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PubMed1984

Humoral immunity in chicks experiencing marginal vitamin B-6 deficiency.

An economical vitamin B-6-deficient ration that was palatable to broiler chickens was prepared and fed to 1-day-old chicks. The experimental ration was a typical soy-glucose ration. Vitamin B-6 was removed by washing the soybean meal with water. Microbiological analysis revealed that the washed ration contained 0.45 mg vitamin B-6 per kilogram. Experimental rations were formulated to contain 0.5, 1.0 and 3.0 mg supplemental pyridoxine x HCl per kilogram of ration. These supplemental levels produced the following total pyridoxine concentrations in the diet: 0.95, 1.48 and 3.18 mg pyridoxine x HCl activity per kilogram of diet. Chicks were grown to 7 weeks of age and characteristic vitamin B-6 deficiency signs were quantitated and/or observed. Notable signs in chicks receiving 0.5 mg added vitamin B-6 were increased mortality, decreased body weight gain and increased incidence of abnormal leg conformation. The humoral immune system of broiler chicks that were moderately deficient in vitamin B-6 was investigated. Marginal pyridoxine deficiency caused significant reduction in antibody levels to sheep red blood cells (SRBC) and relative levels of IgM and IgG during the peak and degradation phases of the primary response. During the hyperimmune response total anti-SRBC levels were not affected; however, relative levels of IgM and IgG were lowered.

Animals↗

PubMed2004

Effects of sarcoptic mange and its control with oil of Cedrus deodara, Pongamia glabra, Jatropha curcas and benzyl benzoate, both with and without ascorbic acid on growing sheep: epidemiology; assessment of clinical, haematological, cell-mediated humoral immune responses and pathology.

The aim of this study was to evaluate the therapeutic efficacy of commonly used acaricidal drugs in India and also to assess the effect of ascorbic acid (AA) as adjunct therapy in 72 growing sheep with sarcoptic mange, aged 5-6 months and weighing 20.4-31.7 kg. Eight replicates of nine animals were formed based on sex, and day 0 body weight. Another set of 12 healthy sheep (5-6 months old) constituted the healthy control group. Drugs were applied locally on the affected parts daily and recovery changes in skin lesions were observed at the time of every application. L-Ascorbic acid was administered intramuscularly. Skin scrapings were collected daily from each group and examined for the presence of mites. Blood samples from each group were collected and analysed for total erythrocytes, leucocytes, haematocrit, haemoglobin and lymphocytes on 0, 14th and 28th day post-treatment (PT). Cell-mediated (CMI) and humoral immune (HI) responses were assessed on 0 and 28 days PT. Within groups treated with the drug alone, recovery in oil of Jatropha curcas group was faster and lesions were free from mites after the eighth application. For each drug, the recovery was faster with AA as an adjunct therapy when compared with the group treated with the drug alone. Within all groups, recovery in oil of J. curcas plus ascorbic acid (OJC-AA) group was fastest and the lesions were mite-free after three applications. The overall mean values were higher for all haematological parameters in OJC-AA group. Recovery with respect to suppressed CMI and HI responses during infection was also faster in this group. Gross and microscopic pathological studies revealed a marked adverse effect of infection on skin, kidney, spleen and liver. The OJC-AA group indicated faster recovery. It is concluded from this study that oil of J. curcas was found more efficacious in controlling sarcoptic mange in sheep and AA might be beneficial as adjunct in case of sarcoptic mange to get quick recovery with lesser applications of main therapy. However, the pharmacology of AA with reference to health of skin needs to be investigated.

Animals↗

PubMed1985

Defective humoral immunity in pediatric acquired immune deficiency syndrome.

