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Results for “Immunity, Humoral”

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At least 145 records · Page 8Linked to original sources

PubMed1995

Effect of HIV vertical transmission on the ontogeny of T cell antigens involved in the regulation of humoral immune response.

HIV infection causes progressive impairment of humoral immunity, including defective specific antibody production. To evaluate whether vertical HIV infection interferes with the expression on CD4+ lymphocytes of developmentally regulated molecules, that play a crucial role in the generation of immunological memory (CD45 isoforms) and in attainment of antibody responses (CD40L), 22 HIV-infected children and 36 seroreverted children born to HIV+ mothers were studied. The percentage of CD40L+ PBMC after activation in vitro with phorbol myristate acetate (PMA) plus ionomycin was lower in HIV-infected children than in controls (P < 0.004). This correlated with the depletion of CD4+ lymphocytes (r = 0.75; P < 0.001). CD40L expression rose progressively with age (r = 0.36; P = 0.03) in seroreverted children, but not in HIV-infected children, suggesting that while in normal children in vivo antigen stimulation results in progressive attainment of CD40L expression (and thus to effective T-B cell cooperation), this process is largely defective in HIV-infected children, contributing to the genesis of humoral immune deficiency. The proportion of CD4+ cells bearing the CD45RO isoform was increased among HIV-infected infants during the first years of life. However, the percentage of CD4+ CD45RO+ peripheral blood mononuclear cells (PBMC) progressively increased with age in controls (r = 0.69; P = 0.03), but not in HIV-infected children, showing that while vertical transmission of HIV does not prevent CD45RO expression early in life, it is associated with a disturbance of the physiological process of antigen priming, contributing to poor immunological memory to T cell-dependent antigens.

Age Factors↗

PubMed1996

Effects of malathion on humoral immunity and macrophage function in mast cell-deficient mice.

Malathion, when administered at noncholinergic doses, was previously shown to enhance the humoral immune response to a T-dependent antigen, sheep red blood cells (SRBC), and macrophage function. In addition, malathion was shown to cause mast cell degranulation. The hypothesis that mast cells contribute to the observed alterations in humoral immunity and macrophage function was determined by examination of the effects of acute administration of malathion to mast cell-deficient mice on macrophage function and the generation of a humoral immune response to SRBC. Initial studies in two strains of mast cell-deficient mice (6-7 weeks old) indicated that oral administration of malathion reduced macrophage function in these mice, but enhanced macrophage function in the wild-type strain. Because both strains reacted in a similar fashion and the defect in the WBB6F1-W/WV strain allowed reconstitution, further studies were conducted with this strain. Exposure of either wild-type mice or mast cell-deficient mice with reconstituted with bone marrow-derived mast cells (BMMC) from the wild-type mice to malathion enhanced macrophage function and the production of circulating IgM, but not IgG, antibodies to SRBC on Days 3 and 5 after immunization. In contrast, administration of malathion to older mast cell-deficient mice suppressed the generation of IgM and IgG antibodies to SRBC on Days 3 and 5 after immunization, but did not affect macrophage function. In summary, the results presented indicate that the presence of mast cells was necessary for the increases in macrophage function and humoral immunity observed after acute oral administration of malathion to mice.

Animals↗

PubMed1976

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

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

Agglutination↗

PubMed2004

The effects of transforming growth factor-beta neutralization on postburn humoral immunity.

