Academic literature on the topic 'Antigen-antibody reactions. Immune serums. Immunoglobulins'

The causes of otitis media (OM) involve bacterial and viral infection, anatomo-physiological abnormalities of the Eustachian canal and nasopharynx, allergic rhinitis, group childcare centers, second-hand smoking, obesity, immaturity and defects of the immune system, formula feeding, sex, race, and age. OM is accompanied by complex and diverse interactions among bacteria, viruses, inflammatory cells, immune cells, and epithelial cells. The present study summarizes the antibodies that contribute to immune reactions in all types of otitis media, including acute otitis media, otitis media with effusion, and chronic otitis media with or without cholesteatoma, as well as the transcription factors that induce the production of these antibodies. The types and distribution of B cells; the functions of B cells, especially in otorhinolaryngology; antibody formation in patients with otitis media; and antibodies and related transcription factors are described. B cells have important functions in host defenses, including antigen recognition, antigen presentation, antibody production, and immunomodulation. The phenotypes of B cells in the ear, nose, and throat, especially in patients with otitis media, were shown to be CD5low, CD23high, CD43low, B220high, sIgMlow, sIgDhigh, Mac-1low, CD80(B7.1)low, CD86(B7.2)low, and Syndecam-1low. Of the five major classes of immunoglobulins produced by B cells, three (IgG, IgA, and IgM) are mainly involved in otitis media. Serum concentrations of IgG, IgA, and IgM are lower in patients with OM with effusion (OME) than in subjects without otitis media. Moreover, IgG, IgA, and IgM concentrations in the middle ear cavity are increased during immune responses in patients with otitis media. B cell leukemia/lymphoma-6 (Bcl-6) and paired box gene 5 (Pax-5) suppress antibody production, whereas B lymphocyte inducer of maturation program 1 (Blimp-1) and X-box binding protein 1 (XBP-1) promote antibody production during immune responses in patients with otitis media.

The endogenous estrogens are important modulators of the immune system and its functions. However, their effects are rather complex and many aspects have not been studied. In this study, we used the 1-chloro-2,4-dinitrobenzene (DNCB)-induced contact dermatitis as a disease model and investigated the effect of estriol (E3), along with two other estrogens, 17β-estradiol and estrone, on the pathogenesis of contact hypersensitivity. A series of parameters, such as ear swelling, skin inflammation, antigen-specific immunoglobulins, and lymphocyte compositions in peripheral lymphoid organs, were evaluated in mice following development of contact dermatitis. We found that administration of all three estrogens elicited strong inhibition of DNCB-induced dermatitis, while E3 exerted the strongest suppressive effect. Administration of E3 alleviated dermatitis, and this effect was accompanied by decreases in serum DNCB-specific immunoglobulins, such as IgA, IgG1, IgG2a, and IgG2b. Besides, treatment with E3 reduced B cell population, especially IgG-producing cells in the peripheral lymphoid organs following the induction of dermatitis. These observations consistently suggest that the antibody (Ab)-mediated humoral immune reactions play a critical role in the pathogenesis of DNCB-induced contact dermatitis. The results from this study demonstrate, for the first time, that estrogen administration has a strong suppressive effect on the pathogenesis of contact dermatitis. These findings offer important insights concerning the pathogenic role of antigen-specific Abs in contact dermatitis and the treatment of chemical-induced, Ab-mediated skin hypersensitivity reactions in humans.

week after immunization (specific activity is identified using neutralization reaction on the model of white mice and dot-blot immunoassay). This level of activity is sufficient for the fractioning of immune serum and extraction of anti-rabies immunoglobulin. Physicochemical and biological properties of the anti-rabies immunoglobulin, obtained with the help of cultural antigen technique, meet the requirements stated in the normative documentation on anti-rabies immunoglobulins extracted from equine blood serum. Specific activity level of experimental batches of anti-rabies immunoglobulin, obtained with the help of cultural technologies, corresponds to 242 and 214 IU/ml.