Specific antibody production was assessed in six young children with the acquired immune deficiency syndrome (AIDS). All patients were immunized with bacteriophage phi X 174, a T cell-dependent neoantigen. In addition, antibody responses to pneumococcal vaccine and tetanus toxoid, lymphocyte responses to mitogens, and serum immunoglobulin levels were determined. Polyclonal hypergammaglobulinemia was documented in three patients. Responses to bacteriophage phi X 174 were abnormal in all patients: primary responses were blunted, secondary responses were markedly decreased, and the class switch (IgM-IgG) was absent in five of six patients. Antibody formation to pneumococcal vaccine and tetanus toxoid was also diminished. Lymphocyte mitogenic responses to phytohemagglutinin, concanavalin A, pokeweed mitogen, and staphylococcal Cowan A were generally decreased. These findings confirm that pediatric patients with AIDS have significant abnormalities in humoral immunity. Dysfunction of both T cells and B cells plays a role in the resultant poor specific antibody production.

Acquired Immunodeficiency Syndrome↗

PubMed1995

Reduced humoral immunity in uremic mice genetically selected for high antibody response.

Biozzi's Selection IV-A mice, genetically selected for 25 generations for high and low antibody response to sheep red blood cells (SRBC), 2-3 months old, were made uremic by subtotal nephrectomy and characterized for antibody production against the selection antigen. T cell activity was evaluated in vitro by lymphocyte proliferation and interleukin 2 (IL 2) production in response to the super antigen staphylococcal enterotoxin B (SEB). Total and IgM antibody titers (log2) were similar in uremic and non-uremic low responder mice (total antibody: 4.0 +/- 0.6 vs 3.6 +/- 0.6; IgG: 3.0 +/- 0.7 vs 2.4 +/- 0.4), while uremic high responders presented with non-uremic animals (total antibody: 10.8 +/- 1.6 vs 13.0 +/- 0.2; IgG: 10.3 +/- 1.5 vs 11.7 +/- 0.3). T cell proliferation and IL 2 production were similar in uremic and non-uremic groups after SEB stimulation. The results indicate a genetic effect on sensitivity to humoral immune response modulation by uremic status, with deficient antibody production despite a normal T cell proliferative response to mitogen stimulation in short-duration renal failure in high responder mice.

Animals↗

PubMed1978

Changing patterns in the humoral immune response to malaria before, during, and after the application of control measures: a longitudinal study in the West African savanna.

A longitudinal seroimmunological investigation of malaria was performed as part of the WHO research project conducted in the northern part of Nigeria from 1970 to 1975. The project included a preintervention phase, an intervention phase with application of malaria control measures (spraying of residual insecticide and mass drug administration), and a postintervention phase. Serological observations were made on the total population of eight villages consisting of approximately 3000 persons. Six immunological parameters were studied, namely, the serum levels of IgG and IgM, the number of bands of precipitation for Plasmodium falciparum in the double diffusion (Ouchterlony) test, the titres of antibodies for P. falciparum and P. malariae in the indirect fluorescent antibody (IFA) test, and the titres of agglutinating antibodies for P. falciparum by the indirect (passive) haemagglutination (IHA) test. The serological results were used to evaluate the impact on the humoral immune response of different levels of parasitaemia resulting, in the unprotected population, from natural factors such as seasons and ageing and in the protected population, from human intervention through the application of control measures and their interruption. The linkage by computer processing of the longitudinal data allowed analysis of the relationship between the results of a serological test in the same person at different surveys, and analysis of correlation between serological results and the concurrent parasitological findings. The correlation between parasitaemia and the results of the different serological tests at the same survey in the same person were also examined and analysed in terms of sensitivity and specificity of the tests.

Adolescent↗

PubMed1979

Plasma membrane and intracellular lipid synthesis in tumor cells rendered sensitive to humoral immune killing after treatment with metabolic inhibitors.