BACKGROUND: Burn injury induces immunosuppression, which is associated with an increased susceptibility to infection. Our laboratory has demonstrated that burn injury also impairs humoral immunity. We reported that burn injury enhanced expression of transforming growth factor-beta (TGF-beta) mRNA and that exogenous TGF-beta further impaired humoral immunity. The objective of this study was to clarify the role of TGF-beta on humoral immunity after burn injury with a neutralizing experiment. METHODS: Twelve BALB/c mice were randomly divided into two groups: sham and burn. Anesthetized mice received a 20% full-thickness burn or sham injury. The murine splenocytes containing 1.5 x 10 cells/mL were cultured with 2.5 microg/mL of lipopolysaccharide with or without 0.5 ng/mL of TGF-beta or 1 microg/mL of anti-TGF-beta neutralizing antibody, if necessary. Concentrations of immunoglobulin (Ig) M in the cell culture supernatant were determined by enzyme-linked immunosorbent assay and the number of IgM-secreting cells in the culture was measured by enzyme-linked immunospot assay. RESULTS: After 2-day culture, neutralization of TGF-beta dramatically restored IgM synthesis after burn injury. After 5-day culture, however, it restored IgM concentration but failed to restore a number of IgM-secreting cells. CONCLUSION: This neutralizing experiment demonstrated that TGF-beta is one of the inhibitors of IgM synthesis after burn injury. However, neutralization of TGF-beta was not enough to completely restore humoral immunity after burn injury. Investigation of the mechanism of impaired IgM synthesis after burn injury should be continued.

Animals↗

PubMed2005

Human tumor cell lysates as a protein source for the detection of cancer antigen-specific humoral immunity.

Measurement of humoral tumor-specific immunity can predict what proteins are specific tumor antigens, be used to evaluate patient diagnosis or prognosis, and function as a method by which one can measure the effects of an immune intervention, such as a vaccine. Antibody assays can easily be adapted to high throughput formats; however, specific reagents needed for assay development often are not available. Developing methods to produce large quantities of purified recombinant tumor antigen proteins for indirect ELISA is both laborious and expensive. In addition, using proteins derived from E. coli might preclude the detection of certain antibody epitopes. We questioned whether a human tumor cell-based ELISA could be developed to assess antibody immunity to common tumor-associated antigens and whether such an ELISA could be optimized to the clinical standards needed for evaluation of large scale trials. Assays were based on the detection of HER-2/neu and p53 antibodies by capture ELISA, using human tumor cell lysate as a protein source. After optimization, the HER-2/neu and p53 ELISA intra-assay coefficients of variation (CV) of positive control sera were consistently 9% and 12%, respectively, at a 1:100 dilution. The HER-2/neu and p53 inter-assay CV of positive control sera over a 5-month time period were 20% and 15%, respectively. The sensitivity and specificity of the ELISAs were evaluated based on comparison to immunoblot. Analysis demonstrated the HER-2/neu ELISA had a specificity of 77% and sensitivity of 89%, and the p53 ELISA had a specificity of 100% and sensitivity of 93%. Cell-based ELISA can be developed to be Clinical Laboratory Improvement Act (CLIA)-compliant and the flexibility of the approach will allow adaptation of the assay to multiple tumor antigen systems.

Antibodies, Neoplasm↗

PubMed1988

Alterations of humoral immunity in patients with gastric cancer.

For better understanding of the alterations of humoral immunity in gastric cancer patients, IgG, IgA, IgM, complement C3, C4, CH50, natural antibody (isohemagglutinin-IgM class), ESR, CRP, albumin and globulin were quantitated in sera taken preoperatively from 81 patients with gastric cancer and from 29 control patients with hernia. The results from patients with gastric cancer were grouped according to pTNM staging (including stage I + II, III, and IV). Serum globulin and IgG levels in all stages of cancer patients were significantly lower than that of the controls (p less than 0.05). The CRP and ESR levels in stage III and IV cancer patients were significantly higher (p less than 0.05). There was no difference between cancer and hernia patient groups in IgA, IgM, isohemagglutinin-IgM class, C3, C4, CH50, albumin, WBC and total lymphocyte counts. In conclusion, the significant changes in humoral immunity in patients with gastric cancer include: (1) decrease in serum IgG and globulin levels, and (2) increased levels of acute phase reactants (ESR, CRP). These results imply that patients with gastric cancer have lower acquired humoral immunity and have acute phase reactions.

Adult↗

PubMed2002

Short-circuiting long-lived humoral immunity by the heightened engagement of CD40.