Modulation of the immune responses to alleviate the diseases has been of interest for many years. Thus a real need exists to protect our immune systems and lead healthier lives. Hence the present study is aimed to evaluate the immunomodulatory activity of Flavanoid of Kigelia africana. The effect of flavanoid of Kigelia africana on the immune system of rats and mice was evaluated by using different experimental models such asmice lethality test, Serum immunoglobulin level, Haemagglutination reaction, hypersensitivity reaction, and delayed type hypersensitivity reaction test. Flavanoid of Kigelia africana was administered orally at low dose and high dose of 100mg/kg/day, poand 200 mg/kg/day, po respectively and Levamisole (2.5 mg/kg/day, po) was used as standard drug. Flavanoid of Kigelia africanain both doses increased the levels of serum immunoglobulin and prevented the mortality induced by bovine Pasteurella multocida in mice. Exhibits a dose related increase in the early hypersensitivity reaction and Delayed type hypersensitivity reaction to the SRBC antigen. It also resulted in a significant increase in the antibody titer value, to SRBC, in experimental animals. Hence, it was concluded that flavanoid of Kigelia africana increases both humoral immunity and cell mediated immunity.

Multiple sclerosis is chronic demyelinating disease of the central nervous system with autoimmune inflammation and accretive neurodegeneration. One of the characteristics of autoimmune inflammation in multiple sclerosis is a polyspecific intrathecal humoral immune response against neurotropic viruses (Measles, Rubella and varicella Zoster) called MRZ-reaction. This immune response is based on polyclonal activation of mature B lymphocytes in the central nervous system and intrathecal synthesis of antibodies to anamnestic antigens unrelated to viral replication in the central nervous system as well as serum antibody release. Immunoglobulins produced against neurotropic viruses are an integral part of the oligoclonal antibody pool in the cerebrospinal fluid. Because immunoglobulins can penetrate the blood brain barrier, not only serum and cerebrospinal fluid specific antibody indices are calculated, but also blood-brain barrier antibody permeability (Qalbumin, QIgG) are taken into account to assess their intrathecal synthesis. The aim of the study was to assess the informative value of the intrathecal antibodies against neurotropic viruses (MRZ-reaction) in multiple sclerosis. There were enrolled 60 patients divided into 2 groups: group 1 — 35 patients diagnosed with multiple sclerosis, group 2 — 25 patients with inflammatory and non-inflammatory disоrders of the central nervous system. Paired cerebrospinal fluid and serum samples were collected from all patients to measure level of oligoclonal IgG, immunoglobulin free kappa and lambda light chains, IgG index and specific antibodies indices, followed by assessing magnitude of MRZ-reaction. We found that the MRZ-reaction was the most specific test to diagnose multiple sclerosis. Intrathecally produced antibodies against neurotropic viruses were detected in 3 of 35 multiple sclerosis patients with lacking oligoclonal IgG antibodies. In addition, a relationship between MRZ-reaction and degree of EDSS disability was found in MS patients: peak EDSS score was reported in patients with intrathecally synthesized antibodies against 3 viral agents, whereas the minimum EDSS score — among MRZ-negative patients. Thus, assessing MRZ-reaction seems rational for confirming MS diagnosis in case of other negative laboratory tests (oligoclonal immunoglobulins and free kappa/lambda light chains in cerebrospinal fluid) allowing to improves diagnostic accuracy and evaluation of MS severity.

ABSTRACT The antibody response patterns of cattle after subcutaneous and intranasal immunizations with adhesin Tf190 of Tritrichomonas foetus were investigated. Reactions of antibody from cattle parenterally immunized with Tf190 revealed antigen specificity and Tf190 sensitization in the majority of the animals, as determined by Western blotting. The results also demonstrated strong preimmune immunoglobulin G2 (IgG2) binding to T. foetus antigens not seen in IgG1 profiles. Subcutaneous injections of Tf190 resulted in significant (P < 0.05) increases in serum IgG1 and IgG2 titers over time, as determined by parasite specific enzyme-linked immunosorbent assay. Immune sera also significantly inhibited parasite adhesion to mammalian cell lines compared to the level of inhibition obtained with preimmune sera (P < 0.05). Intranasal immunization with Tf190 failed to produce measurable parasite-specific antibody in serum; however, this immunization route did result in significant (P < 0.05) increases in parasite-specific IgA titers in cervical mucus secretions from immunized animals that were more resistant to intravaginal challenge with T. foetus than controls. These results suggest that systemic immunization with Tf190 results in serum antibody production and antiparasitic adhesin antibodies. Additionally, the results of challenge experiments with intranasally immunized animals suggests that Tf190 primes protective immune responses that lead to lower rates of infection among these animals.