Line 10 guinea pigs hepatoma cells are resistant to killing by antibody and guinea pig complement. Metabolic inhibitors (adriamycin and actinomycin D) that increase the sensitivity of the cells to antibody-complement (C) killing were examined for their effects on the ability of the cells to synthesize and incorporate specific lipids into plasma membrane and intracellular membrane fractions. Drug-treated cells that had been rendered sensitive to antibody-C killing were inhibited in their incorporation of newly synthesized phosphatidylcholine and cholesteryl ester into the plasma membrane, as well as incorporation of phosphatidylcholine, cardiolipin, cholesteryl ester, and triglyceride into certain intracellular organelles including mitochondria, endoplasmic reticulum, nuclear membrane, or microsomes. Drug-treated cells recultured in the absence of the drug regained their ability to resist antibody-C killing and to synthesize and incorporate lipids into plasma and intracellular membranes. These data suggested that agents modifying the sensitivity of the tumor cells to humoral immune killing have a concomitant effect on plasma membrane and intracellular lipid synthesis.

Animals↗

PubMed1992

A defect in the humoral immune response to protein antigens and haptens in immunoglobulin mu heavy-chain transgenic mice.

We have examined the antibody response in mice expressing a functionally rearranged mu Ig heavy chain derived from a hybridoma antibody with specificity for the hapten 4-hydroxy-3-nitrophenyl (NP). Transgenic mice and their normal littermates were immunized with the antigens NP-OVA, the synthetic polypeptide (Tyr,Glu)-Ala-Lys ((T,G)-A-L), or saline. The presence of serum antibodies to NP-BSA, OVA, (T,G)-A-L, and BSA was examined by ELISA. Sera were evaluated prior to immunization and at periods of up to 4 months following immunization. Prior to immunization, transgenic mice had high levels of IgM anti-NP antibody but no detectable antibody to the other antigens. Both the primary and secondary antibody responses of transgenic mice to NP, OVA, and (T,G)-A-L were depressed when compared with the response of non-transgenic mice. Because of reports that these transgenic mice have increased proportions of CD5 + B-cells, a subpopulation associated with the production of autoantibodies, we examined these mice for the production of both IgG and IgM rheumatoid factors and anti-DNA antibodies. Transgenic mice had a modest increase in the spontaneous production of IgM anti-DNA. These data demonstrate a functional defect in the humoral immune response of mu transgenic mice.

Animals↗

PubMed1988

Characterisation of the humoral immune response during murine pregnancy.

Blood samples from female C57BL/10 mice mated with CBA/Ca males were obtained before, during and after both first and second pregnancies. A cellular enzyme-linked immunospecific assay (CELISA) was used to detect maternal antibodies against antigens on paternal splenocytes. Alloantibodies were detected in 48% of mice during or 9 days after a first pregnancy and in 82% of mice by the ninth day after the second pregnancy; these antibodies were first observed on day 10 of the first pregnancy. In two of four active multigravid sera tested, an increase in IgG1 concentration was detected; the level of all other isotypes remained within normal limits. Weak binding of alloantibody to an antigen of approximate molecular weight 44,000 was detected on CBA/Ca splenocytes by immunoblotting sera from multiparous animals. These sera also recognised an antigen of similar molecular weight on H-2b identical 129J splenocytes but not on splenocytes from the maternal strain. These results provide further information on the maternal humoral immune response during murine pregnancy.

Animals↗

PubMed2005

Humoral immune response and B-cell functions including immunoglobulin class switch are downregulated in aged mice and humans.

Vaccinations are powerful tools for combating infections. Because of the age-related impairment in immune functions, the currently available vaccines are protecting only a small proportion of the elderly population. We, here, provide an overview of age-related changes in innate and adaptive immunity with particular emphasis to changes in antibody production with aging. We also summarize our results showing that the E2A-encoded transcription factor E47, which regulates many B cell functions including class switch recombination (CSR) and somatic hypermutation (SHM), is downregulated in splenic B cells from old mice. This leads to a reduction in the activation-induced cytidine deaminase (AID), which directly induces CSR and SHM, and, in turn, to reduced amounts of switched antibodies produced by splenic activated B cells. Our preliminary results in humans indicate similar reductions: we show herein that the expression of E2A and AID progressively decline with age. Our results provide a possible molecular basis for a decrease in the humoral immune response in aging mice and humans.

