PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Immunity, Humoral”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed2004

Assessment of humoral immune response in patients with chronic hepatitis C virus infection.

Hepatitis C infection is a major public health problem worldwide. Hepatitis C virus (HCV) infection has been identified as a major causative agent of post-transfusion hepatitis. The host immune response to HCV infection is composed of both non- specific immune response, including interferon (IFN) production and natural killer (NK) cell activity and a virus-specific immune response, including humoral and cellular components. Susceptibility to infection has been related to immunological disturbances. Several studies have provided experimental evidence of disorders of both cellular and humoral immunity. Humoral Immunity is dependent mainly on immunoglobulins and little data are available about serum immunoglobulin values in chronic hepatitis C. The present study aimed to evaluate humoral immune response by measuring the concentration of serum immunoglobulin isotypes (IgG, IgM, IgA) and IgG-subclasses level (IgG1-4) in chronic hepatitis C patients and healthy controls. This study included 50 patients with chronic hepatitis C. All of them had positive serum anti-HCV antibodies, positive serum HCV-RNA by PCR, and histologically-proven chronic hepatitis. The results were compared with 25 healthy controls. Total IgG, IgA and IgM were assayed by nephelometry. IgG subclasses were assayed using human IgG subclasses enzyme immunoassay. Serum protein electrophoresis was performed in agarose gel. The results showed that no significant difference in serum immunoglobulin levels were found among patients with chronic hepatitis C of minimal liver damage( Knodell index < or =3) and patients with mild liver disease (Knodell index > 3). A significant increase in total serum IgG, IgG1 and IgG2 levels were found in patients with chronic hepatitis than in healthy controls but no difference was found in IgG3 and IgG4 in both patients and controls. Mean serum IgM was increased in patients with HCV infection compared with healthy controls. No significant difference was found in IgA level in both the patients and healthy controls. Our data revealed an increase of humoral immune response in chronic hepatitis C infection. This is evidenced by an elevation in serum immunoglobulin isotypes; IgG and its subclasses IgG1 and IgG2 and IgM. These findings may provide some new insights into the antibody response to HCV.

Adult↗
PubMedDate not supplied

[Kinetics of the humoral immune response in mice immunized against and inoculated with Trypanosoma cruzi].

Evolution of the immune humoral response against experimentally induced Chagas disease was followed in three groups of white mice CD-1; one group without any previous treatment; a second group that had been immunized with membranes from cultured epimastigotes, and a third group treated only with Freund's adjuvant. The response was observed through immunotransference (Western Blot) against membrane antigens from cultured epimastigotes. As early as 11 days after inoculation, the sera of animals previously immunized showed a great number of recognition bands between 22 and 115 kDa; on the other hand, the animals treated only with adjuvant or those inoculated without any previous treatment, showed antibodies on the 18th day. These reacted against 52 and 62 kDa proteins. Antibodies against 68 and 72 kDa proteins were found on the 32nd day in mice treated with adjuvant and on the 39th day, in mice with no treatment. The antibodies could be relevant in the healing of the animals because they appear at the same time that parasites start disappearing from the blood.

Animals↗
PubMed1991

Lead and immunity: II. Suppression of humoral immune response to Hymenolepis nana in mice.

Serum protein changes in mice treated for varying durations with lead nitrate and subsequently infected with 1000 H. nana eggs were compared with their counterpart controls, only treated and only infected groups. Decreased values of beta and gamma globulins in all the experimental groups along with higher worm recoveries indicate suppression of humoral immune response by lead in association with higher worm recoveries indicate suppression of humoral immune response by lead in association with the cellular components since these globulins are known to contain antibodies. Lead treatment for a duration of 45 days proved to be most effective in suppressing the immune response.

Animals↗
PubMed1987

Suppression of humoral immunity in inbred mice by dieldrin.

The effect of single, sublethal i.p. injection of dieldrin on the primary antibody response to thymodependent (sheep red blood cells, SRBC) and T-cell-independent (lipopolysaccharide, LPS) antigens were investigated in inbred C57Bl/6 mice. Time-course studies showed significant suppression of the anti-SRBC IgM and anti-LPS IgM response at 7-24 days and at 4-14 days, respectively, after exposure to 0.6 LD50 of dieldrin. The anti-SRBC IgG response was also suppressed by dieldrin exposure, however, maximal suppressory effect was found at 48 days after the pesticide exposure. Similar patterns of the dieldrin-induced suppression of the primary IgM response to the thymodependent and T-cell-independent antigens, in addition to the overall control of cytotoxicity of lymphoid cell populations, suggest rather dysfunction of cellular cooperation during the inductory phase of the immune humoral response.

