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Results for “Immunity, Humoral”

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PubMed1987

Protein transfer at the blood cerebrospinal fluid barrier and the quantitation of the humoral immune response within the central nervous system.

The cerebrospinal fluid (CSF)/serum concentration quotients of albumin and the immunoglobulins G, A and M have been determined for 396 patients with a normal blood CSF barrier function or a pure barrier impairment without a humoral immune response within the central nervous system. The ratios between the concentration quotients of the three immunoglobulins and that of albumin increase in a nonlinear fashion with progressive impairments of the blood CSF barrier, i.e. the molecular size dependent discrimination of the protein transfer ('selectivity') decreases. The upper reference values of the concentration quotients for the whole range of passive transfer comply with the hyperbolic function: Q(IgX) = a/b square root Q(Alb)2 + b2 - c with different constants a/b, b2, c for IgG (0.8, 15 X 10(-6), 1.8 X 10(-3), IgA (0.72, 80 X 10(-6), 5.1 X 10(-3) and IgM (0.65, 150 X 10(-6), 7.5 X 10(-3). With these discriminatory functions the locally synthesized fractions IgX(loc) of IgG, IgA and IgM in CSF can be calculated by the general formula: IgX(loc) = [Q(IgX) - a/b square root Q(Alb)2 + b2 + c] X IgX(Ser).

Albumins↗

PubMed2000

Modulation of humoral immune responses in the rat by centrally applied Met-Enk and opioid receptor antagonists: functional interactions of brain OP1, OP2 and OP3 receptors.

We have previously demonstrated that central application of leucine-enkephalin (Leu-Enk) elicits potentiation and suppression of humoral immune responses through OP(1) (delta) and OP(2) (kappa) receptors, respectively. Interestingly, both effects were found to be additionally dependent on OP(3) (mu) receptor function. In the present study, we have further investigated whether opioid receptor interactions underlie the immunomodulatory effects of endogenous opioids as well as exogenously applied methionine-enkephalin (Met-Enk). For that purpose, the plaque-forming cell (PFC) response was determined in rats injected intracerebroventricularly (i.c.v.) with opioid receptor-selective antagonists and Met-Enk. Application of the OP(1) antagonist ICI 174864, but not naltrindole, resulted in suppression of the PFC response. In contrast, i.c.v. injection of the OP(2) selective antagonist nor-binaltorphimine (nor-BNI) significantly potentiated the PFC response. Both effects, presumably mediated by endogenous opioid peptides, were antagonized by the OP(3) receptor antagonist beta-funaltrexamine (beta-FNA) at a dose that was devoid of immunomodulatory activity. The immunopotentiation of the PFC response induced by Met-Enk was reversed by OP(1) receptor antagonists, naltrindole and ICI 174864, but not by beta-FNA or nor-BNI. On the basis of these and previous findings, it may be concluded that central OP(3) receptors are permissive for the central immunomodulatory action of endogenous opioid peptides and Leu-Enk. In contrast, the central immunoenhancing effect of Met-Enk appears to be mediated through OP(3)-independent OP(1) receptors.

Adjuvants, Immunologic↗

PubMed1996

Markedly impaired humoral immune response in mice deficient in complement receptors 1 and 2.

Complement receptor 1 (CR1, CD35) and complement receptor 2 (CR2, CD21) have been implicated as regulators of B-cell activation. We explored the role of these receptors in the development of humoral immunity by generating CR1- and CR2-deficient mice using gene-targeting techniques. These mice have normal basal levels of IgM and of IgG isotypes. B- and T-cell development are overtly normal. Nevertheless, B-cell responses to low and high doses of a T-cell-dependent antigen are impaired with decreased titers of antigen-specific IgM and IgG isotypes. This defect is not complete because there is still partial activation of B lymphocytes during the primary immune response, with generation of splenic germinal centers and a detectable, although reduced, secondary antibody response. These data suggest that certain T-dependent antigens manifest an absolute dependence on complement receptors for the initiation of a normally robust immune response.

Animals↗

PubMedDate not supplied

High concentrations of interleukin-2 selectively suppress T-cell dependent humoral immune responses.

