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Results for “Immunity, Humoral”

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PubMedDate not supplied

The late effects of selected immunosuppressants on immunocompetence, disease incidence, and mean life-span. I. Humoral immune activity.

The effect of different immunosuppressive treatments during young adulthood or humoral immune competence late in life was determined. It was found that the marked reduction in humoral immune competence in aged mice is further compromised when severe insults are administered early in life. Thus, thymectomy, splenectomy, and sublethal X-irradiation produced lasting immunodepression as measured (1) in situ and (2) by the hemolysin, direct and indirect plaque forming cell responses of adoptively transferred spleen cells. In contrast, treatment with cyclophosphamide and cortisone acetate were without effect, indicating that drug-damaged cells of the immune system were replaced by competent cells during the course of time. Decrease in immune competence of aged thymectomized animals could not be correlated with a decrease in numbers of theta-bearing T or immunoglobulin receptor-bearing B lymphocytes. The significance of the observed unequal effects of these immunosuppressants on immune competence, as they relate to disease incidence and life expectancy, are dealt with in the third paper in this series.

Age Factors↗

PubMedDate not supplied

Effect of chronic or cyclic exposure to estradiol on the humoral immune response and the thymus.

Estradiol (E2) is known to enhance humoral immunity. Previous studies examining serum immunoglobulin levels on days within the estrous cycle or in the ovariectomized, chronically E2-implanted rat have determined a positive correlation between serum E2 concentrations and antibody responsiveness. No previous study has investigated the effect of fluctuating E2 concentrations, as during the estrous cycle, throughout the course of a specific humoral immune response. Therefore, in the present study we addressed the influences of cyclic and tonic E2 exposure on the anti-fluorescein response in the rat. Ovariectomized rats were submitted to a 2 x 2 factorial design of chronic E2 implants and 4-day E2 injection (and vehicle control) regimens. Anti-fluorescein antibody production and thymic weights were measured. Animals given a 4-day cycle of E2 showed significantly (p less than 0.001) greater anti-fluorescein responses than did animals given tonic or no E2 replacement. Animals which were given implants, with or without cyclic E2 injections, experienced significant (p less than 0.001) thymic involution relative to those without implants. The 4-day E2 injections alone did not lead to thymic atrophy. These results indicate that while chronic E2 treatment induced thymic atrophy, cyclic exposure to E2 exerted a greater immunoenhancing influence than did tonic E2 exposure.

Animals↗

PubMed1994

Humoral immunity to Malassezia furfur serovars A, B and C in patients with pityriasis versicolor, seborrheic dermatitis and controls.

This study examined the humoral immune responses to Malassezia furfur serovars A, B and C of 10 patients with pityriasis versicolor, 10 patients with seborrheic dermatitis and 20 age- and sex-matched controls. A transferable solid-phase ELISA was used to determine titres of total Igs, IgM, IgA and IgG specific to M. furfur serovars A, B and C. The results demonstrated that patients with seborrheic dermatitis had a significantly higher titre of total Igs to serovar A than patients with pityriasis versicolor; and that patients with seborrheic dermatitis had a significantly higher titre of IgA to serovar C than patients with pityriasis versicolor. The titres of total Igs for controls and patients with seborrheic dermatitis were significantly lower to serovar B than to serovar C. A modified TSP ELISA was used to determine the titres of the IgG subclasses. Titres of IgG1,3,4 to serovar B were significantly higher in seborrheic dermatitis patients than pityriasis versicolor patients and titres of IgG3 to serovar A were significantly higher in seborrheic dermatitis patients than pityriasis versicolor patients. However, despite the differences between the patient groups, none of these results was significantly different to those of controls. Thus, this study did not demonstrate any differences in humoral immunity of patients suffering from Malassezia-associated dermatoses when compared to normal controls. These results may suggest that the humoral immune response to M. furfur is not related to the pathogenesis of Malassezia-associated dermatoses, but simply to the carriage of M. furfur on the skin.

Adult↗

PubMed1998

Role of the humoral immune system in Salmonella enteritidis phage type four infection in chickens.

