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Results for “Immunity, Humoral”

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PubMed1984

Host defenses in murine malaria: humoral immunity to Plasmodium berghei in mice.

Humoral immunity to Plasmodium berghei infection of F1 hybrid B6D2 (C57B1/6 X DBA/2) mice was investigated using an immune serum prepared from mice which survived a lethal challenge of erythrocytic stage P. berghei because of previous vaccination with formalin-killed P. berghei. Immune serum, but not normal serum, if injected intraperitoneally or intravenously soon after infection, during rapidly increasing parasitemia, transiently inhibited the progress of infection in a pattern which was directly related to the dose and timing of serum injection. However, the level of restriction of parasitemia caused by the intravenous injection of 1 ml of immune serum could not be improved upon by subsequent additional 1-ml injections of the same serum, and parasitemia in all mice, whether delayed by immune serum or not, ultimately progressed to death. The protective capacity of the immune serum was markedly specific for plasmodial species but absorption with formalin-killed homologous parasites failed to remove the protective component. No variants of P. berghei insensitive to inhibition by immune serum were detected. The results support the view that humoral immunity to P. berghei may be mediated by more than one soluble factor and effected through at least two different pathways.

Animals↗

PubMed2000

Interactions between the cellular and humoral immune responses in Drosophila.

Drosophila has highly efficient defenses against infection. These include both cellular immune responses, such as the phagocytosis of invading microorganisms, and humoral immune responses, such as the secretion of antimicrobial peptides into the hemolymph [1] [2]. These defense systems are thought to interact, but the nature and extent of these interactions is not known. Here we describe a method for inhibiting phagocytosis in Drosophila blood cells (hemocytes) by injecting polystyrene beads into the body cavity. This treatment does not in itself make a fly susceptible to Escherichia coli infection. However, when performed on flies carrying the mutation immune deficiency (imd), which affects the humoral immune response [3], the treatment results in a striking decrease in resistance to infection. We therefore carried out a sensitized genetic screen to identify immunocompromised mutants by co-injecting beads and E. coli. From this screen, we identified a new gene we have named red shirt and identified the caspase Dredd as a regulator of the Drosophila immune response. The observation that mutants with defects in the humoral immune response are further immunocompromised by blocking phagocytosis, and thus inhibiting the cellular immune response, shows that the Drosophila cellular and humoral immune responses act in concert to fight infection.

Animals↗

PubMed2002

Immune responsiveness in renal transplant recipients: mycophenolic acid severely depresses humoral immunity in vivo.

BACKGROUND: Current immunosuppressive drug treatments for renal transplant recipients result in high one-year graft survival rates. Despite adequate suppression of the immune response directed to the allograft, the immune system remains able to cope with many infectious agents. METHODS: To define the influence of distinct immunosuppressive treatment protocols, primary and secondary cellular and humoral immune responses in groups of renal transplant recipients were studied: patient treated with prednisolone and cyclosporine A (P/CsA); with IgA CD3 monoclonal antibody as a rejection treatment superimposed on prednisolone and cyclosporine A (IgA CD3 mAb+P/CsA); and with prednisolone, cyclosporine A and mycophenolate mofetil (P/CsA/MMF). RESULTS: Primary in vitro proliferative responses to the protein antigen keyhole limpet hemocyanin (KLH) were not significantly disturbed in P/CsA treated patients, or in IgA CD3 mAb+P/CsA and P/CsA/MMF treated patients. In vitro proliferative responses to the recall antigen tetanus toxoid (TT) were similarly unaffected. Antigen-specific antibody responses to immunization with KLH and TT were not affected by treatment with P/CsA, or by IgA CD3 mAb+P/CsA, but were severely disturbed in patients treated with P/CsA/MMF. All patients displayed a profound inhibition of the delayed-type hypersensitivity skin reactivity to KLH and recall antigens. Nevertheless, in most patients with P/CsA treatment, T cell infiltrates were observed in skin biopsies from the site of KLH challenge, while expression of intercellular cell adhesion molecule-1 (ICAM-1) expression in challenged skin was significantly decreased in these patients. The balance between T helper 1 and T helper 2 cells was unaffected by immunosuppressive treatments during one year of follow-up. CONCLUSIONS: Immunosuppressive drug treatment with P/CsA inhibits delayed-type hypersensitivity skin reactions to both primary and frequently encountered antigens. Histological studies indicate an effect on ICAM-1 expression, leaving the influx of CD3pos T cells unaffected. Administration of a 10-day course of IgA CD3 mAb does not add profound immunosuppressive effects on the measured parameters. In contrast, addition of treatment with MMF profoundly decreases both primary and secondary humoral immune responsiveness in vivo. Finally, no effect of the studied immunosuppressive drugs on Th1/Th2 balance in vivo was measured.

