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Results for “Immunity, Humoral”

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PubMed2001

The effects of melatonin on humoral immune responses of young and aged rats.

The pineal gland with its effects on immune system and free radicals may have a role on aging process. In this study, we investigated the effects of melatonin (10 mg/kg/d, s.c. for 7 days), the main secretion of the pineal gland, on the humoral immune responses of aged and young male Wistar rats. Eighteen aged (28 months old; 6 in control group and 12 in melatonin group) and 25 young (9 months old; 10 in control group and 15 in melatonin group) rats were given 4 x 10(8) sheep erythrocytes i.p. in order to evoke humoral immune responses. After a booster injection at the end of a period of three-weeks following the last melatonin injection, IgM and IgG1 levels were measured. Melatonin was found to increase IgG1 and IgM responses of aged rats when compared to controls (p = 0.049 and p = 0.007), respectively. In the young rats, while the IgG1 levels of control group were significantly higher than that of the melatonin group (p =0.021), IgM levels were not significantly different (p = 0.563). It is concluded that exogenous melatonin may augment the depressed humoral immune responses seen aged rats.

Aging↗

PubMed1991

[Cellular and humoral immunity in patients with chronic bronchitis and hereditary variants of alpha 1-proteinase inhibitor].

Cellular and humoral immunity was investigated in practically healthy subjects with PLM allele subtypes in the homozygotic form, PiM3M3 phenotypical variants and normal phenotypical variant PiM1M1 in the presence of which practically healthy subjects show a 100% antitryptic activity in the blood serum. A study of the immunological reactivity of 225 patients with chronic obstructive bronchitis revealed in these patients disorders of the cellular and humoral immunity and they were more pronounced in patients with PiM3M3 phenotypical variant.

Adult↗

PubMed1983

B cell activity in systemic lupus erythematosus: depressed in vivo humoral immune response to a primary antigen (haemocyanin) and increased in vitro spontaneous immunoglobulin synthesis.

B lymphocyte studies, in vivo and in vitro, were performed in 28 patients with systemic lupus erythematosus (SLE). After immunization with the primary test antigen haemocyanin, a decreased antigen specific humoral immune response was observed for all three Ig classes, irrespective of disease activity or the use of corticosteroids. Levels of antibodies against (recall) viral and nuclear antigens were increased during active disease. The in vitro spontaneous production of IgM and IgG, determined in the supernatant of 8 days cultures by ELISA, was highly increased in patients with active disease (reversely correlated with levels of complement C3, r = 0.74). Pokeweed mitogen-induced synthesis was decreased in all patients. The distribution of T cell subsets (OKT3, Leu 3a and OKT8 positive cells) was not different from controls, irrespective of disease activity. It is concluded that the primary humoral immune response is decreased in SLE, whereas a polyclonally activated B cell appears to be present. The normal T cell subset distribution does not support the primary role of the cell in the state of hyperactivity of the B cell.

Adolescent↗

PubMed1988

Persistent suppression of humoral immunity produced by 7,12-dimethylbenz(A)anthracene (DMBA) in B6C3F1 mice: correlation with changes in spleen cell surface markers detected by flow cytometry.

The purpose of these studies was to examine the effects of DMBA on subpopulations of splenocytes obtained from B6C3F1 mice, using cell surface markers defined by monoclonal antibodies and multiparameter flow cytometry. Changes were correlated with alterations in humoral immune function assessed in vitro. Mice were treated for 10 days during a 2 week period by subcutaneous (s.c.) injections of DMBA in corn oil at doses of 0.5, 5 and 10 micrograms/g/day (5-100 micrograms/g total dose). Four mice from each exposure group and an additional corn oil control group of mice were studied at 4 and 8 weeks following the last injection with DMBA. These studies demonstrated a dose-dependent decrease in the total number and percentage of spleen cells expressing B-cell markers (mu heavy chain, kappa light chain and 14.8 antigen) as well as T-cell markers (Thy 1.2, Lyt-1 and Lyt-2). The percentage of splenocytes expressing Mac-1 was increased by DMBA. Helper T-cells appeared to be a very sensitive population of spleen cells to DMBA exposure, as suggested by a decrease in the number and percentage of Lyt-1 positive cells recovered from the spleen 4 weeks after exposure to DMBA. DMBA produced a dose-dependent suppression of the in vitro primary humoral immune responses to SRBC, TNP-Ficoll and TNP-LPS. The fact that a functional suppression of humoral immunity was accompanied by a decrease in the number of mature B-cells and T-cells in the spleen suggests that cell surface markers may be useful indicators of immunotoxicity in animals receiving DMBA in sub-chronic studies.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1995

Humoral immunity in DiGeorge syndrome.