Abstract Zone electrophoresis on agarose gel was performed on serum samples from HIV-antibody carriers and negative controls. Nitrocellulose strips precoated with an HIV preparation were then placed on top of the gels and developed by an immunoblotting procedure. A positive reaction was demonstrated between the HIV antigens and the HIV-antibody-positive serum samples with hypergammaglobulinemia and oligoclonal IgG bands. A negative reaction was found between the HIV antigens and HIV-antibody-negative serum samples from a normal person and a patient with monoclonal gammopathy. The presence of oligoclonal IgG bands in the serum of HIV-antibody carriers, and their positive identification with HIV antigens, indicates a specific immune response of the host to the HIV infection and supports the use of oligoclonal IgG bands as markers to follow the course of HIV infection.

Abstract Background: Lysolipids have been claimed to be involved in the origin of sporadic monoclonal gammopathy of undetermined significance (MGUS) and multiple myeloma (MM) and of Gaucher's associated MGUS/MM because lyso-glucosylceramide (LGL1) and lysophosphatidylcholine (LPC) were purported to be the target of the clonal immunoglobulin in 31% of patients with sporadic and 85% with Gaucher's associated MGUS/MM(Nair et al. N Engl J Med 2016;374:555-61). The low titers (1:250) of the reported anti-lysolipid reactivity raised doubts as to whether these reactivities were indeed mediated by the clonal immunoglobulin (paraprotein). Patients and Methods: We analyzed the sera from 96 patients with MGUS/MM for the presence of anti-lysolipid reactivity by means of immunofixation, ELISA, serum protein electrophoresis (SPSP) before and after absorption with sphingosine beads to remove antibodies against lysolipids and paraprotein-specific antigens (paratarg-7 and sumoylated HSP90), respectively, and Western blots. Moreover, the BCR from MGUS/MM with a paraprotein-mediated reactivity against paratarg-7 and HSP90 were cloned and expressed as Fab fragments and used to determine antigen specificity by direct antigen binding and antigen-competition assays. Results: The presence of antibody reactivity against LGL1 and LPC was demonstrated in 28/96 (29%) MGUS/MM patients, confirming the rate observed in Nair's study (31%). Seven of these 28 sera also contained reactivity against paratarg-7 and 2 against HSP90 (always at titers >1x106). In none of the 28 lysolipd-reactive cases was the anti-lysolipd reactivity mediated by the clonal immunoglobulin as demonstrated by low antibody titers (<1:500), immunoglobulin subclasses different from the clonal immunoglobulin (as shown by immunofixation), inability of lysolipids to compete with specific antigens for binding with the clonal immunoglobulin or the recombinant B-cell receptor and demonstration by immunoglobulin affinity chromatography, that separated LGL1 reactivity from the monoclonal immunoglobulin. Absorption with sphingosine-beads completely removed the anti-lipd reactivity from the respective sera and the LGL1 immunoreactive bands after SPEP, but did not remove the monoclonal peak from the serum electrophoresis, while this was always the case with paratarg-7 (see figure) and HSP90 when they were the antigenic targets of the paraproteins. Anti-lysolipid reactivities were rare in 140 healthy controls (6%), but more frequent in 140 patients with autoimmune diseases (19%; p=0.002). Conclusions: Our data disprove a role of lysolipids in the origin of sporadic MGUS/MM. While we had no access to sera from patients with Gaucher'sassociated MGUS/MM, the report that lysolipds are the targets of the paraproteins in 85% of these cases and hence play a role in the pathogenesis of these diseases must also be met with caution. To prove that an observed antibody reactivity is mediated by the clonal immune globulin all of the following prerequisites must be met: 1st, the clonal immunoglobulin and the antibody mediating the reactivity against the antigen have the identical light and heavy chains; 2nd, the reaction has a serum titer >1x106; 3rd, absorption with the antigen removes the monoclonal peak in the serum electrophoresis; 4th, a specific reactivity of the expressed (clonal) B-cell receptor with the antigen is demonstrated; and 5th, convincing data is provided by competition assays that the paraprotein and the B-cell receptor recognize the same antigen and epitope of the antigen under investigation. Not a single one of these prerequisites has been met in the study of Nair et al. A role of lysolipids in the pathogenesis of any form of MGUS/MM cannot be assumed until the complete set of the 5 prerequisites is demonstrated for these autoantigens. A request for exchange of sera has been forwarded to Nair et al., and if granted, results will be reported. Supported by Wilhelm-Sander-Stiftung. Figure Figure. Disclosures No relevant conflicts of interest to declare.