Adolescent↗

PubMedDate not supplied

Pathophysiology of viral myocarditis: the role of humoral immune response.

The pathophysiology of viral myocarditis is still a matter of debate. Humoral autoimmunity in postviral heart disease remains an attractive but complex hypothesis. Antigenic mimicry with or without cytolytic antibody properties has been shown to play a role in the immunopathogenesis of myocarditis with respect to sarcolemmal/myolemmal epitopes (including the beta-receptor), myosin and some mitochondrial proteins including the antinucleotide translocator (ANT)-carrier and dihydrolipoamid dehydrogenase. Today, refined two-dimensional Western blots are able to identify receptors and enzymes that are target of a humoral immune response or the consequence of an "immunization process." A humoral immune response to an invading agent will most likely lead to immunodestruction first. After conversion to IgG, the continuing antibody response may indicate the healing or healed process and last for many years or life-long. This paper reviews our present knowledge on the humoral immune response in myocarditis and its interplay with the viral agents and the other components of the immune system.

Animals↗

PubMed1976

Cytomegalovirus infection and immunity in renal allograft recipients: assessment of the competence of humoral immunity.

Cytomegalovirus (CMV) infections are prevalent in renal allograft recipients. The purpose of this ongoing study is to attempt to elucidate the mechanism(s) responsible for the enhanced susceptibility to CMV infections on the part of transplant patients and for their apparent inability to eradicate the infection once it starts. The present report assesses the competence of humoral immunity to CMV in renal allograft recipients. The total study population was comprised of 41 renal allograft recipients (10 followed prospectively) and 38 age-matched control subjects. The overall CMV infection rate in renal allograft recipients was 90.2%, and in 11 cohort control subjects it was 45.5%. Active infection was present in 61.0% of transplant patients (24.0% of these had CMV disease) and in 18.2% of the cohorts. THESE DIFFERENCES ARE SIGNIFICANT. CMV complement fixation and neutralization antibody prevalence was similar in 10 patients with renal failure undergoing hemodialysis before transplantation and in 23 control subjects. There was similarly no difference in antibody response between allograft recipients in whom the infection was primary (eight subjects) or secondary (17 subjects). We conclude that despite immunosuppressant therapy (with azathioprine and corticosteroids), humoral immunity to CMV is not impaired in transplant patients with either a primary or secondary infection.

Age Factors↗

PubMed1994

Cell-mediated and humoral immunity in bulls infected with IBR/IPV virus (BHV 1).

Time-related changes in specific cell-mediated immunity (CMI) and in humoral immunity were monitored in 20 bulls, aging 12 to 16 months, in four groups, each consisting of 5 animals. Group I was experimentally and group III-naturally infected with BHV 1 virus, groups II and IV serving as control animals. Tests for CMI included delayed type hypersensitivity (DTH), leukocyte migration inhibitory factor (LMIF) and granulocyte migration inhibitor factor (GMIF-LIF-buffy coat leukocyte migration inhibitory factor) in the presence of BHV I antigen while humoral immunity was tested by serum induced neutralization of the virus (SN) and by estimation of serum IgG, IgG1, IgG2, IgM and IgA levels. Immunologic, virologic and clinical studies were performed two days before infection and 17 timed within 91 days after the infection in bulls of group I and II and 7 times within 42 days after developing the disease in bulls of groups III and IV. The results showed that positive CMI reactions appeared 3 to 4 weeks earlier than positive antibody titers in SN test. The antibodies belonged most probably to IgG1 and IgG2 subclasses.

Animals↗

PubMed1999

The immune system in the elderly: I. Specific humoral immunity.