The recent therapeutic application of immunoregulatory cytokines, most notably the T-cell growth factor, interleukin-2 (IL-2), marks the advent of a new class of pharmacologic agents. In the present studies the effects of exogenous IL-2 on in vitro humoral immune responses in spleen cells isolated from female B6C3F1 mice were investigated. In vitro direct addition of low concentrations of rmIL-2 (25 U/ml) to naive spleen cells induced a moderate enhancement of the T-cell dependent antibody forming cell (AFC) response to sRBC. Similarly, low concentrations of rmIL-2 (10-50 U/ml) enhanced T-cell independent AFC responses to DNP-Ficoll and LPS. Interestingly, high concentrations of rmIL-2 (100 or 250 U/ml) selectively suppressed the T-cell dependent AFC response but not T-cell independent AFC responses to either DNP-Ficoll or LPS. Neither immunoenhancing (25 U/ml) nor immunosuppressive (200 U/ml) concentrations of rmIL-2 altered the kinetics of the sRBC response. Temporal addition studies indicated that high concentrations of rmIL-2 (200 U/ml) were only inhibitory when added to the cultures during the first 24 h following antigen sensitization. Conversely, a significant enhancement of the response was observed when 200 U/ml rmIL-2 was added 48 h following antigen sensitization. These results are in agreement with previous reports that the presence of high concentrations of IL-2 render T-cells unresponsive to subsequent antigen stimulation but that the high concentrations of IL-2 enhance immune responses when added at 48 h following antigen sensitization.

Animals↗

PubMed2007

SAP regulation of follicular helper CD4 T cell development and humoral immunity is independent of SLAM and Fyn kinase.

Mutations in SH2D1A resulting in lack of SLAM-associated protein (SAP) expression cause the human genetic immunodeficiency X-linked lymphoproliferative disease. A severe block in germinal center development and lack of long-term humoral immunity is one of the most prominent phenotypes of SAP(-) mice. We show, in this study, that the germinal center block is due to an essential requirement for SAP expression in Ag-specific CD4 T cells to develop appropriate follicular helper T cell functions. It is unknown what signaling molecules are involved in regulation of SAP-dependent CD4 T cell help functions. SAP binds to the cytoplasmic tail of SLAM, and we show that SLAM is expressed on resting and activated CD4 T cells, as well as germinal center B cells. In addition, SAP can recruit Fyn kinase to SLAM. We have now examined the role(s) of the SLAM-SAP-Fyn signaling axis in in vivo CD4 T cell function and germinal center development. We observed normal germinal center development, long-lived plasma cell development, and Ab responses in SLAM(-/-) mice after a viral infection (lymphocytic choriomeningitis virus). In a separate series of experiments, we show that SAP is absolutely required in CD4 T cells to drive germinal center development, and that requirement does not depend on SAP-Fyn interactions, because CD4 T cells expressing SAP R78A are capable of supporting normal germinal center development. Therefore, a distinct SAP signaling pathway regulates follicular helper CD4 T cell differentiation, separate from the SLAM-SAP-Fyn signaling pathway regulating Th1/Th2 differentiation.

Animals↗

PubMed1999

Humoral immune responses among mucosal and cutaneous leishmaniasis patients caused by Leishmania braziliensis.

Mucosal leishmaniasis is arguably the most morbid sequelae of cutaneous leishmaniasis. The importance of early diagnosis for effective therapy, coupled with the difficulty of diagnosing the disease parasitologically, prompted this investigation of humoral immune markers of mucosal disease. Promastigote soluble antigens of Leishmania braziliensis, isolated from cutaneous and mucosal lesions, were separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis; antigens were identified by immunoblotting with parasite-specific IgG antibody-positive sera of patients with mucosal disease (n = 18) and cutaneous disease (n = 23). For antigens of the cutaneous parasite WR 2095, mucosal sera generally reacted intensely to antigens of 75, 66, and 45 kDa and weakly to 48-50-kDa antigens, whereas cutaneous sera generally detected weakly the first 3 antigens and intensely the latter doublet. The data suggest that the transition from the cutaneous antigenic profile to a mucosal antigenic profile could be used to predict mucosal disease in approximately half of mucosal patients. An additional finding was that antibodies present in the sera of patients with mucosal disease labeled a 66-kDa peptide of normal human lip mucosa more intensely than did cutaneous sera. Autoimmune processes stimulated by the reaction of IgG, originally directed against the 66-kDa of L. braziliensis, to the 66-kDa antigen of mucosal tissue may contribute to the clinical presentation of mucosal leishmaniasis.