Agonistic alpha CD40 Ab's have been shown to be potent immune adjuvants for both cell- and humoral-mediated immunity. While enhancing short-lived humoral immunity, the administration of a CD40 agonist during thymus-dependent immune responses ablates germinal center formation, prematurely terminates the humoral immune response, blocks the generation of B cell memory, and prevents the generation of long-lived bone marrow plasma cells. Interestingly, some of these effects of heightened CD40 engagement could be mimicked by enhancing the magnitude of antigen-specific T cell help. Taken together, these studies demonstrate that as the magnitude of CD40 signaling intensifies, the fate of antigen-reactive B cells can be dramatically altered. These are the first studies to describe the multifaceted function of CD40 in determining the fate of antigen-reactive B cells and provide novel insights into how CD40 agonists can short-circuit humoral immunity.

Animals↗

PubMed2006

A novel chitosan CpG nanoparticle regulates cellular and humoral immunity of mice.

OBJECTIVE: To develop a safe and novel immunoadjuvant to enhance the immunity and resistance of animals against E. coli infection. METHODS: An 88-base immunostimulatory oligodeoxynuleotide containing eleven CpG motifs (CpG ODN) was synthesized and amplified by PCR. The chitosan nanoparticle (CNP) was prepared by ion linking method to entrap the CpG ODN that significantly promotes the proliferation of lymphocytes of pig in vitro. Then the CpG-CNP was inoculated into 21-day old Kunming mice, which were orally challenged with virulent K88/K99 E. Coli 35 days after inoculation. Blood was collected from the tail vein of mice on days 0, 7, 14, 21, 28, 35, 42, and 49 after inoculation to detect the changes and content of immunoglobulins, cytokines and immune cells by ELISA, such as IgG, IgA, IgM, IL-2, IL-4, and IL-6. RESULTS: The CpG provoked remarkable proliferation of lymphocytes of pig in vitro in comparison with that of control group (P < 0.05). The inoculation with CpG-CNP significantly raised the content of IgG, IgM, and IgA in the sera of immunized mice (P < 0.05). The levels of IL-2, IL-4, and IL-6 in the mice significantly increased in comparison with those in controls (P < 0.05), so was the number of white blood cells and lymphocytes in immunized mice. The humoral and cellular immunities were significantly enhanced in immunized mice, which resisted the infection of E. coli and survived, while the control mice manifested evident symptoms and lesions of infection. CONCLUSIONS: CpG-CNP can significantly promote cellular and humoral immunity and resistance of mice against E. coil infection, and can be utilized as an effective adjuvant to improve the immunoprotection and resistance of porcine against infectious disease.

Adjuvants, Immunologic↗

PubMed1996

An orally supplemented mononucleotide mixture prevents the decrease in T cell-dependent humoral immunity in C57BL/6 mice fed a nucleotide-free diet.

T-cell-dependent humoral immune responses are lower in mice fed a nucleotide-free (NF) diet. In a previous study, a mononucleotide and nucleoside mixture prevented the decrease in humoral immune responses in mice fed a NF diet when a total of seven doses [2100 micromol/(kg x dose)] were administered intraperitoneally. In the present study, C57BL/6 (B6) mice were fed a NF diet for 3 wk with or without mononucleotide mixture (MM) supplementation. The MM was given at the levels of 14 or 70 micromol/(kg x d) by daily gavage feeding for 3 wk. Control mice were fed a NF diet without supplements (negative control) or a NF diet plus the mononucleotide/nucleoside mixture administered intraperitoneally (positive control). Both doses of MM prevented the decrease in T-dependent antibody (Ab) production in mice fed a NF diet as effectively as positive controls. T-helper (Th) spleen cells from mice of each diet group were enriched, mixed with Th cell-depleted spleen cells from each diet group, and antigen-primed in the culture. The number of Ab-secreting cells formed was higher with Th cells from mice with oral MM supplements or from positive controls than with those from mice without nucleotide supplement. The source of Th cell-depleted spleen cells did not influence the number of Ab-secreting cells. Thus, orally supplemented nucleotides can prevent the suppression of Th cell-dependent humoral immunity in mice fed a NF diet with doses likely to be provided by dietary sources.