Abstract Background The antibody repertoire in an infant/toddler develops in response to the microbiome, infections, environmental exposures, and vaccinations. Monitoring the specificity of these antibody responses in normal toddlers will provide indicators of disease susceptibility. Methods The serum Immunoglobulin (Ig)G and IgM antibody reactivity patterns in 1- and 2-year-old healthy toddlers was determined by examining the Ig specificity to diverse infectious agents, autoantigens and vaccine antigens with an antigen array. The toddlers were stratified based on their antibody reactivity to these diverse antigens with a normalized fluorescence intensity measure. Repeat profiling was performed at year 2 to reveal longitudinal changes in the IgG and IgM responses. Clinical information, along with DNA sequencing, and selected cytokine assays were used to establish an odds ratio for immune disease potential among the cohort. Results Healthy 1- and 2- year old IgG responses revealed cohorts of low, moderate, and high Ig responder groups that was unconnected with total serum IgG levels. The high responder group had elevated IgG reactions to selected pathogens, particularly viruses as well as to autoantigens. This high reactivity group, representing 17% of the cohort, had high odds ratios with maternal gestational diabetes, age, and a family history of asthma. While all toddlers developed strong antibody responses to Measles-Mumps-Rubella vaccines (MMR), more variation was noted towards other vaccines. In infections to Molluscum contagiosum, the IgG serum levels were transient regardless of the responder group. The high responder group had DNA polymorphisms linked to enhanced immune responses that correlated with elevated cytokine levels as well as eczema and asthma. A subset of toddlers has strong IgG responses to pathogens and vaccines Conclusion A subset of normal healthy toddlers has a high potential for immune system abnormalities and autoimmunity based on higher serum antibody responses to pathogens and autoantigens, genetic polymorphisms, and elevated cytokine responses. Disclosures All Authors: No reported disclosures

ABSTRACT The purpose of the present study was to determine the extent of immunologic responses, particularly immunopathologic responses, within the upper and lower respiratory tracts after intranasal immunization using the mucosal adjuvant cholera toxin (CT). BALB/c mice were nasally immunized with influenza virus vaccine combined with CT. The inclusion of the mucosal adjuvant CT clearly enhanced generation of antibody responses in both the nasal passages and lungs. After nasal immunization, antigen-specific immunoglobulin A (IgA) antibody-forming cells dominated antibody responses throughout the respiratory tract. However, IgG responses were significant in lungs but not in nasal passages. Furthermore, parenteral immunization did not enhance humoral immunity in the upper respiratory tract even after a nasal challenge, whereas extrapulmonary lymphoid responses enhanced responses in the lung. After nasal immunization, inflammatory reactions, characterized by mononuclear cell infiltration, developed within the lungs of mice but not in nasal passages. Lowering dosages of CT reduced, but did not eliminate, these adverse reactions without compromising adjuvancy. Serum IgE responses were also enhanced in a dose-dependent manner by inclusion of CT. In summary, there are differences in the generation of humoral immunity between the upper respiratory tract and the lung. As the upper respiratory tract is in a separate compartment of the immune system from that stimulated by parenteral immunization, nasal immunization is an optimal approach to generate immunity throughout the respiratory tract. Despite the promise of nasal immunization, there is also the potential to develop adverse immunopathologic reactions characterized by pulmonary airway inflammation and IgE production.