OBJECTIVE: To assess humoral immunity after immunization and natural infection in patients with clinical manifestations of the DiGeorge anomalad. DESIGN: Retrospective review of cases. SETTING: Ambulatory immunology clinic of a tertiary care teaching hospital. PATIENTS: The 13 patients had a symptom complex including congenital heart disease, characteristic facies of the DiGeorge anomalad, possible hypocalcemia, and thymic hypoplasia or aplasia. Molecular and cytogenic studies of 12 patients demonstrated that all had 22q11 microdeletions. METHODS: Serial studies included lymphocyte population enumeration by flow cytometry, lymphocyte proliferation assays with the mitogens phytohemagglutinin and pokeweed mitogen and Staphylococcus aureus, and immunoglobulin quantitation. Specific antibody studies included virus neutralization assays for poliovirus antibodies, and enzyme-linked immunosorbent assay for diphtheria, tetanus, measles, rubella, varicella-zoster virus (VZV), and cytomegalovirus (CMV) antibodies. Avidity of rubella, VZV, and CMV antibodies was tested by enzyme-linked immunosorbent assay modified to include a mild protein denaturant in the first wash after incubation with sera. RESULTS: All patients had a CD3+ cell count greater than 0.500 x 10(9)/L and a CD4+ cell count greater than 0.350 x 10(9)/L). One patient had low proliferation responses to S. aureus, and one to phytohemagglutinin and pokeweed mitogen. Immunoglobulin levels, compared with those in age-related control subjects, were normal except that two patients had transient, borderline low IgG levels and two had elevated IgA levels. Specific antibody tests showed (No. of patients with positive results/No. tested) the following: diphtheria (13/13); tetanus (13/13); poliomyelitis caused by polio virus type 1 (5/9), type 2 (9/9), and type 3 (8/9); measles (11/13); rubella (11/13); and infection with VZV (5/5) and CMV (7/13). There were no significant differences in antibody avidity results between patients and control subjects for rubella (mean avidity index, 83.5 +/- 8.79 vs 85 +/- 17.6), VZV (81.6 +/- 3.98 vs 65.1 +/- 12.38), or CMV (69.3 +/- 22.31 vs 73.3 +/- 12.46). CONCLUSIONS: Patients with "partial" DiGeorge anomalad, defined by clinical and immunologic criteria, can be immunized and for the most part can generate good antibody responses.

Adolescent↗

PubMed1989

The time course of the humoral immune response to rhinovirus infection.

The specific humoral immune response of 17 volunteers to infection with human rhinovirus type 2 (HRV-2) has been measured both by neutralization and by ELISA. Six volunteers who had HRV-2-specific antibodies in either serum or nasal secretions before HRV-2 inoculation were resistant to infection and illness. Of the remaining 11 volunteers who had little pre-existing HRV-2-specific antibody, one was immune but 10 became infected and displayed increases in HRV-2-specific antibodies. These antibodies first increased 1-2 weeks after infection and reached a maximum at 5 weeks. All six resistant volunteers who had high pre-existing antibody and eight of the volunteers who became infected maintained their HRV-2-specific antibody for at least 1 year. At this time they were protected against reinfection. Two volunteers showed decreases in HRV-2-specific antibodies from either serum or nasal secretions. They became infected but not ill after HRV-2 inoculation 1 year later.

Adult↗

PubMed1995

In vitro evaluation of the role of humoral immunity against Bartonella henselae.

The contribution of humoral immunity against Bartonella henselae was evaluated by examining the in vitro bactericidal activity of sera and the ability of these microorganisms to activate complement and stimulate phagocytosis and an oxidative burst in polymorphonuclear leukocytes. The organism was killed by complement-mediated cytolysis. Complement activation preferentially proceeded by the alternative pathway. The presence of specific antibodies did not increase the serum bactericidal activity or complement activation. However, phagocytosis and the subsequent production of oxygen radicals, evaluated by flow cytometry, were significantly enhanced in the presence of bacteria previously opsonized with immune sera.