Aging↗

PubMed2005

In vivo humoral immune responses to isolated pneumococcal polysaccharides are dependent on the presence of associated TLR ligands.

We determined whether T cell-independent Ig isotype responses to isolated pneumococcal polysaccharides (PPS) required TLR signaling in vivo. IgG anti-PPS responses to PPS3, PPS14, and C-polysaccharide (C-PS) were virtually undetectable in TLR2(-/-) mice, whereas specific IgM induction was variably reduced compared with wild-type mice. All PPS-containing preparations induced IL-6 and TNF-alpha from wild-type, but not TLR2-/-, macrophages. TLR2 activity was distinct from that of PPS, in that it was phenol extractable. Immunization of wild-type mice with phenol-extracted PPS14 also resulted in a marked reduction in the IgG, although not the IgM-anti-PPS14, response compared with untreated PPS14. The commercial 23-valent PPS vaccine, Pneumovax-23 also contained TLR ligands (TLR2 and TLR4), which were absolutely critical for the IgG-inducing activity of the vaccine in mice. Finally, the commercial pneumococcal conjugate vaccine, Prevnar, contained a TLR2 ligand(s) that substantially enhanced both the primary and secondary anti-PPS responses in mice, especially the type 1 IgG isotypes. These data strongly suggest the absolute need for a distinct, TLR-dependent second signal for inducing in vivo IgG T cell-independent humoral immune responses to isolated pneumococcal polysaccharide Ags and highlight the potential importance of previously unappreciated copurified and/or contaminating TLR ligands in PPS vaccine preparations.

Animals↗

PubMed1995

Lymphotoxin-alpha-deficient mice. Effects on secondary lymphoid organ development and humoral immune responsiveness.

Targeted mutagenesis in embryonic stem cells was used to generate mice deficient in lymphotoxin-alpha (LT-alpha). Mice lacking LT-alpha -/- (LT-alpha -/- mice) exhibit a phenotype dominated by defects in secondary lymphoid organ development. LT-alpha -/- mice lack lymph nodes and Peyer's patches, and possess spleens in which the usual architecture is disrupted. However, in a few of the mutants, abnormal lymph node-like structures were observed, mainly within the mesenteric fat. Abnormal clusters of lymphocytes were also found to accumulate in the periportal and perivascular regions of the liver and lung of LT-alpha -/- mice. Yet, lymphocytes from LT-alpha -/- mice appeared phenotypically normal, expressing the expected ratios of B and T cell surface markers as well as the lymphocyte homing marker, L-selectin. In addition, bone marrow cells from LT-alpha -/- mice were able to successfully reconstitute the lymphoid organs of severe combined immunodeficient mice. However, LT-alpha -/- mutant mice examined for humoral immune responsiveness were found to be impaired in their ability to respond to different Ag. These data illustrate the utility of this mouse model as a system for understanding lymphoid organ development and its effects on immune responsiveness.

Animals↗

PubMed1987

Cellular and humoral immune responses to synthetic peptides deduced from the amino-acid sequences of Epstein-Barr virus-encoded proteins in EBV-transformed cells.

Ten synthetic peptides containing 18-22 residues deduced from the amino-acid sequences of the EBV-encoded latent-infection-associated membrane protein (LMP) and the 2 principal nuclear antigens, EBNA-1 and EBNA-2, were tested for their ability to induce lymphokine release from sensitized T-cells of EBV-seropositive donors, as measured by the leukocyte migration inhibition assay (LMI). Only one of the 10 free peptides induced EBV-specific LMI. After Sepharose-coupling, 4 additional peptides were regularly active. In parallel, the sera of the same and other donors were screened for synthetic peptide-binding antibodies, as measured by an ELISA assay. Antibodies to 9 of the 10 peptides were detected in 25-80% of EBV-antibody-positive, but not in EBV-antibody-negative sera. A comparison of the two responses indicates that the humoral immune system tends to react with more epitopes on a given protein than the cellular immune system. Furthermore, the antibody reactivity pattern to different epitopes is more variable from individual to individual than the T-cell response. Also, the epitopes detected by antibodies and sensitized T-cells are often not identical.