Adolescent↗

PubMed1985

[Genetic aspects of the reactions of humoral immunity to collagen in man and animals. II. Modifications of the autoimmune status to collagen type I in NZB x NZW (F1) mice by sex hormones during ontogeny].

The sex hormones, estradiol and testosterone, are able to modulate the status of spontaneous reactions of humoral immunity to type I collagen in ontogenesis of NZB x NZW (F1) females. Administration of estradiol to puber and unpuber females leads to a significant increase in the reactivity levels. The autoimmune status to type I collagen in NZB x NZW (F1) males is nonreactive to sex hormones influence. The results obtained corroborate the suggestion of the important role of sex hormones in formation of sex dimorphism and age variability to autoimmunity to type I collagen.

Animals↗

PubMed2006

Improved uptake of plant-derived LTB-linked proteins in carp gut and induction of specific humoral immune responses upon infeed delivery.

Oral vaccination of fish is an effortless and stress free immunisation method which can be used for almost any age. However, vaccination via the mucosal route does have disadvantages. For example, the vaccine may induce tolerance and has to be protected to escape digestion. Also the vaccine should be efficiently delivered to immune-competent cells in the gut or other lymphoid organs. In addition, it should be cost effective. Here we present a novel fish vaccination model using potato tubers as vaccine production and delivery system. The model vaccines discussed here include fusion proteins consisting of a gut adhesion molecule (LTB) and a viral peptide or green fluorescent protein (GFP) expressed in potato tubers. The adhesion molecule mediates binding to and uptake from the gut, whereas the viral peptide or GFP functions as model vaccine antigen provoking the induction of an immune response. We demonstrate that fusion to LTB facilitates an elevated uptake of the model vaccines in carp gut mucosa. The plant-derived fusion proteins also elicit a specific systemic humoral immune response upon oral application of crude tuber material incorporated into a standard dietary feed pellet. The data presented here show the promising potentials of the plant as a production system for oral vaccines in aquaculture and feed mediated immunisation of fish.

Administration, Oral↗

PubMed1999

The humoral immune response to human T-cell lymphotropic virus type 1 envelope glycoprotein gp46 is directed primarily against conformational epitopes.

Individuals infected with human T-cell lymphotropic virus type 1 (HTLV-1) develop a robust immune response to the surface envelope glycoprotein gp46 that is partially protective. The relative contribution of antibodies to conformation-dependent epitopes, including those mediating virus neutralization as part of the humoral immune response, is not well defined. We assess in this report the relationship between defined linear and conformational epitopes and the antibodies elicited to these domains. First, five monoclonal antibodies to linear epitopes within gp46 were evaluated for their ability to abrogate binding of three human monoclonal antibodies that inhibit HTLV-1-mediated syncytia formation and recognize conformational epitopes. Binding of antibodies to conformational epitopes was unaffected by antibodies to linear epitopes throughout the carboxy-terminal half and central domain of HTLV-1 gp46. Second, an enzyme-linked immunoadsorbent assay was developed and used to measure serum antibodies to native and denatured gp46 from HTLV-1-infected individuals. In sera from infected individuals, reactivity to denatured gp46 had an average of 15% of the reactivity observed to native gp46. Third, serum antibodies from 24 of 25 of HTLV-1-infected individuals inhibited binding of a neutralizing human monoclonal antibody, PRH-7A, to a conformational epitope on gp46 that is common to HTLV-1 and -2. Thus, antibodies to conformational epitopes comprise the majority of the immune response to HTLV-1 gp46, and the epitopes recognized by these antibodies do not appear to involve sequences in previously described immunodominant linear epitopes.