The role of avian humoral immunity in the clearance of S. enteritidis was evaluated through bursectomy. After oral inoculation of bursectomized and sham-treated chickens with S. enteritidis, faecal excretion of S. enteritidis was examined. Organs were collected weekly until six weeks post-inoculation (pi) for bacteriological enumeration. Antibody isotypes in serum and bile were quantified by ELISA. Faecal excretion of S. enteritidis was significantly lower in controls from 13 days pi. Numbers of S. enteritidis in caeca from controls were significantly decreased from three weeks pi. Numbers of S. enteritidis were significantly decreased at two weeks pi in the spleen and the liver and at six weeks pi in the liver. Antibodies to S. enteritidis peaked at two weeks pi in controls and were absent in bursectomized chickens. These findings indicate that elimination of S. enteritidis partly depends on humoral immunity. The intestinal humoral response appeared more effective than the systemic humoral response for elimination of S. enteritidis.

Animals↗

PubMedDate not supplied

[Effect of trypsin on the development of a humoral immune response and of delayed hypersensitivity].

Trypsin was found to stimulate the development of humoral immune response to the thymus-dependent antigen when administered simultaneously with immunization and to exert no influence on this form of immune response being injected 4 days after immunization. Trypsin fails to affect the development of humoral immune response induced by the thymus-independent antigen. Trypsin was shown to enhance the development of hypersensitivity of delayed type at administration simultaneously with the sensitizing or resolving dose of the antigen. Trypsin appeared to attenuate the antigen-specific immunosuppressing effect of lymphocytes of the hyperimmunized animal spleen.

Animals↗

PubMed1991

The human humoral immune response to Salmonella typhi Ty21a.

The short-term kinetics and the effects of different dose regimens and formulations on the humoral immune response induced in human subjects by the live attenuated typhoid vaccine Salmonella typhi Ty21a were examined. Antibody responses in jejunal fluid and serum and by specific antibody production in vitro by peripheral blood lymphocytes to S. typhi lipopolysaccharide were determined. A short vaccination schedule of three doses of 10(11) live organisms over 5 days induced significantly greater intestinal IgA antityphoid antibody responses than did two comparable doses 21 days apart. The humoral immune response was dose dependent with 10(10) and 10(11) live organisms stimulating greater intestinal immune responses than did 10(11) killed organisms. No responses were evident with either 10(9) viable organisms or with an enteric-coated preparation. In the continued development and assessment of oral typhoid vaccines, the effects of different doses and formulations and the timing of sampling on the humoral immune response should be considered.

Administration, Oral↗

PubMedDate not supplied

Down regulation of humoral immunity in chickens due to carbendazim.

This study was planned to investigate the effect of very low dose of carbendazim on the humoral immune response in the chicken. Sixteen adult chickens, earlier vaccinated against New Castle Disease were divided in two experimental groups. Chickens of group I served as control, while group II birds were given a feed containing 200 ppm of carbendazim, which is considered no observable effect level (NOEL) dose, for a period of 6 months. The Humoral immune response was measured by the B-lymphocyte blastogenesis assay using lipopolysaccharide as mitogen and the quantitation of IgG, IgA, IgM levels by using respective antichicken conjugates, through an ELISA method. Total serum proteins, serum gamma-globulins and globulins were measured using commercially available kits. Carbendazim significantly (P< or =0.05) reduced both the B-lymphocyte proliferation and serum IgG, IgM and IgA levels, leading to decreased immunocompetence. At the end of experiment percent decrease in B-lymphocyte proliferation was 20.5% and that in serum IgG, IgM and IgA were 11.2, 22.9 and 28.8%, respectively. The percent decrease in total serum protein, serum gamma-globulins and serum globulins were 14.6, 18.5 and 9.7%, respectively. Results clearly indicated down regulation of humoral immunity by carbendazim at NOEL dose.

Animal Feed↗

PubMed1990

Similarities in intestinal humoral immunity in dermatitis herpetiformis without enteropathy and in coeliac disease.