Adult↗

PubMed1981

Humoral immune response in vitamin A deficient children.

Humoral immune response was evaluated in children with vitamin A deficiency. The percentage of B lymphocytes and the initial levels of plasma IgA, IgG and IgM were normal. Two weeks after the immunisation with diphtheria and tetanus toxoids, there was a marked increase in the antibody titers. There were no significant differences between the deficient and the normal children. The results indicate that the antibody production is not altered in children with vitamin A deficiency.

Antibody Formation↗

PubMed1982

[Humoral immune defects in adults].

The importance of humoral immune defects and of the antibody deficiency syndrome, respectively, at adult age was examined on 69 patients. As immunological methods the estimation of the immunoglobulins G, A, M, D with Mancini's technique, of IgA-antibodies with Ouchterlony's technique, of T-lymphocytes with the sheep erythrocyte rosette test, of B-lymphocytes with direct immunofluorescence and mouse erythrocyte rosette test were used. The enzyme adenosine deaminase was determined in the plasma, the erythrocytes and the lymphocytes. 31 patients with primary antibody deficiency syndrome, of them 22 patients with selective IgA-deficiency could be diagnosed. 38 patients with secondary antibody deficiency syndrome came from groups of patients with lymphoproliferative diseases (non-Hodgkin-lymphoma and plasmocytoma), chronic dialysis and other haematological diseases. In 80% of the patients clinical symptoms of an immune defect could be proved. Chronically relapsing infections of the respiratory tract are in the first place. Familial accumulation, allergic reactions, antibodies against IgA, statistically significant accumulation of gastric and duodenal ulcers set off the anyway large group of patients with selective IgA-deficiency. An antibody deficiency syndrome with IgA-deficiency could be proved in 5 of 16 patients undergoing the dialysis programme, but clinically it is perhaps insignificant. Disturbances of the cell-mediated immune reaction occurred in a child with teleangiectatic ataxia and lymphoproliferative diseases. A deficiency of adenosine deaminase, which is of importance in combined immune defects syndrome at adult age, but it is to be proved in the plasmocytoma and the non-Hodgkin-lymphoma. The necessity of the knowledge of forms of the antibody deficiency syndrome at adult age results from the increasingly immunosuppressively acting therapeutic measures, correct and well-timed diagnosing as well as the necessity of aimed consultation of the physician in institutions specialised in immunology.

Adult↗

PubMed2005

The role of the humoral immune system in multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE).

The pathogenic events in multiple sclerosis (MS) that result in immune cell infiltration, multifocal demyelination and axonal loss have been focused by the strong impact of the classical MS model experimental autoimmune encephalomyelitis (EAE) towards the hypothesis that MS is an entirely T cell-mediated disease. Although conspicuous humoral immune responses have been known since Kabal's seminal finding of elevated immunoglobulins (Igs) in the cerebrospinal fluid (CSF), only in the past few years evidence derived from recent studies of the MS lesion of anti-myelin antibodies (Abs) in patients with early MS and of MS animal models has led to a renewed interest in the role for B cells, plasma cells and their products in the pathogenesis of MS. This review surveys the actual data concerning the role of the humoral immune system in MS and EAE and explains potential modes of action and long-time persistence in the inflamed brain tissue as a B cell-supportive microenvironment in MS. These mechanisms include the modulation of antigen presentation and costimulation to T cells, increased myelin opsonisation und recruitment of inflammatory cells to the CNS, but also immunoregulatory influences on the remyelination by anti-myelin B cells and Abs. So, affecting the humoral immune system in MS would be a reasonable therapeutic option.

Animals↗

PubMed1979

[Exploration of humoral immunity in man using blood lymphocytes cultures (author's transl)].

New methods allow the study of humoral immunity in man using blood lymphocyte cultures. A primary in vitro antibody response can be induced, characterized by the appearance of antibody forming cells, and its pattern is as follows: stringent culture requirements, which have been so far obtained in few laboratories; the kinetics of the response, with a peak on day 7--8; and exclusively IgM response; a T-cell requirement. Among these methods, the model we have described has the advantage of allowing a reproductible response in a given individual. The in vitro study of humoral immunity has limitations, the most apparent of which is that it addresses itself to only one lymphoid population, that in peripheral blood, easily accessible. It presents several advantages, as compared to an in vivo study after injection of an antigen: absence of ethical problem; the necessity of only one blood sample, at a given time, avoiding the interference of a treatment started after the test; the possibility of performing successive primary stimulations for a longitudinal study.