Profound and complex changes in the immune response occur during the aging process. Immunosenescence is reflected by a sum of disregulations of the immune system and its interaction with other systems. Many of the changes would appear to implicate age-related deficiencies of the immune responses. The term immunosenescence designates therefore a sort of deterioration of the immune function which is believed to manifest itself in the increased susceptibility to cancer, autoimmune disease, and infectious disease. Evidence has been accumulating from several studies which suggest an association between immune function and individual longevity. However, there are observations, especially in very old healthy people, that several immune functions are unexpectedly well preserved and substantially comparable to those observed in young subjects. These findings raise the question of whether the alterations that can be observed in the immune parameters of the elderly are a cause or a result of underlying disease processes. Moreover, studies on centenarians revealed a remodeling of the immune system rather than a deterioration, suggesting that the changes observed during immunosenescence do not correspond to immunodeficiency. The underlying mechanisms of these events are however still unclear. The purpose of the present review is to assess the status of research on the immunobiology of aging. In this first section, we focus attention on the B cell biology of aging. In clinical practice, the changes in humoral immune responsiveness and antibody-mediated defense mechanisms could greatly influence the incidence and outcome of bacterial infections and autoimmune diseases as well as the response to vaccines.

Aged↗

PubMed1991

Serological evidence for major histocompatibility complex (B complex) antigens in broilers selected for humoral immune response.

Genetic selection for early humoral immune responsiveness against two simultaneous antigens, namely, heat-killed Escherichia coli and Newcastle disease virus vaccine (NDV), was performed in a heterogenic population of broiler chickens. The humoral immune response was measured prior to 24 days of age, depending on the vaccine. Chicks were divided into two populations according to their antibody response: a population of high responders to both antigens and a population of low responders. After four generations of selection, a significant difference was observed in the immune response of the two populations, and therefore, an attempt was made to identify possible differences in the segregation of major histocompatibility complex genes. Using alloantisera prepared in B-congenic White Leghorn, the high responders exhibited a high percentage of chickens having erythrocytes agglutinated with B5 antisera, and the low responders exhibited a high percentage of chicks with erythrocytes agglutinated with B15 and B19 antisera. The B13 antisera agglutinated cells of similar proportions of chickens in the two populations. A random commercial broiler flock was screened with the antisera, and correlation was high between B haplotype and antibody level to E. coli following vaccination. The present work indicated the possibility of a direct association between the genetic characteristics represented in the B complex and humoral antibody response in a broiler population.

Animals↗

PubMedDate not supplied

Immunology of chronic generalized periodontitis. 1. Estimation of cellular and humoral immune status.

Cell-mediated and humoral immune responses were assessed in forty patients with chronic generalized periodontitis (CGP), and in an equal number of control subjects. The cell mediated immunity assessed by enumeration of total rosette forming cells [TRFC] and high affinity rosette forming cells [HARFC], were found to be slightly depressed in CGP patients compared controls. The humoral immune response was assessed by estimation of serum immunoglobulins G,A,M,D and E by single radial immunodiffusion technique (RID). Except IgD all the other immunoglobulins were found to be elevated significantly. These immunological derangements found in CGP patients may be the cause or effect of the disease process.

Adult↗

PubMed1982

Genetic regulation of the immune response to hepatitis B surface antigen (HBsAg). I. H-2 restriction of the murine humoral immune response to the a and d determinants of HBsAg.

In hepatitis B virus (HBV) infection correlation of disease activity with major histocompatibility complex (MHC) antigens has been suggested. However, no data are available regarding the nature and regulation of the immune response to the surface viral protein (HBsAg). This consideration and the current emphasis on production of an HBV vaccine led us to investigate the humoral immune response to HBsAg in inbred strains of mice to assess genetic factors that may regulate the humoral anti-HBs response. Studies with H-2 congenic and noncongenic inbred strains revealed the T-dependent humoral immune responses to the group-specific a and subtype-specific d determinants of HBsAg are regulated by gene(s) mapping to the murine MHC. The H-2q haplotype conferred high responsiveness, the H-2s,f haplotypes conferred low to nonresponsiveness, and the H-2a,b,d,k haplotypes were intermediate. Studies of H-2 recombinant strains allowed tentative mapping of regulation of the anti-a response and possibly the anti-d response to the K/I-A, I-B region of the MHC. The H-2-restricted regulation of the humoral immune response to HBsAg was circumvented by immunization with 10-fold higher HBsAg doses. These findings demonstrate a clear linkage between the murine MHC and the regulation of the immune response to specific determinants on HBsAg.

Animals↗

PubMed1986

Humoral immune responses within the human central nervous system following systemic immunization.

We investigated sequential humoral immune responses in the CSF and blood of 6 stable multiple sclerosis (MS) patients without decreases in the blood-brain barrier. Anti-tetanus toxoid antibodies (anti-TT Ab) increased to a similar relative degree within the CSF and blood starting within 2 weeks after subcutaneous booster injection of TT. In 3 of 4 subjects, CSF lymphocytes obtained at 2 weeks secreted anti-TT Ab to the same degree as autologous blood lymphocytes when cultured with pokeweed mitogen. These findings suggest a prompt antibody response within the CSF to systemically administered antigen, not due to diffusion from the serum, with active trafficking of TT-sensitized lymphocytes into the central nervous system.