Animals↗

PubMed1992

Direct evidence that primary acquired cell-mediated immunity is less resistant than is primary thymus-dependent humoral immunity to the depressive influence of wasting protein-energy malnutrition in weanling mice.

Wasting protein-energy malnutrition (PEM) was induced in male C57BL/6J mice fed a low-protein diet ad libitum from 23 to 37 d of age. In comparison with a complete diet, the low-protein formulation reduced delayed hypersensitivity to sheep red blood cells (SRBCs) assessed on day 14 of feeding by measuring increased footpad thickness (mean +/- SD: 4 +/- 4% vs 22 +/- 8%, P less than 0.01), after immunization on day 9, and after challenge with SRBCs on day 13. By contrast, the low-protein diet did not affect the anti-SRBC hemagglutinin titer (8.3 +/- 2.2 vs 9.1 +/- 1.1, P greater than 0.30) despite profound reduction in numbers of splenic plasma cells secreting IgM-class anti-SRBCs (7.3 +/- 3.1 vs 49.9 +/- 23.8 x 10(-3), P less than 0.001), after immunization on day 9 and assessment on day 14. Thus, direct experimental evidence, previously altogether lacking, is provided in support of the concept, central to nutritional immunology, that acquired cell-mediated immunity is less resistant than is systemic humoral immunity to the depressive influence of pre-adolescent, wasting PEM.

Animals↗

PubMed1992

[Humoral immunity following splenectomy in adults].

Humoral immunity was examined in a population of one hundred adult patients splenectomized after abdominal trauma without associated disease, and the results were compared with those observed in healthy individuals. We found, in addition to the disorders, a large increase in the seric concentration of total IgE, and increased presence of autoantibodies and circulating immunocomplexes. These alterations were not correlated with the asplenia period.

Adult↗

PubMed1992

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

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

Animals↗

PubMed1994

Stress and humoral immunity: a review of the human studies.

Many studies have examined the relationship between stress and immunity, however, only a few have explored associations between stress and humoral immunity. In our review of this literature, three ways of characterizing the response of the humoral immunity system to stress were identified: total immunoglobulins, antibody to latent viruses and antibody to vaccines. These studies provide some support for the hypothesis that stress affects humoral immunity, particularly response to latent virus, but further research is required to confirm these observations. Several directions for future research are proposed.

Adult↗

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↗

PubMed2004

Humoral immune responses to model antigen co-delivered with biomaterials used in tissue engineering.

A model shed antigen, ovalbumin (OVA), was co-delivered with polymeric biomaterial carrier vehicles in C57BL6 mice to test whether the presence of the biomaterial acted as an adjuvant in the immune response towards the associated antigen. The biomaterials tested were non-biodegradable polystyrene microparticles and biodegradable 50:50 or 75:25 poly(lactic-co-glycolic acid) (PLGA) microparticles or scaffolds. For each biomaterial carrier vehicle, to assess the resulting time-dependent systemic humoral immune response towards the co-delivered OVA, the OVA-specific IgG concentration and isotypes (IgG2a or IgG1, indicating a predominant Th1 or Th2 response, respectively) were determined using ELISA. OVA co-delivered with biomaterial carrier vehicles supported a moderate humoral immune response that was maintained for the 18-week duration of the experiment. This humoral immune response was primarily Th2 helper T cell-dependent as indicated by the predominant IgG1 isotype. Furthermore, this humoral immune response was not material chemistry-dependent within the material set tested here. With the presence of the biomaterial resulting in an enhancement of the humoral immune response to co-delivered antigen, it appears that the biomaterial acts as an adjuvant in the development of an adaptive immune response to co-delivered antigen.