Acrylamides↗

PubMed1998

The humoral immune response to Haemophilus influenzae type b: a mathematical model based on T-zone and germinal center B-cell dynamics.

Through careful mapping of the physiology of the T-zone and GC B-blast dynamics to a mathematical representation of the cell processes including proliferation, migration, differentiation, and cell death, a mathematical model is constructed to capture the dominant nominal primary, late follicular, and secondary humoral response to Haemophilus influenzae Type b. This model explicitly incorporates the dynamics of memory B-cells, T-zone and GC B-dynamics, IgM and IgG antibodies, avidity maturation, and IC presentation by FDCs into a coherent framework. This paper describes the relevant immunology, the pertinent physiological assumptions, the developed model, and the parameter identification procedure. The model parameters were found using a parameter identification procedure that capitalizes on the timing and interactions of certain dominant physiological attributes. Simulation results and validation tests indicate that the model reflects not only a nominal primary and secondary humoral immune response but also the tertiary and T-independent responses. The model shows robustness to variations in infection dosage, bacterial growth rate (virulence of the strain), and onset-timing of the secondary response. The utility of this model in studying the humoral immune response is demonstrated through suggested physiological assumptions, mechanisms, and rates to be eventually clinically evaluated as well as insights into vaccination design. The model and parameter identification techniques are easily adapted to other diseases which primarily evoke a humoral immune response.

Antibodies, Bacterial↗

PubMed1982

Potentiation of the primary humoral immune response in vitro by C5a anaphylatoxin.

The effect of the anaphylatoxin C5a on the primary humoral immune response to SRBC was studied in culture of spleen cells from C3H mice. The addition of human C5a to antigen-stimulated cultures resulted in a significant, dose-dependent augmentation of the primary PFC response to antigen. The specificity of this effect was affirmed by the ability of C5ades Arg, but not of the structurally analogous C3a anaphylatoxin, to act in a parallel fashion. Enhancement could be observed over a range of doses of antigen. Brief preincubation of macrophages, but not of lymphoid cells, with C5a was sufficient to cause subsequent enhancement of the primary humoral immune responses. The duration of preincubation required for this effect closely paralleled that for binding of C5a to peritoneal cells. Immunopotentiation by C5a appears to involve the function of C5a receptor-bearing, Ia- accessory cells as well as Ia+ antigen-presenting cells. Immunopotentiation could be observed when the addition of C5a was delayed for up to 24 hr after initiation of culture. Additionally, augmentation of tritiated thymidine uptake in mixed lymphocyte reactions was enhanced by the addition of C5a in a fashion parallel to that for the primary response to SRBC. These observations support a role for C5a as a modulator of cellular immunity in addition to its role in acute inflammation. Possible cellular mechanisms and implications for immunomodulation of immune responses are discussed.

Adjuvants, Immunologic↗

PubMed1988

[Effect of unilateral nephrectomy in mice on the level of the humoral immune response to T-independent antigen].

The influence of unilateral nephrectomy on the degree of humoral immune response to T-independent (polyvinylpyrrolidone, PVP) and T-dependent (sheep red blood cells, SRBC) antigens was studied. The increase in the number in antibody-forming cells (AFC) and nonspecific immunoglobulin-forming cells (nIFC) was investigated by means of the adaptive transfer model. The lethally irradiated recipients were injected with the antigen and also the spleen cells of operated and intact donors. PVP did not induce significant alterations of antibody genesis in mice receiving spleen cells of unilaterally nephrectomized animals comparing with recipients of intact spleen cells. At the same time, the kidney operation induced the increase in the number of AFC and nIFC when the SRBC were used. Hence the activation of humoral immune response induced by kidney operation was related not to the direct activation of B-lymphocytes but to T-cells. The possible causes of this activation were analyzed. Spleen cells of operated animals enhance both specific and antigen-dependent nonspecific immune response.

Animals↗

PubMedDate not supplied

Nature of the decline in antigen-induced humoral immunity with age.