Amino Acid Sequence↗

PubMed2001

Assessment of HIV-intrathecal humoral immune response in AIDS-related neurological disorders.

Intrathecal synthesis of IgG directed to HIV antigens was investigated by antibody specific index (ASI), affinity-mediated immunoblot (AMI) and Western blot (WB) assay in a group of 88 AIDS patients of which 28 with HIV-associated neurological disorders (HAND), 13 without associated neurological disorders (WAND) and 47 with non-HIV-associated neurological disorders (non-HAND). CD4+ count was above 50 cells/mm3 (CD4+>50) in 30 and below 50/mm3 (CD4+<50) in 58 patients, respectively. A significantly higher frequency for CSF complete anti-gag profile (p<0.001), and for HIV-specific oligoclonal patterns ("mixed" pattern=p<0.01) was observed in HAND as compared to patterns from the other clinical groups. A decrease in complete anti-env, anti-pol and anti-gag reactivity was present in CSF of patients with CD4+<50 as compared to those with CD4+>50. Our findings suggest that AIDS appears to be characterized by an anti-HIV intrathecal humoral immune response which is principally directed to env products with a prevalence of oligoclonal patterns and CSF complete anti-gag profile in HIV-associated neurological involvement.

AIDS Dementia Complex↗

PubMed2000

Evaluation of an ELISA and immunoblotting for studying the humoral immune response in Anguillicola crassus infected European eel Anguilla anguilla.

The applicability of an enzyme-linked immunosorbent assay (ELISA) for the detection of anguillicolosis in feral eels was examined using a crude antigen preparation from the body wall of adult Anguillicola crassus. The screening consisted of samples from 100 feral European eels Anguilla anguilla. As a reference the actual status of infection was determined by dissection of the eels' swim-bladders. The ELISA results were compared with a background value calculated from the results obtained from 43 non-infected farm eels. The screened samples had a high prevalence of A. crassus (83 %); however, the specificity and the negative predictive value of the ELISA were low compared to the high positive predictive value. Nonetheless, the reproducibility (precision) of the test was satisfactory, and for the non-infected reference group specificity was 97.7 %. Although the ELISA, as used in the present study, is not applicable for diagnostic purposes, it represents a useful tool for the investigation of the specific humoral immune response of eels against A. crassus under controlled experimental conditions. Immunoblots using crude antigen preparations from different parts of adult A. crassus as well as a crude somatic third-stage (L3) antigen preparation illustrated that only antigens associated with the body wall of adult A. crassus are potentially suitable for diagnostic purposes. Despite the fact that antibodies against Raphidascaris acus cross-reacted with 3 body wall antigens of A. crassus, the most encouraging results were obtained with the antigen preparation from the outer cuticle of adult A. crassus which yielded a conspicuous, broad band at about 100 kDa.

Air Sacs↗

PubMed1994

Modulation of a specific humoral immune response and changes in intestinal flora mediated through fermented milk intake.

This study was undertaken to elucidate whether eating a fermented milk containing Lactobacillus acidophilus La1 and bifidobacteria could induce changes in intestinal flora and modulate the immune response in man. Volunteers consumed a fermented milk containing L. acidophilus La1 and bifidobacteria over a period of three weeks during which an attenuated Salmonella typhi Ty21a was administered to mimic an enteropathogenic infection. A control group ate no fermented foods but received the S. typhi Ty21a. Faecal flora analyses showed an increase in L. acidophilus and bifidobacterial counts during fermented milk intake. The specific serum IgA titre rise to S. typhi Ty21a in the test group was > 4-fold and significantly higher (P = 0.04) than in the control group. An increase in total serum IgA was also observed. These results indicate that lactic acid bacteria which can persist in the gastrointestinal tract can act as adjuvants to the humoral immune response.

