral immunity. In combination with vitamin E, however, beta carotene significantly increased disease protection and reduced hepatomegaly caused by E. coli infection.

Agglutination Tests↗

PubMed1990

[The role of T-lymphocytes in the development of a humoral immune response to the corpuscular antigen of Staphylococcus aureus].

The dependence of humoral immune response and the formation of immunological memory to corpuscular staphylococcal antigen (CSA) on the T-system of immunity was studied in experiments on B-mice and on mice with the congenital absence of the thymus (nude). Primary and secondary immune response to CSA in athymic mice was found to be considerably less than in normal animals. After the repeated immunization of genetically athymic mice the pronounced secondary reaction of the formation of antibodies to CSA was observed. As shown in this investigation carried out with the use of adoptive transfer techniques, the induction of memory B-cells to CSA may occur in animals with congenital or experimentally induced T-immunodeficiency. The conclusion was made on the T-dependence of humoral immune response to CSA, the formation of immunological memory to this antigen being relatively T-independent.

Animals↗