Intestinal humoral immunity was examined in eight patients with dermatitis herpetiformis and normal jejunal histology (as determined by quantitative morphometry) on a gluten-containing diet. Jejunal aspirate was taken at the time of jejunal biopsy, and levels of total immunoglobulins (IgA, IgM, IgG) and specific antibody to gliadin and two other dietary proteins, betalactoglobulin and ovalbumin, were measured. The pattern of secretory immune responses in the dermatitis herpetiformis patients was similar to that in twenty-six patients with untreated coeliac disease--ie, higher than normal concentrations of IgA, IgM, and IgG and high levels of specific antibodies (IgA and IgM) to the three dietary proteins. Serum levels of IgA antigliadin were similar in the dermatitis herpetiformis and control (twenty-eight patients who underwent jejunal biopsy to exclude coeliac disease) groups, and serum levels of IgG antigliadin were intermediate between those of the control and coeliac disease groups. These findings suggest that investigation of gut humoral immunity may provide a diagnostic index of latent coeliac disease. The definition of coeliac disease as a permanent gluten-sensitive enteropathy may have to be revised if the proposed two-stage model is confirmed.

Adolescent↗

PubMed2006

Humoral immune response against mycobacterial antigens in children with tuberculosis.

Different clinical outcomes of tuberculosis (TB) are related to the balance between cell-mediated and humoral immunity and may depend on environmental and individual factors including age and sex. The purpose of this study was to analyze the humoral immune response to recombinant and native mycobacterial antigens in relation to clinical presentations of pulmonary TB in children. We examined 224 serum samples including 81 primary and 31 postprimary TB cases, 30 cases of latent TB infection, and 82 nontuberculosis controls. Commercially available ELISA assays detecting IgG, IgA, and IgM against antigens: 38 kDa, 16 kDa, 38 kDa, lipoarabinomannan (LAM), and A-60 were used. The results indicate that IgG production was very low in primary compared with postprimary TB (P<0.0001). IgM levels did not differ between the examined groups. Antibody levels strongly depended on the child's age. In infants aged below 1 there was no difference in the antibody level between the TB and control cases. Most positive cases were observed in children aged above 10. The influence of BCG vaccination on the antibody level was not seen. In all subgroups, person-to-person heterogeneity of antigen recognition was observed. We conclude that humoral immune response is associated with the phase of TB and is stronger in more advanced TB forms. IgG and IgA production against mycobacterial antigens is very low in young children.

Adolescent↗

PubMed1986

Reconstitution of in vitro humoral immune function in bone marrow transplant recipients.

The process by which humoral immune function is re-established following bone marrow transplantation was investigated in 50 transplant recipients. The recovery of in vitro-specific antibody production directed at sheep red blood cells was found to proceed through three phases. B cell function and helper T cell function were undetectable in the first phase (encompassing the first 5 months after transplantation), in which only suppressor cells reached functional maturity. Suppressor cells controlled responsiveness in the second phase (encompassing the period 5 to 15 months postgrafting). During this period, B cells and helper T cells became fully responsive; their activity became measurable, however, only after removal of Sephadex G-10-adherent suppressor cells. Normal responsiveness (associated with the loss of excessive suppressor cell activity) was characteristic of the third phase (over 15 months posttransplantation). Particular attention was paid to the role of suppressor cells in the recovery of humoral immune function. Their activity was positively correlated with graft-versus-host disease (GVHD), particularly of the chronic type. Suppressor cell activity in the early posttransplant period was predominantly mediated by OKT8-positive T lymphocytes, whereas suppressor cell activity in chronic GVHD patients was predominantly mediated by peripheral blood mononuclear cells that were retained on Sephadex G-10 columns, but did not express OKT8 antigen.

Acute Disease↗

PubMed1998

Evaluation of the primary humoral immune response following exposure of male rats to 17beta-estradiol or flutamide for 15 days.

