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PubMed1976

[Cerebral auto-antigens in the serum of schizophrenic patients].

Brain autoantigens in the blood of 200 schizophrenic patients were investigated. It was established that the introduction of brain autoantigens caused the formation of antibrain antibodies in the animals. The brain autoantigen, limitted by the species, is also present, and there is a possibility of autoimmunization by each of them. It is shown that the autoantigen which is connected with the species of the brain, is stable to organic dissolvent activity in the paranoid form of schizophrenia (87.5%) and in the malignant and shift-like form (20%). In the other forms of schizophrenia and also in epilepsy and viluy encephalitis its inactivation is marked. The qualitative heterogeneity of brain autoantigen in different forms of schizophrenia is suggested.

Antigens↗
PubMed2025

PhIP-Seq uncovers marked heterogeneity in acute rheumatic fever autoantibodies.

Acute rheumatic fever (ARF) and associated rheumatic heart disease are serious sequelae after infection with group A Streptococcus (Strep A). Autoantibodies are thought to contribute to pathogenesis, with deeper exploration of the autoantibody repertoire needed to improve mechanistic understanding and identify new biomarkers. Phage immunoprecipitation sequencing (PhIP-Seq) with the HuScan library (>250,000 overlapping 90-mer peptides spanning the human proteome) was utilized to analyze autoreactivity in sera from children with ARF, uncomplicated Strep A pharyngitis, and matched healthy controls. A global proteome-wide increase in autoantigen reactivity was observed in ARF, as was marked heterogeneity between patients. Public epitopes, common between individuals with ARF were rare, and comprised less than 1% of all enriched peptides. Differential analysis identified both unknown and previously identified ARF autoantigens, including PPP1R12B, a myosin phosphatase complex regulatory subunit expressed in cardiac muscle, and members of the collagen protein family, respectively. Pathway analysis found antigens from the disease-relevant processes encompassing sarcomere and heart morphogenesis were targeted. In sum, PhIP-Seq has substantially expanded the spectrum of autoantigens in ARF, and reveals the rarity of public epitopes in the disease. It provides further support for the role of epitope spreading in pathogenesis and has identified PPP1R12B as an enriched autoantigen.

Humans↗
PubMed1977

[Activity of different antigenic preparations from the retina to induce experimental auto-immune uveo-retinitis (EAU) in guinea pigs (author's transl)].

24 different antigenic preparations from bovine or guinea pig retina and 3 from bovine uvea were tested for their ability to induce uveo-retinitis in guinea pigs. Each animal received one injection into the hind foot pads of 0.1 ml og the tissue preparation mixed with an equal volume of complete Freund's adjuvant. The intensity of the disease was assessed by clinical and histological criteria. Homogenates and extracts from whole guinea pig retina are more active than the same preparations from bovine retina. Autologous retinal extract is slightly more active than homologous in low doses. In bovine retina, the autoantigen(s) is localized in the photoreceptor structures and the pigment epithelium. Bovine uveal preparations seem to be inactive when the epithelium has been removed. Purified outer segments are very active, as well as soluble extracts of outer segments. Highly purified bovine rhodopsin has no immunopathogenic activity. A soluble autoantigen (autoantigen S) has been isolated by preparative isoelectrofocusing from retinas of several species. Autoantigen S from guinea pig induces the disease in guinea pigs at a dose of a few micrograms.

Animals↗
PubMedDate not supplied

[Comparative study of immunopathogenic ability of autologous and allogeneic spermatozoa in Hartley guinea-pigs (author's transl)].

Autologous or allogeneic spermatozoa in amounts of 10(8), 10(7), 10(6) or 10(5) incorporated in complete Freund's adjuvant were injected into hemiorchidectomized Hartley guinea-pigs. The course of autoimmune aspermatogenic orchi-epididymitis, delayed hypersensitivity and humoral responses to autologous and allogeneic spermatozoa and to spermatozoa autoantigens S, P and T (isolated from a large pool of spermatozoa) were investigated after 1,2,3 or 4 weeks of evolution. Testicular and epididymal lesions and the cellular and humoral responses to autoantigens S and T were nearly identical in autoimmunized and alloimmunized guinea-pigs; but the delayed hypersensitivity responses to whole spermatozoa was more frequent in alloimmunized than in autoimmunized guinea-pigs. This latter result might not be due to the addition of two responses on to autoantigens and one to alloantigens (both present in allogeneic spermatozoa) since the positive responses of the alloimmunized guinea-pigs to autologous spermatozoa compared to allogeneic were found more frequent. From the technical conditions of the experiments, especially due to the use of complete Freund's adjuvant, a helper effect originating in allotypic determinants on allogeneic spermatozoa seems an unlikely explanation. Autoimmunization or alloimmunization in incomplete Freund's adjuvant instead of complete adjuvant provoked a weak response. However, the antibody response to antigen S was significantly more frequent in alloimmunized than in autoimmunized animals; in this case allotypic determinants in autoantigen S responsible for a helper effect might be the cause.