Adult↗

PubMed2003

Mechanisms of hypergammaglobulinemia and impaired antigen-specific humoral immunity in HIV-1 infection.

Hypergammaglobulinemia and defective humoral immunity are hallmarks of HIV-1 infection. Naive B cells have been recently suggested as the major source of hypergammaglobulinemia in chronic viral infections. We recently reported that HIV-1-infected patients carry low levels of memory B cells. Here we studied whether defects in the naive and memory B cells in HIV-1-infected patients translated into hypergammaglobulinemia and defective humoral immunity against specific antigens. Naive B cells from HIV-1-infected patients exhibited abnormal expression of the activation/differentiation markers CD70 and leukocyte-associated Ig-like receptor (LAIR-1). Activated naive B cells from patients showed a significant increase in the intracellular immunoglobulin G (IgG) content ex vivo and this activated phenotype correlated to hypergammaglobulinemia and to the ability of naive B cells from patients to secrete IgG in vitro. We analyzed the levels of antibodies to tetanus toxoid, measles, and HIV-1 in relation to memory B cells and observed a significant reduction of antigen-specific antibodies in patients with low-memory B lymphocytes. Nevertheless, hypergammaglobulinemia and levels of polyspecific self-reactive antibodies were comparable in patients with normal and low memory B cells. We conclude that reduction of memory B lymphocytes in HIV-1 infection correlates with defective humoral immunity and that hyperactivated naive B cells may represent the source of abnormal IgG production in HIV-1 infection. Our results may be relevant to the design of HIV-1 therapeutical vaccines and to the clinical management of HIV-1-infected patients.

Adult↗

PubMed1987

[Role of helper T-lymphocytes in modulating the humoral immune response to cholera enterotoxin].

The role of helper T-lymphocytes in the modulation of humoral immune response to sheep red blood cells with choleragen has been studied in vivo, the populations of cooperating marrow cells, formed in mice under the action of hydrocortisone being used as a model. In adoptive transfer marrow cells, taken from mice on day 12 after thymectomy and from mice previously treated with antithymocyte serum, have proved incapable of humoral immune response. Choleragen, similarly to theophylline, normalizes the humoral immune response of marrow cells in thymectomized mice, but inhibits this response in intact ones, while thymosin fraction 2 restores it again, thus abolishing the action of choleragen and theophylline. The opposite effects rendered by choleragen and theophylline on humoral immune response, depending on the hormonal status of the animals and the possibility of influencing these effects by means of thymosin fraction 2 indicate that the population of helper T-lymphocytes are selectively sensitive to changes in the concentration of intracellular cAMP. Their capacity for cooperative interaction in the immune process is regulated by thymic hormones and forms the basis of the mechanism permitting the modulation of humoral immune response with choleragen.

Animals↗

PubMed1987

The role of humoral immunity in Lactobacillus casei cell wall induced arthritis.

Although both cellular and humoral immunity have been shown to play important roles in the development of collagen induced arthritis, their roles in the pathogenesis of bacterial cell wall induced arthritis remain unclear. Previous studies of humoral immunity in bacterial cell wall induced arthritis were carried out in outbred animals and measured the humoral response to only the eliciting bacteria. We compared the humoral immune responses of arthritis susceptible Lewis and arthritis resistant Fisher rats after the injection of arthritogenic group B Lactobacillus casei cell wall fragments. Both strains developed significant IgG and IgM responses to the Lactobacillus casei cell wall fragments. Neither strain developed a significant immune response to types I, II, IX or 1a2a3a collagens. These data suggest that humoral immune responses to the Lactobacillus casei cell wall fragments and types I, II, IX, or 1a2a3a collagens do not play a significant role in determining the differing arthritis susceptibilities of Lewis and Fisher rats.

Animals↗

PubMed1977

[Effects of anesthesia and surgery on certain parameters of humoral immunity].

Research on certain parameters of humoral immunity was undertaken in 10 patients who had undergone a major surgical operation. The control subjects were chosen among 10 subjects in good health. The tests were carried out within 24-72 hours after the operation. The determination of cytolytic lymphocyte activity, in the presence of specific antibodies, was strongly lowered in the postoperative period. This was also the case with the capacity to form EAC lymphocyte rosettes. Finally total serum complement was lowered significantly whereas factor C3 remained normal. These results show a change in humoral immunity in the postoperative period together with a reduction in complement activity.