There is a concern that certain industrial chemicals found in the environment may mimic or antagonize endogenous hormones and adversely affect the endocrine as well as the immune system. The objective of this study was to determine if exposure of Crl:CD (SD)BR male rats to 17beta-estradiol (17beta-E2), an estrogen receptor agonist, or flutamide (FLUT), an androgen receptor antagonist, would significantly alter the primary IgM humoral immune response to sheep red blood cells (SRBC). This study was conducted in the context of a male in vivo Tier I battery designed to identify endocrine-active compounds (EACs). The Tier I male battery consists of organ weights coupled with a comprehensive hormonal assessment. Rats were dosed by the intraperitoneal route for 15 days with vehicle or 0.001, 0.0025, 0.0075, or 0.050 mg/kg/day 17beta-E2 or 0.25, 1, 5, or 20 mg/kg/day FLUT. Six days prior to termination, selected rats were injected intravenously with SRBC for assessment of humoral immune function. Spleen cell number and spleen and thymus weights were obtained. Serum was analyzed for anti-SRBC IgM antibody by using an enzyme-linked immunosorbent assay. At 0.050 mg/kg/day 17beta-E2, mean final body and absolute thymus weights were significantly decreased to 84 and 65% of control, respectively. 17beta-E2 did not significantly alter spleen weight, spleen cell number, or the primary IgM humoral immune response to SRBC. The no-observed-adverse-effect level (NOAEL) for immune system alteration was 0.050 mg/kg/day 17beta-E2 since the decrease in absolute thymus weight was judged to be secondary to the decrements in body weight. In the Tier I male battery, responses to 17beta-E2 included decreased absolute testis and epididymis weights, decreased relative accessory sex gland unit weights, hormonal alterations (decreased serum testosterone (T), dihydrotestosterone (DHT), and luteinizing hormone (LH), and increased serum prolactin and E2 levels). The lowest-observed-adverse-effect level (LOAEL) for the reproductive indices was 0.001 mg/kg/day 17beta-E2 based on the hormonal alterations seen at this level; no NOAEL was established. Exposure to FLUT did not significantly alter mean final body, spleen, or absolute thymus weights, spleen cell number, or the primary IgM humoral immune response to SRBC. A significant increase (118% of control) in relative thymus weight was observed at 20 mg/kg/day FLUT. The NOAEL for immune system alteration was 5 mg/kg/day FLUT based on the increased relative thymus weights that were judged to be compound-related. In the Tier I male battery, responses to FLUT included decreased absolute epididymis and relative accessory sex gland unit weights and hormonal alterations (increased serum T, DHT, E2, and LH, and decreased follicle stimulating hormone levels). The LOAEL for the reproductive indices was 0.25 mg/kg/day FLUT based on the hormonal alterations seen at this level; no NOAEL was established. Based on these data, the reproductive and not the immune system appears to be the primary target organ of toxicity in young adult male rats treated with either 17beta-E2 or FLUT.

Androgen Antagonists↗

PubMed2003

Intrathecal B-cell clonal expansion, an early sign of humoral immunity, in the cerebrospinal fluid of patients with clinically isolated syndrome suggestive of multiple sclerosis.

The development of somatically mutated memory and plasma B cells is a consequence of T cell-dependent antigen-challenged humoral immunity. To investigate the role of B cell-mediated humoral immunity in the initiation and evolution of multiple sclerosis (MS), we analyzed Ig variable heavy chain genes of intrathecal B cells derived from patients with a first clinical manifestation suggestive of MS. Sequences of Ig variable regions showed that B cells in the cerebrospinal fluid from most of these patients were clonally expanded and carried somatic hypermutated variable heavy chain genes. The mutations showed a high replacement-to-silent ratio and were distributed in a way suggesting that these clonally expanded B cells had been positively selected through their antigen receptor. In comparison, intrathecal B-cell clonal expansion often precedes both oligoclonal IgG bands and multiple magnetic resonance imaging lesions. Clinical follow-up study showed that patients with clonally expanded intrathecal B cells had a high rate of conversion to clinically definite MS. The findings provide direct evidence of recruitment of germinal center differentiated B lymphocytes into the central nervous system during the initiation of MS. These results indicate B cell-mediated immune response in the cerebrospinal fluid is an early event of inflammatory reaction in the central nervous system of MS. This procedure also provides a more sensitive method to evaluate the association of humoral immunity in the evolution of MS.

Adult↗

PubMed2000

[Local cellular and humoral immunity in pneumonia patients].