Animals↗

PubMed2005

Cellular and humoral immunity following Snow Mountain virus challenge.

Little is known about the immune response to noroviruses. To elucidate the immunobiology of norovirus infection in humans, 15 volunteers were challenged with Snow Mountain virus (SMV), a genogroup 2 norovirus. We assessed the cellular and humoral immune response and infection by analyzing stool, serum, saliva, and peripheral blood mononuclear cell (PBMC) responses pre- and postchallenge. In contrast to Norwalk virus (NV), SMV infection was not dependent upon blood group secretor status. Nine of 15 volunteers were infected and showed a >/=4-fold increase over the prechallenge anti-SMV serum immunoglobulin G (IgG) titer, mostly subclass IgG1. Although serum IgG elicited by SMV infection was cross-reactive with Hawaii virus (HV), another genogroup 2 norovirus, salivary IgA was less cross-reactive. Neither SMV-elicited serum IgG nor salivary IgA cross-reacted with NV, a genogroup 1 norovirus. Significant increases in serum gamma interferon (IFN-gamma) and IL-2, but not IL-6 or IL-10, were noted on day 2 postchallenge. For the majority of volunteers, both infected and uninfected, PBMCs stimulated with norovirus virus-like particles secreted IFN-gamma and other Th1 cytokines, suggesting previous norovirus exposure in most volunteers. Like the IgG antibodies, the SMV-activated T cells were cross-reactive with HV but not NV. IFN-gamma production was dependent upon CD4(+) cells, consistent with a predominant, but not exclusive, Th1 response. To our knowledge, this is the first report characterizing T-cell and cytokine responses following live norovirus challenge.

Adult↗

PubMed1985

Ablation of humoral immunity in 15I5 x 72 chickens is not predisposing to the formation of subgroup G virus-induced distal sarcomas.

Clone (cl.) 85 infection of 15I5 x 72 chickens at 4 weeks posthatch results in a lower frequency of distal sarcomas than does Prague (Pr)-B infection. As higher titers of virus-neutralizing antibody are generated in the cl.85-infected chickens, the possibility was addressed in the present study that the low frequency of cl.85-induced distal sarcomas is a direct consequence of the strong neutralizing response. Our observations indicate that ablation of humoral immunity by embryonic bursectomy does not serve to increase this frequency, implying that the antiviral humoral response is not required to limit formation of cl.85-induced distal sarcomas.

Animals↗

PubMed1997

Cellular and humoral immunity to the 60-kD heat shock protein in inflammatory bowel disease.

BACKGROUND: Mycobacteria have been considered a possible etiological agent in Crohn's disease. Since cross-reactivity between epitopes of mycobacterial and self-heat shock protein might represent a potential disease mechanism, we determined the cellular and humoral immune responses to the mycobacterial and the human 60-kD heat shock protein, as well as various control antigens. METHODS: We studied samples from 19 patients with Crohn's disease, 12 patients with ulcerative colitis, and from 19 healthy individuals. T cell responses were studied using a standard proliferation assays to purified recombinant mycobacterial and human 60-kD heat shock protein. Antibody levels were measured by establishing an enzyme-linked immunosorbent assays to recombinant purified 60-kD heat shock protein. RESULTS: The proliferative responses to the mycobacterial and the human 60-kD heat shock protein were closely correlated, but the cellular immune response to both antigens was not significantly different between the two patient groups and healthy controls. In addition, antibody levels to heat shock protein were also not significantly different between the three groups. CONCLUSIONS: These results argue strongly against a role for mycobacterial heat shock protein in the pathogenesis of Crohn's disease. However, in view of previous data demonstrating overexpression of 60-kD heat shock protein in inflammatory Crohn's disease tissue, this considerable cellular and humoral autoreactivity suggests an important immunoregulatory role for the 60-kD heat shock protein.

Adult↗

PubMed1996

Suppression of humoral immunity by monoclonal antibody to CD79b, an invariant component of antigen receptors on B lymphocytes.