Animals↗
PubMed1999

[The changes in the humoral immune system during pregnancy with diabetes].

Gestational diabetes (GDM) is a carbohydrate intolerance of different severity with the onset during the pregnancy. GDM is a complication observed in 1-3% of pregnancies and has an important negative influence on foetal development. However most women with GDM do develop diabetes type 2, gestational diabetes could also be the beginning of a slow-progress towards the clinical onset of diabetes type 1. It is now possible, on the basis of the presence of antibodies directed against pancreatic autoantigens (ICA, GADA, IA-2A, IAA) to detect in the early stage of the autoimmune process leading to development of insulin-dependent diabetes (IDDM). In the present review we have summarised actual studies concerning the immune humoral alterations directed against pancreatic B cells in pregnant women with diabetes. We have also discussed the potential clinical implications of the presence of pancreatic autoantibodies in pregnant women with diabetes for the future risk of IDDM.

Antibody Formation↗
PubMed1982

In vitro assessment of humoral immunity following exposure to heavy metals.

The immune system of animals and man is extremely complex. This report will discuss the effect metals has on one segment of the immune system; that is, humoral immunity. Humoral immunity is essentially the production of antibody in response to an antigen. The B-lymphocyte is the primary cell responsible for producing antibody. However, this cell is regulated by T-lymphocytes and macrophages. Many methods are available to assess humoral immune responses. A multitude of immunoassays have been developed for enumeration of serum antibody. Some of these are immunodiffusion, complement fixation, serum neutralization, hemagglutination, radioimmunoassay and enzyme-linked immunosorbent assay (ELISA). Detection of antibody-forming cells distinguishes between effect on antibody production compared to degradation of preformed antibody. Other available methods are measurement of surface receptor (Fc and complement) activity on B-cells. Mitogens (T-independent) have also been regarded as a measurement for humoral immunity. In our laboratory, we have developed an ELISA technique that is appropriate for general assessment of humoral immune responses resulting from chemical exposure. This technique is highly sensitive and can be mechanized. The assay can easily be incorporated into the drug and chemical efficacy testing programs of industry.

Antibody Formation↗
PubMed2005

Both innate immunity and type 1 humoral immunity to Streptococcus pneumoniae are mediated by MyD88 but differ in their relative levels of dependence on toll-like receptor 2.

Little is known regarding the role of Toll-like receptors (TLRs) in regulating protein- and polysaccharide-specific immunoglobulin (Ig) isotype production in response to an in vivo challenge with an extracellular bacterium. In this report we demonstrate that MyD88(-/-), but not TLR2(-/-), mice are markedly defective in their induction of multiple splenic proinflammatory cytokine- and chemokine-specific mRNAs after intraperitoneal (i.p.) challenge with heat-killed Streptococcus pneumoniae capsular type 14 (S. pneumoniae type 14). This is correlated with analogous responses in splenic cytokine protein release in vitro following addition of S. pneumoniae type 14. Consistent with these data, naive MyD88(-/-), but not TLR2(-/-), mice are more sensitive to killing following i.p. challenge with live S. pneumoniae type 14, relative to responses in wild-type mice. However, prior immunization of MyD88(-/-) mice with heat-killed S. pneumoniae type 14 protects against an otherwise-lethal challenge with live S. pneumoniae type 14. Surprisingly, both MyD88(-/-) and TLR2(-/-) mice exhibit striking and equivalent defects in elicitation of type 1 IgG isotypes (IgG3, IgG2b, and IgG2a), but not the type 2 IgG isotype, IgG1, specific for several protein and polysaccharide antigens, in response to i.p. challenge with heat-killed S. pneumoniae type 14. Of note, the type 1 IgG isotype titers specific for pneumococcal surface protein A are reduced in MyD88(-/-) mice but not TLR2(-/-) mice. These data suggest that distinct TLRs may differentially regulate innate versus adaptive humoral immunity to intact S. pneumoniae and are the first to implicate a role for TLR2 in shaping an in vivo type 1 IgG humoral immune response to a gram-positive extracellular bacterium.

Adaptor Proteins, Signal Transducing↗
PubMed2006

Oral ingestion of cow's milk immunoglobulin G stimulates some cellular immune systems and suppresses humoral immune responses in mouse.