Anesthesia↗

PubMed2007

Potential role of humoral immunity in the pathogenesis of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE).

The earliest research literature addressing sub-clinical characteristics of Multiple Sclerosis was largely focused on humoral immune components, particularly antibodies in the cerebrospinal fluid of MS patients. However, two decades later, in the 1990's, T cells were established as a major component of the underlying mechanism(s) of MS pathogenesis, especially since EAE, the mouse model of MS, could be readily induced by immunization with myelin derived peptides or passive transfer of encephalogenic T cells. This data has contributed to the concept that the role of humoral immunity in MS pathogenesis may be negligible. However, more recent studies have provided important insights regarding the role of humoral immunity in MS pathogenesis. The goals of this review are to 1) summarize evidence for and against the hypothesis that humoral immunity plays a central role in the pathogenesis of MS, and 2) summarize studies in the EAE model that directly tested the role of humoral immunity in pathogenesis of the disease. With this information, we hope to convince the reader that great strides have been made towards defining a central role of humoral immunity in MS pathogenesis, but that there is a substantial amount of work to be done (especially in the EAE model) to ensure that the contribution of humoral immunity to MS pathogenesis is effectively addressed.

Animals↗

PubMed1997

Effect of age on humoral immunity, selection of the B-cell repertoire and B-cell development.

The age-associated changes in humoral immunity affect the quality more than the quantity of the antibody response. Changes in the quality of the antibody response with age include shifts in antibody specificities from foreign to autoantigens, in antibody isotypes from IgG to IgM, in antibody affinities from high to low and in the antibody idiotypic repertoire. These changes can be traced to an impaired capacity of T cells to facilitate: (a) the maturation of B cells with respect to isotype and affinity maturation in the periphery and (b) the development of a diverse B-cell repertoire from precursors within the bone marrow. In contrast, there is no evidence that the amount of immunoglobulin produced before or after immunization diminishes with age. Nonetheless, the impaired responses of the elderly to most vaccines and the greater susceptibility of the elderly to infections has fostered a view that immune senescence leads to a state of immune deficiency. However, it is more precise to describe immune senescence as leading to a state of immune dysregulation. The dysregulation of the humoral immunity is manifested by a shift from adaptive humoral immunity, characterized by the production of a highly specific, high-affinity, IgG antibody response to foreign antigens, to a process of natural antibody-mediated immunity, dominated by low-affinity, polyreactive, IgM antibodies which react with autoantigens. Age-associated T-cell impairments appear to be the basis for the shift from adaptive to natural humoral immunity and their reversal should permit the restoration of an adaptive antibody response in the elderly.

Aging↗

PubMed2006

Evidence for a novel endocrine disruptor: the pesticide propanil requires the ovaries and steroid synthesis to enhance humoral immunity.

Steroid hormones are known to affect the humoral immune response to a variety of antigens. However, the mechanisms regulating these effects are poorly understood. The immunotoxic chemical propanil and estrogen have similar effects on the immune system including augmentation of humoral immune responses. Propanil enhances the number of phosphorylcholine (PC)-specific IgG2b, IgG3, and IgM antibody-secreting cells (ASCs) in the spleen four- to sixfold 7 days after vaccination of female C57BL/6 mice with heat-killed Streptococcus pneumoniae. Several experiments were performed to test the hypothesis that propanil increases the response via an estrogenic pathway. Ovariectomy abrogated the effect of propanil on the PC-specific ASC response. Both in vitro and in vivo assays indicate that propanil does not bind either estrogen receptor (ER) alpha or beta. Exogenous estradiol administration in ovariectomized mice failed to restore the effect of propanil on the PC response. Treatment of female mice with a pure ER antagonist, ICI 182,780, or the progesterone antagonist RU486 did not inhibit the increase in ASCs. These data suggest that estrogen and progesterone do not regulate the effect of propanil. However, complete inhibition of steroid synthesis with the gonadotropin-releasing hormone (GnRH) antagonist antide abrogated the increased response in propanil-treated mice, indicating a necessary role for steroid synthesis. Experiments in male mice demonstrated that propanil increased the number of ASCs comparable to female mice. However, orchiectomy did not inhibit this effect, suggesting that androgens do not regulate the amplification of the humoral response. These data suggest a novel role for the ovarian hormones in the regulation of the PC-specific antibody response.

Animals↗