CD79b is an invariant component of antigen receptors on B lymphocytes. Previous data have suggested that monoclonal antibody (mAb) to CD79b would introduce negative signals into B lymphocytes and suppress humoral immunity. We tested this hypothesis in this study using in vitro assay systems, and revealed that anti-CD79b mAb effectively suppressed the antibody response to a T-cell dependent antigen. The speculated mechanisms for this immunosuppression were: (i) down-modulation of antigen receptors, (ii) inhibition of B lymphocyte differentiation, and (iii) induction of B lymphocyte unresponsiveness. Of these three, we confirmed that the first two were actually induced by anti-CD79b mAb treatment, whereas the in vitro system could not induce the unresponsiveness of B lymphocytes.

Antibodies, Monoclonal↗

PubMed2006

The humoral immune response and protective efficacy of vaccination with inactivated split and whole influenza virus vaccines in BALB/c mice.

Recently the urgency of developing a pandemic influenza vaccine has lead to the re-evaluation of the use of whole virus vaccine. We have compared the humoral immune response and the protective efficacy of whole and split influenza virus vaccines in mice. Whole virus vaccine was more immunogenic particularly after the first dose of vaccine, generally eliciting higher numbers of systemic antibody secreting cells and an earlier and higher neutralising antibody response. Immunisation with one dose of whole virus vaccine more effectively reduced viral shedding upon non-lethal homologous viral challenge, but two doses of split virus vaccine was most effective at limiting viral replication and this was correlated with high influenza specific serum IgG concentrations. The two vaccine formulations induced different T helper profiles particularly after one dose of vaccine; split virus vaccine induced a type 2 bias response, whereas whole virus vaccine elicited a dominant type 1 response.

Animals↗

PubMed2004

Impairment of humoral immunity to Plasmodium falciparum malaria in pregnancy by HIV infection.

BACKGROUND: HIV infection increases the risk of malaria infection in pregnant women. Antibodies to variant surface antigens (VSA) on infected erythrocytes might protect against malaria in pregnancy. We postulated that HIV-induced impairment of humoral immunity to VSA mediates the increased susceptibility to malaria. METHODS: We compared serum concentrations of antibodies to VSA by flow cytometry or agglutination, and to merozoite proteins AMA-1 and MSP119 by ELISA, in 298 pregnant Malawian women, and related the findings to malaria and HIV infection, CD4-positive T-cell count, and HIV-1 viral load. FINDINGS: Concentrations of IgG to placental type VSA were lower in HIV-infected women than in HIV-uninfected women (median 8 units [IQR 4-23] vs 20 [12-30]; p<0.0001), among women with malaria (p=0.009) and those without malaria (p=0.0062). The impairment was greatest in first pregnancy. Agglutinating antibodies to placental VSA were present in a lower proportion of HIV-infected than HIV-uninfected women (58 [35.1%] of 165 vs 50 [53.8%] of 93, p<0.001). The degree of antibody binding by flow cytometry was correlated with CD4-positive T-cell count (r=0.16, p=0.019) and inversely with HIV-1 viral load (r=-0.16, p=0.030). Concentrations of antibodies to AMA-1 were lower in HIV infection (p<0.0001) but were not correlated with CD4-positive T-cell count or viral load. Responses to MSP119 were little affected by HIV infection. In multivariate analyses, HIV was negatively associated with amount of antibody to both VSA and AMA-1 (p<0.001 for each) but not MSP119. INTERPRETATION: HIV infection impairs antimalarial immunity, especially responses to placental type VSA. The impairment is greatest in the most immunosuppressed women and could explain the increased susceptibility to malaria seen in pregnant women with HIV infection.

Adult↗

PubMed1993

Retrobulbar adipocytes and humoral immunity in Graves' ophthalmopathy.