Four-week-old male C3H/HeN mice were bred with diets consisting of ovalbumin alone (OVA, control diet) or mixtures of OVA and cow's milk immunoglobulin G (IgG-added diets) as a protein source for 4 or 5 weeks, and both the cellular and humoral immune properties of the mice were investigated. The number of interleukin (IL)-12+CD11b+ cells in spleens and the formation of superoxide by peritoneal macrophages were higher in mice given the IgG-added diet than in those given the control diet. The number of natural killer cells in Peyer's patches or spleens and the cytotoxic activity of spleen cells toward an erythroleukemia cell line, K562, were also higher in mice given the IgG-added diet. In contrast, the numbers of interferon-gamma+CD4+ and IL-4+CD4+ cells in Peyer's patches or spleens and the levels of total or OVA-specific intestinal IgA and serum IgG were significantly lower in mice given the IgG-added diet than in those given the control diet. In addition, the number of cells expressing CD19 in spleens was significantly higher in mice given the IgG-added diet. These results indicate that oral ingestion of cow's milk IgG may stimulate some innate cellular immune systems, while suppressing humoral adaptive immune responses in the mouse.

Administration, Oral↗
PubMed2002

Initiation of humoral immunity. I. The role of cytokines and hormones in the initiation of humoral immunity using T-independent and T-dependent antigens.

The early events during the initiation of immune responses following the injection of T-independent (lipopolysaccharide, LPS) and T-dependent (bovine serum albumin, BSA) antigens were studied in immature male chickens. Specifically, the role of cytokines and hormones in the initiation of humoral immunity against these antigens was investigated. Both interleukin-1 (IL-1) and tumor necrosis factor (TNF-alpha) increased significantly post-LPS but not post-BSA injection. While interleukin-2 (IL-2) significantly decreased post-LPS injection, IL-2 significantly increased post-BSA injection. Furthermore, corticosterone levels significantly increased and tri-iodothyronine (T(3)) levels significantly decreased post-LPS but not post-BSA injection. In this study, the results indicate that although LPS and BSA can induce a humoral antibody response in chickens, they activate different cytokines and neuroendocrine network systems.

Animals↗
PubMed1982

[Dynamics and factors regulating the humoral immune response to Staphylococcus].

After repeated immunization of CBA mice with corpuscular staphylococcal antigen the titer of serum antibodies to staphylococci was the same as after single immunization, irrespective of the duration of the interval between injections. The increase of the interval between injections contributed to an increase in the titer of antibodies resistant to 2-mercaptoethanol. Mouse serum obtained 6 days after immunization suppressed humoral immune response to staphylococci. When injected intravenously into syngeneic mice, splenocytes taken from immune mice 3, 6 and 10 days after their immunization with staphylococcal antigen enhanced humoral immune response to staphylococci.

Animals↗
PubMed2005

Semliki forest virus and Kunjin virus RNA replicons elicit comparable cellular immunity but distinct humoral immunity.

RNA replicons offer a number of qualities which make them attractive as vaccination vectors. Both alphavirus and flavivirus replicon vaccines have been investigated in preclinical models yet there has been little direct comparison of the two vector systems. To determine whether differences in the biology of the two vectors influence immunogenicity, we compared two prototypic replicon vectors based on Semliki Forest virus (SFV) (alphavirus) and Kunjin virus (KUN) (flavivirus). Both vectors when delivered as naked RNAs elicited comparable CD8+ T cell responses but the SFV vectors elicited greater humoral responses to an encoded cytoplasmic antigen beta-galactosidase. Studies in MHC class II-deficient mice revealed that neither vector could overcome the dependence of CD4+ T cell help in the development of humoral and cellular responses following immunization. These studies indicate that the distinct biology of the two replicon systems may differentially impact the adaptive immune response and this may need to be considered when designing vaccination strategies.

Alphavirus Infections↗
PubMed1976

Experimental stimulation of cell-mediated immunity without concomitant stimulation of humoral immunity in graft-versus-host immunosuppressed mice.