Adult↗

PubMed1980

Contact hypersensitivity, humoral immunity, and specific unresponsiveness can be induced in Syrian hamsters with simple haptens.

Several inbred strains of Syrian hamsters have been immunized by skin painting with highly reactive haptens. Classical contact hypersensitivity has been assayed by the ear swelling response: the response is hapten-specific, exaggerated after re-immunization with the original hapten, and can be transferred adoptively to naive syngeneic hamsters with viable lymphoid cells, suggesting that contact hypersensitivity is mediated in hamsters by T lymphocytes. Moreover, skin painting with hapten induces significant serum titers of anti-hapten antibodies, indicating that antigen-specific B lymphocytes are also activated. Hamsters can be rendered unresponsive to these same haptens by conventional methods: 1) i.v. inoculation of the soluble hapten sulfonate or 2) inoculation of hapten-derivatized syngeneic lymphoid cells. Hamsters treated with these "tolerizing" maneuvers develop profound hapten-specific unresponsiveness that can be adoptively transferred to naive recipients with living lymphoid cells. "Unresponsive" animals, however, make strong anti-hapten antibody responses that rival the humoral immune responses found after skin sensitization. The data suggest that an active process is involved in the induction and maintenance of the unresponsive state, but responsibility can not be assigned firmly to putative suppressor T cells or to an antibody-mediated B suppressor modality.

Animals↗

PubMed1987

Model analysis of the bases of multistationarity in the humoral immune response.

A formal analysis of the regulation of antibody production has been developed. It comprises two complementary approaches: a logical analysis in terms of discrete (boolean) variables and functions and a more classical analysis in terms of differential equations. A first paper dealt mostly with the logical description which provided global information on how complex the network needs to be in order to account for some main aspects of the immune response, without having to specify the details of the cellular interactions or to introduce a great number of parameters. Here we present the continuous approach and, in particular, a detailed study of the steady states and a discussion of their role in the dynamics of the immune response. The model subject to this analysis is a minimal one, which takes into account a small number of well-established facts concerning lymphocyte interactions and some reasonable assumptions. The core of the model is a negative feedback loop between the helper (TH) and suppressor (TS) T lymphocytes on which autocatalytic loops of the TH and TS populations on themselves are grafted. The salient feature of this minimal scheme is the prediction, for given environmental and parametrical conditions, of a multiplicity of steady states. This multistationarity occurs both in the absence of antigen or for constant antigen levels. Variations in the external constraints provoke switches among the steady states which might be related to the various modes of the humoral immune response, and depend on the doses of antigen injected and on the previous antigenic history of the system. In particular, high and low dose paralysis appear to be associated with two distinct steady state branches.

B-Lymphocytes↗

PubMed1991

Investigations on etiology of Crohn's disease. Humoral immune response to stress (heat shock) proteins.

Many investigators have tried to prove a relationship between Crohn's disease and Mycobacteria. Recent evidence suggests that some autoimmune diseases may be initiated through "molecular mimicry" between mycobacterial stress protein antigens and their human homologs. We investigated whether antibody to stress proteins was more frequent in patients with Crohn's disease than controls. We used ATP binding to separate stress proteins (heat-shock-induced, de novo-synthesized, and constitutively expressed ATP-binding proteins) from crude extracts obtained from Mycobacteria and from an SV40-transformed human epithelial cell line that expresses a heat-shock protein, hsp73, as a complex with SV40 T antigen. We used immunoblots to compare sera from 34 patients with Crohn's disease, 14 with ulcerative colitis, and 14 with duodenal or gastric ulcers (noninflammatory bowel disease control patients). We found no statistically significant pattern or frequency of antibodies against single proteins or a combination of mycobacterial or human stress proteins. These observations do not support the hypothesis that a humoral immune response to stress proteins of Mycobacteria is important in the pathogenesis of Crohn's disease.

Antibody Formation↗