Animals↗
PubMed1977

Autoantibodies against the inner aspect of erythrocyte membranes in NZB mice.

Erythrocyte autoantibodies in NZB mice react by hemagglutination methods with exposed and hidden red cell antigens. The hidden antigens can be exposed by treatment with proteolytic enzymes. By indirect immunofluorescence one antibody population can be shown to react with modified red cells. In the present study the location of the corresponding autoantigen within the membrane was studied. Mechanical or hypotonic lysis of the red cells exposed the antigen. Proteolytic digestion known to expose other erythrocyte autoantigens had no effect. The autoantigen was exposed on 'inside out' erythrocyte membrane vesicles, but not on 'right-side out' vesicles, prepared from isolated erythrocyte ghosts. Frezzing and thawing as well as mechanical disintergration of red cells liberated antigenically active material as saline-insuluble fibrillar material. The observations indicate that the autoantigen studied is located at the inner aspect of the erythrocyte membrane and suggest that it is associated with fibril-forming structural components. The observed reactivity distinguishes the described antibodies from previously identified erythrocyte autoantibodies.

Animals↗
PubMedDate not supplied

Cell mediated immune regulation in autoimmunity.

Autoimmunity is the term for the immune conditions characterized by a specific humoral or cell mediated response to the body's own tissues. The termination of the natural state of self tolerance may lead to immunopathological manifestations with clinical consequences, i.e. autoimmune diseases. In a very general sense, one may classify autoimmune diseases into two groups with respect to the underlying mechanism: 1. There are autoimmune diseases which develop in the presence of a normal intact regulation mechanism. 2. Another group whose development must be understood on the basis of a cellular dysfunction. In the first case, dequestered or semi-sequestered autoantigens are liberated as a consequence of exogenic influences inducing the sensitization of immunocompetent cells. The immune system then reacts with these autoantigens in the same way as with foreign substances. This kind of autoimmune disease will, however, not be dealt with here. In the second case, autoantigens are normally, i.e. in healthy individuals, accessible to the immunocompetent cells. To understand the reason for the development of an autoimmune reaction one must first clarify the mechanism of self tolerance. Then one must examine the way in which a break of this physiological state takes place. One of the major unanswered questions is the relative importance of antibody-mediated and cell-mediated immune mechanisms in the onset and further development of autoimmune diseases. Recently it has been suggested that a dysfunction at the cellular level might represent the basic cause which induces the termination of selftolerance. Most of the conceptions about the mechanism by which autoimmune diseases are triggered were gained through experiments with animals. It is, however, difficult to use these experimental results to explain human diseases; in humans many questions are still open. Undoubtedly, the mechanisms of induction and maintenance of self tolerance and also the ways in which autoimmune diseases may be induced, are not uniform. In all these cases, cells and cellular interactions as well as the corresponding cellular products are decisive. The majority of autoimmune diseases are mediated by antibodies as can be demonstrated in transfer experiments, for instance. Experimental Autoimmune Thyroiditis (EAT), rather than by sensitized cells. An example of the latter would be Experimental Autoimmune Encephalitis (EAE). In principle the following can be said of all these kinds of autoimmune diseases as well as of selftolerance: 1. Induction of autoantibodies is in principle possible. 2. Self antigens important in autoimmune diseases are T-dependent. 3. Self-reacting lymphocytes (T- and/or B-cells) are present in "normal" individuals.

Antibody Formation↗
PubMed2026

Molecular biomarker profiling in noninfectious uveitis: a chronological review of discovery.

PURPOSE OR REVIEW: Noninfectious uveitis (NIU) encompasses a heterogeneous group of immune-mediated intraocular inflammatory diseases whose complexity has driven systematic molecular biomarker discovery. This review presents NIU molecular biomarkers organized by biological category; autoantigens, human leukocyte antigens (HLA) and genetic markers, cellular immune subsets, cytokines, chemokines, and multiomics platforms including proteomics, microbiome metagenomics, metabolomics, and single-cell transcriptomics with each category presented in strict chronological order of landmark discovery. RECENT FINDINGS: We present a review organized along two nested timelines. Categories are presented in the order they historically emerged in the field, and within each category, landmark discoveries appear in chronological sequence. This allows the reader to trace how each biomarker category evolved: from foundational autoantigen identification in experimental uveitis models, through the genomic revolution of HLA association studies, into cellular immunophenotyping, cytokine profiling of aqueous humor, chemokine mapping of intraocular trafficking, and finally the emerging omics platforms that may potentially anchor precision medicine in NIU. Each biomarker is paired in line with its linked targeted therapeutic. SUMMARY: Biomarker research has transformed the understanding of NIU from a clinically defined syndrome into a group of molecularly distinct immune disorders. Advances spanning autoantigens, genetics, immune-cell profiling, cytokines, chemokines, and multiomics have revealed novel pathogenic mechanisms and therapeutic targets. Integration of these biomarkers with targeted therapies may accelerate the transition toward precision medicine in uveitis care.

cytokines↗
PubMed1977

Evidence for a B lymphocyte defect underlying the anti-X anti-erythrocyte autoantibody response of NZB mice.