The immunosuppressive effect of the graft-versus-host (GVH) reaction was studied in CBA X A F1 (CAF1) mice which had been rendered immunologically unresponsive by the injection of parental A strain lymphoid cells (GVH mice). Suppression of both cell-mediated and humoral immune responses was demonstrated by the prolonged survival of C57BL/6 (B6) skin allografts and by the inability of GVH mice to produce detectable antibody following stimulation with sheep erythrocytes (SRBC). Appropriate stimulation of GVH mice induced cell-mediated immune reactions to xeno- and allogeneic antigens while the humoral immune responses to the same antigens remained suppressed. Multiple challenges of the GVH mice with B6 tissue caused a rapid rejection of subsequent B6 skin grafts but failed to stimulate the production of any detectable antibodies to B6 allotransplantation antigens. Sensitization of GVH mice with SRBC in Freund's complete adjuvant stimulated a delayed hypersensitivity response to SRBC, although no humoral response to SRBC could be detected, even after three challenges with SRBC. The experimental results are discussed in terms of a proposed model for GVH-induced immunosuppression.

Animals↗
PubMed1996

Immunogenicity of bovine herpesvirus 1 glycoprotein D in mice: effect of antigen form on the induction of cellular and humoral immune responses.

For the development of veterinary subunit vaccines, modifications to the antigen may be needed to make the production of these vaccines cost effective. To investigate the effect of antigen modifications on immune response, we used glycoprotein D, one of the major glycoproteins of bovine herpesvirus-1 (BHV-1), as a model antigen. We developed a mouse model to assess the immune response elicited by immunization with either a recombinant truncated (tgD) or the authentic full-length (gD) form of BHV-1 gD in VSA3, a novel water-in-oil adjuvant. Both forms of BHV-1 gD antigen induced good levels of cell-mediated immunity, as evaluated by antigen-specific proliferative response and cytokine (IFN-gamma and IL-4) production. Following primary immunization, the humoral immune response induced by gD was superior to that elicited by vaccination with tgD. However, after a secondary immunization, a strong and similar antibody response to BHV-1 gD was induced by both forms of the antigen. The difference in immunogenicity between gD and tgD after primary immunization was not due to the loss of immunogenic epitopes in the truncated antigen or the ability to associate with the adjuvant VSA3. Our results indicate that both gD and tgD are capable of efficiently inducing a cell-mediated immune response, and although recombinant tgD is less efficient in inducing a primary humoral immune response when compared to the full-length gD, tgD effectively primed for a secondary antibody response.

Animals↗
PubMed1993

[Studies of humoral immunity induced by proteins of the cell wall of Hafnia alvei].

It was found that cell wall proteins (CWP) of Hafnia alvei applied intraperitoneally to mice are inducing, beside previously detected cellular immunity, also humoral immunity. Applying ELISA immunoenzymatic test in which a conjugate enabling demonstration of IgG antibodies was applied, it was found that CWP of Hafnia alvei induce appearance of specific antibodies in a high titer, but their presence in mouse serum is short and independent from applied doses of CWP. Humoral immunity induced by CWP can be transferred passively to nonimmunized animals by application of high level immune serum, which protected fully the animals against infection with homological strains of Hafnia alvei even in dilution 1:100. Investigated serum did not exhibit protective activity against infection with heterological strains of Hafnia alvei.

Animals↗
PubMed1998

The role of neuroendocrine immune interactions in the initiation of humoral immunity in chickens.

The presence of neuroendocrine immune interaction in mammalian species has been studied extensively and has been established. However, such an interaction is not as well established in avian species. Furthermore, the role of such an interaction in the initiation of humoral immunity is not well understood. Therefore, the present studies were conducted to determine mechanisms involved in the initiation of humoral immunity in chickens. Cornell K-strain White Leghorn immature male chickens were used for all the experiments. Changes in hormonal and leukocyte profiles after antigen stimulation were studied. The ability of different leukocytes to produce ACTH was also investigated. It was concluded that the first step in the initiation of humoral immunity after antigen exposure is the release of interleukin-1 by macrophages, which in turn stimulates the production of CRF by hypothalamus and/or leukocytes. It is important to mention that CRF production could also be a direct effect of antigen stimulation. The CRF will then stimulate ACTH production by anterior pituitary and/or leukocytes. In addition, CRF will directly enhance lymphocyte activities in the spleen. Corticosteroid production will be stimulated by ACTH and will cause redistribution of lymphocytes from circulation to secondary lymphoid organs such as the spleen for antigen processing and eventual production of antibodies against the invading antigens. Finally, both ACTH and corticosteroids will later act in a negative feedback manner to regulate and control the process of antibody production by inhibiting lymphocyte activities and/or reducing the responsiveness to different stimuli.

Adrenocorticotropic Hormone↗