An attempt has been made to summarize our present knowledge of the influence of age on humoral immunity, as judged by the ability of an individual to generate antibody in response to antigenic stimulation. In general, humoral immunity declines with age, and the onset can occur as early as when an individual reaches sexual maturity. The decline is due to changes in the immune cells and their milieu. Cell loss, shift in the proportion of subpopulations, and qualitative cellular changes have all been detected. The most prominent cellular target of aging appears to be T cells involved in the regulation of humoral response. Since the changes are closely associated with the involution and atrophy of the thymus, an understanding of its changes could be the key to understanding immunosenescence.

Aging↗

PubMed2000

Regulation of humoral immune responses by CD21/CD35.

Before antigen-specific immunity arises, the complement system responds by activation through the classical and/or alternative pathways leading to the covalent deposition of complement fragments. Three models, not mutually exclusive, have been proposed to explain how these complement fragments interact with their receptors, CD21/CD35, to enhance humoral immune responses: i) CD21/CD35 retain and focus antigens for optimal presentation; ii) CD21/CD35 on B cells serve as enhancing co-receptors for B-cell antigen receptor (BCR) signaling; iii) CD21/CD35 regulate B-cell responses, by CD19 aggregation. The coreceptor model led us to predict that CD21/CD3 5 may lower the threshold of BCR affinity to diversify the repertoire of humoral immune responses, but surprisingly, CD21/CD3 5-deficient mice expressing a transgenic BCR with very low affinity (Kalpha approximately =1.2 x 10(5) M(-1)) for the (4-hydroxy-3-nitrophenyl)acetyl hapten generated significant antibody and germinal center responses to even low doses of antigens in alum. The magnitudes of these responses were much below those of normal controls but higher doses of antigens substantially rectified these deficits. Thus, while CD21/CD35 play important roles in humoral immunity, our observations provide little support to the hypothesis that CD21/CD35 promote clonal diversity in immune responses by helping recruit low-affinity B cells.

Animals↗

PubMed1999

Role of maternal humoral immunity in vertical transmission of HIV-1 subtype E in Thailand.

The significance of the maternal humoral immune response in relation to vertical transmission of HIV-1 was investigated in 123 mothers infected with subtype E from Thailand. Antibody binding titers to HIV-1 env domains (monomeric gp120, the CD4/gp120 binding site [BS], V3 loop, and gp41) and antibody-mediated neutralization of primary and T-cell line-adapted (TCLA) subtypes B and E HIV-1 isolates were investigated. No correlation between maternal anti HIV-1 antibodies at delivery and vertical transmission of HIV-1 subtype E was found. However, a trend to higher titer antibody-mediated cross-neutralization of a heterologous subtype B TCLA isolate, HIV-1MN, was observed in nontransmitting mothers postpartum. The HIV-1-specific antibody titers in these infected mothers increased significantly from delivery to 6 months postpartum (p < .05), but this was only partially attributable to hemodilution and an additional factor or factors appear to affect humoral immunity to HIV-1 during late pregnancy.

Adult↗

PubMed2000

Dynamics of the humoral immune response of calves infected and re-infected with Cooperia punctata.

The dynamics of the humoral immune response of calves were analysed after primary infection and re-infection with the intestinal nematode Cooperia punctata. 12 male 5 month-old Holstein-Friesian calves were randomly divided into two groups A and B. At the beginning of the experiment Group A animals were each infected experimentally with a single oral dose of 130,000 infective third stage larvae (L3) of C. punctata. The animals of Group B were kept as non-infected controls. The two calves from Group A with the highest infections died of cooperiosis at 32 and 44 days after infection (DAI), respectively. On DAI 100 the calves were treated with the recommended dose of oxfendazole. On DAI 180 the remaining four calves of Group A and three animals of Group B (B1) were infected with 260,000 L3 of C. punctata, while the other three calves of Group B (B2) served as non-infected controls. Monitoring of the humoral immune response predominantly demonstrated an IgG1 response against both adult and L3 antigen of C. punctata. Moreover, re-infections increased the levels of these immunoglobulins. IgA levels were less increased than IgG1 and no significant increase was observed in IgG2 and IgM levels. Immunoblotting analysis showed that total IgG present in the serum of the primary infected animals mainly reacted against adult proteins of 12-14 and 17-20 kDa and against L3 proteins of 33 and 43 kDa. After re-infection total IgG reacted with the same adult proteins but also with an adult 29 kDa protein.

Animals↗