The paper reports a study of some local immunity factors in pneumonia aimed at specification of mechanisms inducing respiratory immunodeficiency and their effects on the disease course. Local cellular immunity of the lungs was studied by estimation of the total number of cells in the bronchoalveolar lavage, their viability, alveolar macrophages (AM), neutrophils, T- and B-lymphocytes, AM and neutrophil phagocytic index and number, receptor apparatus. The lavage IgA, IgM, IgG, lysozyme were estimated. It was found that local cellular and humoral immunity depend on clinicoetiological form of pneumonia. Cellular and humoral immunodeficiency was the greatest in staphylococcal infection. The role of cellular and humoral immunity dysfunction in the lungs in genesis of bronchoobstructive syndrome is specified. Recovery of cellular and humoral immunity in pneumonia reconvalescents is behind clinical recovery. Grave immunodeficiency in severe or lingering pneumonia may be a pathogenetic factor of chronic inflammation in the lungs. To evaluate functional condition of local immunity of the lungs it is valid to study cellular and humoral factors of local pulmonary immunity in bronchoalveolar lavage.

B-Lymphocytes↗

PubMed1968

The effect of measles infection and of vaccination with certain live vaccines upon humoral immunity to smallpox.

The results of a study of the effect of measles infection and of vaccination with live measles vaccine (Leningrad-16 strain) on the level of humoral immunity to smallpox in children previously vaccinated against smallpox show that a measles infection markedly depressed the humoral immunity to smallpox, which did not reach its initial level in the 2-3 months of observation that followed clinical recovery. Immunoglobulin administered during the incubation period did not prevent the fall in smallpox antibody titres.It was also found that live measles vaccine, however intense the clinical reaction to the vaccination may be, does not have any marked effect on the smallpox antibody level in children. Similarly, 2 administrations of live trivalent poliomyelitis vaccine had no effect on humoral immunity to smallpox.

Child↗

PubMed1978

Identification of lipids associated with the ability of tumor cells to resist humoral immune attack.

Certain metabolic inhibitors or chemotherapeutic agents that increase the susceptibility of line-1 or line-10 guinea pig hepatoma cells to humoral immune attack were studied for their effects on the ability of the cells to synthesize lipids. A direct correlation was found between the drug-induced increase in sensitivity to antibody-C mediated killing and the inhibition of the ability of the cells to incorporate acetate, glycerol, and fatty acids into complex cellular lipids. Drug-treated cells recultured in drug-free medium regained their resistance to antibody-C mediated killing; these cells recovered their ability for complex lipid synthesis at this time. Thin layer chromatography of CHCl3:CH3OH lipid extracts from these cells indicated that the drug-induced increase in susceptibility to humoral immune attack correlated with the inhibition of acetate, glycerol, and fatty acid incorporation into cardiolipin and triglyceride in line-10 cells and the inhibition of incorporation of these compounds into cardiolipin alone in line-1 cells. No direct correlation was found between the sensitivity of the cells to humoral immune attack and the ability of the cells to incorporate precursors of lipid synthesis into other lipid moieties (sphyngomyelin, phosphatidyl serine, phosphatidyl choline, phosphatidyl glycerol, or cholesterol esters). The synthesis of cardiolipin and triglycerides, therefore, appears to be associated with the mechanism whereby these tumor cells resist antibody-C mediated killing.

Acetates↗

PubMed1992

Morphine suppresses primary humoral immune responses by a predominantly indirect mechanism.

Morphine suppresses humoral immune responses, causes thymic hypoplasia and suppresses NK (natural killer) activity in animal models. There is evidence that thymic hypoplasia and NK suppression are predominantly mediated by indirect mechanisms. The mechanism of morphine-induced humoral immunosuppression is less certain. Recent reports suggest that morphine and other opioids can directly act on cells of the immune system to suppress the generation of antibody-forming cells (AFC) in Mishell-Dutton cultures. The present study was designed to assess the roles of direct and indirect mechanisms in morphine-induced suppression of humoral immunity. Splenocytes from mice treated with morphine by s.c. implantation of a slow-release 75 mg pellet were dysfunctional in Mishell-Dutton cultures. Exposure to morphine in vivo for 12 or 24 hr caused significant suppression of the AFC production stimulated by sheep erythrocytes in Mishell-Dutton cultures. In contrast, direct addition of morphine or the kappa selective opioid agonist U50,488H to Mishell-Dutton cultures under a variety of conditions had little or no effect on AFC generation. These results indicate that suppression of humoral responses by morphine is not primarily mediated by direct action of morphine on the immune system. Suppression of AFC responses by administration of morphine in vivo was substantially blocked by treating mice with the glucocorticoid antagonist RU 38486, suggesting that glucocorticoids may be involved in the indirect mechanism by which morphine causes splenocyte dysfunction.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed1998