Animals↗

PubMed2000

Augmented humoral immune function in metallothionein-null mice.

Stress response proteins can play integral roles as modulators of cellular function and can be involved in mechanisms that are important to immune function. Metallothionein (MT), a cysteine-rich stress response protein, has been shown to play numerous roles in the cell: it serves as a reservoir of essential heavy metals, it scavenges free radicals, and it can sequester heavy metals. These various functions suggest that MT may also participate in modulating immune responses. In previous work, we have shown that exogenous metallothionein can suppress the developing humoral immune response when coinjected with antigen. The present study was designed to evaluate the effects of endogenous MT on the development of humoral immunity. We compared the humoral immune function of animals with a targeted disruption of Mt-1 and -2 genes (MTKO) and their wild-type counterparts. MTKO mice displayed a significantly higher humoral response to challenge with ovalbumin (OVA) compared to wild-type controls. The secondary anti-OVA response in MTKO mice is as much as 58% higher than the response in control mice injected at the same time. Overall circulatory immunoglobulin levels are also substantially higher in MTKO mice (0.039 mg/ml IgM and 0.42 mg/ml IgG) than wild-type controls. MTKO mice displayed increased B cell differentiation following OVA challenge and an enhanced lymphoproliferative response to mitogenic stimulation. These changes in immune functional capacity occur in the context of changes in the makeup of the lymphoid compartments of the blood and spleen. There are substantially fewer T and B cells in the circulation of MTKO mice, but more T cells in the spleen of these mice than in control animals. Finally, we have found that splenocytes from MTKO animals displayed significantly elevated levels of NF-kappaB activity compared to wild-type controls. In conclusion, we have provided evidence that endogenous metallothionein can modulate the immune response in vivo and that intracellular MT may modulate immune function by regulation of transcription factor activity.

Animals↗

PubMed1991

[The effects of ciprofloxacin and ofloxacin on the cellular and humoral immune response in mice].

The effects of a 7 days chemotherapy with ciprofloxacin or ofloxacin on the cellular and humoral immune responses in albino mice were studied. The non-toxic doses of the drugs (10 or 30 mg/kg/day) were used. The delayed-type hypersensitivity reaction to sheep blood cells and skin biopsy were evaluated for cellular immune response. The complement fixation method was applied for the determination of the humoral immune response. Both drugs increased the cellular and humoral immune responses.

Animals↗

PubMed2005

Essential role for humoral immunity during Ehrlichia infection in immunocompetent mice.

Although cellular immunity is essential for host defense during intracellular bacterial infections, humoral immunity can also play a significant role in host defense during infection by some intracellular bacteria, including the ehrlichiae. Antibodies can protect susceptible SCID mice from fatal Ehrlichia chaffeensis infection, an observation that has been hypothesized to involve the opsonization of bacteria released from host cells. To determine whether humoral immunity plays an essential role during ehrlichia infection in immunocompetent mice, we utilized a murine model of fatal monocytotropic ehrlichiosis caused by Ixodes ovatus ehrlichia. Mice lacking either B cells or FcgammaRI were unable to resolve a low-dose (sublethal) I. ovatus ehrlichia infection, which suggested that humoral immunity is essential for resistance. Polyclonal sera generated in I. ovatus ehrlichia-infected mice recognized a conserved ehrlichia outer membrane protein and, when administered to infected mice, caused a significant decrease in bacterial infection. Mice experimentally depleted of complement, or deficient for complement receptors 1 and 2, were also susceptible to sublethal I. ovatus ehrlichia infection, as were mice that lacked the phox91 subunit of NADPH oxidase. The data are consistent with a mechanism whereby bacteria released from infected cells are lysed directly by complement or undergo antibody-mediated FcgammaR-dependent phagocytosis and subsequent exposure to reactive oxygen intermediates. The findings suggest mechanisms whereby antibodies contribute to immunity against intracellular bacteria in immunocompetent mice.

Animals↗