As CT and MR-imaging revealed an enlargement of retrobulbar fat tissue in patients with Graves' ophthalmopathy, the role of the retrobulbar adipocytes in the pathogenesis of this disorder remains to be elucidated. To evaluate the in vitro influence of humoral immunity on retrobulbar adipose tissue, the effects of IgG and sera from 56 euthyroid ophthalmopathy patients and 53 controls on both porcine and human (patients' and controls') retrobulbar adipocytes were measured by means of several assays: An enzyme-linked immunosorbent assay was employed to reveal specific binding of antibodies to the adipocytes. Metabolic activity was determined by means of a colorimetric dimethyl thiazolium-diphenyl-tetrazolium bromide test which quantifies the activity of mitochondrial dehydrogenases; cell proliferation was measured by incorporation of [3H]-thymidine in 24 h, and activities of adipocyte specific enzymes, such as membrane-bound lipoprotein lipase and 1-glycerol-3-phosphate-dehydrogenase were determined. By means of these specific enzyme tests no distinctions could be made between patients and controls. Furthermore, a significant difference between patients' (untreated and treated) and controls' IgG to bind to, to activate or to stimulate the proliferation of porcine or human (patients' and controls') retrobulbar adipocytes could not be detected under the employed experimental conditions. The effects of patients' heat-inactivated and non-inactivated sera were indistinguishable from those of the controls. Incubation with autologous sera, however, led to an activation of the retrobulbar adipocytes which was higher than the median caused by the patients' group and that engendered by incubation with autologous IgG.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipocytes↗

PubMed1993

Humoral immune response to human cytomegalovirus infection: diagnostic potential of immunoglobulin class and IgG subclass antibody response to human cytomegalovirus early and late antigens.

For the development of effective prophylaxis (hyperimmune globulins) and improvement of serological testing for human cytomegalovirus (HCMV) infection in immunocompromised patients it is essential to characterize the viral encoded proteins and the humoral immune response in terms of neutralizing antibodies and immunoglobulin class and IgG subclass reactivity to "early" and "late" HCMV proteins. The major neutralizing epitopes have been identified and screening of donor sera for neutralizing antibody by either conventional neutralization assays or enzyme-linked immunosorbent assay using recombinant antigens may help to improve the efficacy of hyperimmune globulin prophylaxis. The humoral response to individual HCMV proteins has been thoroughly investigated in immunocompromised patients. Antibodies against HCMV induced "early" antigens are not exclusively associated with active infection but may indicate an elevated risk for cytomegalic inclusion disease in immunocompromised patients. With a sensitive western blot technique. IgM and IgA antibodies against HCMV "late" proteins can be detected in sera from healthy seropositive individuals. Serum samples from subjects suffering from cytomegalic inclusion disease show significantly larger broader immune responses compared with healthy HCMV antibody carriers. Promising results using recombinant antigens corresponding to immunodominant epitopes for the detection of HCMV specific antibodies have been published.

Antibodies, Viral↗

PubMed1999

Hyporesponsiveness of the systemic and mucosal humoral immune systems in chickens infected with Salmonella enterica serovar enteritidis at one day of age.

Newly hatched chicks lack immunological maturity, which could compromise their ability to respond to infection by pathogens such as Salmonella enterica serovar enteritidis (S. enteritidis; SE). A study was conducted in which chicks were infected with a sublethal dose of SE at 1 d posthatch, and the systemic and intestinal immune responses to the challenge were followed over time. Birds infected at this age experienced difficulty in clearing the infection, and 50% of the individual birds remained persistently infected until 23 wk of age. These birds exhibited only a marginal systemic and mucosal humoral immune response to the infection. No response or little response was observed 1 wk postchallenge; responses increased somewhat over time. On many of the sampling times, 50% or more of the culture-positive birds lacked a detectable plasma or intestinal response. Levels of 10(3) to 10(5) SE/g of feces could be found in the intestines of birds eliciting a good IgA response, indicating that, when these birds did respond mucosally, the IgA produced was incapable of clearing the organism once the infection was established. Birds infected during this time also experienced reduced ability to respond to vaccination. Compared with uninfected controls, depressed responsiveness to an S. enteritidis bacterin was observed in infected birds 1 and 2 wk after administration, whereas those individuals receiving an inactivated Newcastle disease vaccine (NDV) experienced a reduced response 4 and 6 wk postvaccination, indicating that the persistent infection affected the ability of the immune system to respond to homologous and heterologous antigens. These results demonstrate that exposure of chickens to SE early in life interferes with the ability of these individuals to respond humorally to the infection and to other antigenic stimuli; such effects can be observed for at least 23 wk.

Animals↗