Exogenous melatonin enhances cell-mediated, but not humoral, immune function in adult male deer mice (Peromyscus maniculatus).

Many nontropical rodent species display seasonal changes in reproductive physiology and metabolism, as well as in immune function. Field studies of seasonal changes in immune function typically report decreased immune function in the short days of winter compared to summer; presumably, reduced immunity in winter reflects increased glucocorticoid secretion in response to environmental stressors. In contrast, laboratory studies of photoperiodic changes in immunity invariably demonstrate increased immune function in short compared to long days. Although the precise mechanisms regulating short-day enhancement of immune function are not known, it is hypothesized that increased immunity is due to the increased duration of melatonin secretion in short compared to long days. However, melatonin can act both directly (i.e, via melatonin receptors located on lymphatic tissue) and indirectly (i.e., via alterations in gonadal steroids) to affect immune function. The present study examined the effects of exogenous melatonin administration on both cell-mediated and humoral immune function in adult male deer mice (Peromyscus maniculatus), as well as the role of gonadal steroid hormones in mediating these effects. Mice either were castrated to remove circulating androgens or received sham operations and were implanted with empty capsules or capsules containing melatonin. Individual mice implanted with melatonin underwent reproductive regression and displayed enhanced splenocyte proliferation to the T-cell mitogen concanavalin A; antigen-specific serum immunoglobulin M production was unaffected by melatonin treatment. Castration had no effect on either cell-mediated or humoral immune function. Taken together, these results suggest that exogenous melatonin enhances cell-mediated, but not humoral, immune function in adult male deer mice and that this effect is independent of gonadal steroid hormones. These results are consistent with a direct effect of melatonin on immunity.

Analysis of Variance↗

PubMed2005

Enhancement of humoral immune responses to HBsAg by heat shock protein gp96 and its N-terminal fragment in mice.

AIM: Most studies on the immune effect of gp96 were focused on its enhancement of CTLs. It is interesting to know whether gp96 could influence the humoral immune response, and whether the recombinant N-terminal fragment of gp96 could substitute native gp96 to stimulate the immune system. METHODS: gp96 isolated from livers of normal mice and its N-terminal fragment (amino acid 22-355) expressed in E coli were used for immunization of BALb/c mice. Eight groups of mice received one of the following regiments subcutaneously in 100 microL phosphate buffered saline (PBS) at an interval of 3 wk. Group 1: PBS only; group 2: gp96 only; group 3: N-terminal fragment only; group 4: HBsAg only; group 5: HBsAg+gp96; group 6: HBsAg+N-terminal fragment; group 7: HBsAg+incomplete Freud's adjuvant; group 8: HBsAg+N-terminal fragment (95 degrees heated for 30 min). Serum anti-HBsAg antibody levels were assayed by ELISA. CTL responses in splenocytes were analyzed by ELISPOT after the last vaccination. RESULTS: The average titer of serum anti-HBsAg antibody in the mice immunized with HBsAg together with gp96 or its N-terminal fragment were much higher than those immunized with HBsAg alone detected by ELISA. The cellular immune response of the mice immunized with HBsAg together with gp96 or its N-terminal fragment was not different with those immunized with HBsAg alone measured by ELISPOT assay. CONCLUSION: gp96 or its N-terminal fragment greatly improved humoral immune response induced by HBsAg, but failed to enhance the CTL response, which demonstrated the potential of using gp96 or its N-terminal fragment as a possible adjuvant to augment humoral immune response against HBV infection.

Animals↗