The autoimmune hemolytic anemia of NZB mice is pathogenetically mediated by a genetically prescribed anti-erythrocyte autoantibody response directed to the X erythrocyte autoantigen. The cellular locus of the immunoregulatory defect underlying the anti-X response was explored by adoptively transferring bone marrow cells (BMC) from NZB mice to lethally irradiated histocompatible recipients. Before adoptive transfer, BMC from donor mice were assayed for antigen-binding lymphocytes with receptors for the X autoantigen (X-ABL) by immunocytoadherence assays and for anti-X autoantibody-secreting cells (X-PFC) by plaque-forming cell assays. Twelve weeks after adoptive transfer, splenic lymphocytes from recipient mice were assayed for X-PFC and humoral anti-X autoantibody by Coombs' tests. Transfer of 15 to 30 x 10(6) BMC containing 6 to 12 x 10(3) X-ABL but no X-PFC from 6- to 8-week-old NZB mice to lethally irradiated BALB/c, B10.D2, C57BL/Ks, and DBA/2 mice produced X-PFC in 70% of the recipients. Development of X-PFC was not simply dependent upon available X-ABL since transfer of 15-30 x 10(6) BMC, containing comparable numbers of X-ABL, from BALB/c, B10.D2, C57BL/Ks, or DBA/2 mice to NZB or syngeneic recipients did not produce X-PFC. Transfer of BMC from NZB mice to BALB/c, B10.D2, and DBA/2 mice with weekly administrations of AKR anti-theta antiserum had no effect on the development of X-PFC; Tlymphocyte ablation was evidenced by the absence of theta+ spleen cells. These results suggest that the pathogenetic anti-X response is not genetically prescribed at the level of macrophages, humoral factors, or T cells, but rather appears to be a phenotypic expression of a primary B lymphocyte defect permitting or promoting differentiation of NZB X-ABL.

Anemia, Hemolytic, Autoimmune↗
PubMed1978

A model for the autosensitization autoantibody production associated with xenogeneic thymic RNA.

Normal C57BL/6 bone marrow cells cultured for 3 weeks with xenogeneic thymic RNA and syngeneic C57BL/6 antigens (immunoglobulin G or red blood cells) produced anti-immunoglobulin antibody or anti-mouse red blood cell antibody (hemolysin). Addition of both xenogeneic thymic RNA and autoantigens to bone marrow cultures was necessary to elicit autosensitization. Syngeneic thymic RNA would not substitute for xenogeneic RNA. Normal recipients inoculated with syngeneic kidney or spinal cord homogenates and xenogeneic thymic RNA developed albuminuria or motor neuropathies within 10 days. Histologic examination of tissues from these animals revealed immunoglobulin deposits on glomerular or tubular basement membranes or on myelin sheaths. These changes were not observed in tissues from control animals inoculated with only the organ homogenates. Normal mice injected with syngeneic bone marrow cells, which had been autosensitized in vitro against kidney or spinal cord homogenates, also developed albuminuria or motor neuropathies, respectively. These abnormalities were observed only if bone marrow cells had been cultured with both xenogeneic thymic RNA and autoantigens. Histologic examination of tissues from these mice also revealed immunoglobulin deposits in kidney or spinal cord tissues. These results demonstrate that xenogeneic thymic RNA can play important roles in the formation of autoantibodies.

Animals↗
PubMed1978

[Clinical and pathogenetic characteristics of cardiogenic shock].

The clinical course of cardiogenic shock was studied in 441 patients with myocardial infarction. The incidence of this complication was found to be dependent on the variant of myocardial infarction and was 7.4% in primary, 14.2% in repeated myocardial infarction, and 22.2% in the recurrent variant. The duration of the shock was 3 to 4 days and its course indulant. Disorders of central and peripheral hemodynamics are of principal pathogenetic importance in cardiogenic shock; these were studied by the method of dilution of T-1824 dye. Of auxiliary importance are autoantigens entering the blood from the zone of myocardial infarction 6 hours after the onset of the disease and possessing depressor, negative inotropic and cardiotoxic properties. This was established in experiments on intact and sensitized dogs. One of the components of the shock in a second attack of myocardial infarction or in recurrent infarction may be anaphylactic shock due to reaction of autoantibodies, circulating in blood after the first myocardial infarction, with the autoantigens arriving from the focus of the fresh necrosis.

Animals↗
PubMed1975

Functional role of cholesterol in infection and autoimmunity.

Cholesterol binds to streptolysin O and related bacterial toxins. In normal serum, only a fraction of the cholesterol attached to lipoprotein is available for binding, probably as a cholesterol-peptide complex formed during catabolic breakdown of the lipoprotein. Cholesterol esterase produced by certain organisms--e.g., Staphylococcus pyogenes and Pseudomonas oeruginosa--augments this fraction both in vitro and in vivo. Endogenous esterase similarly increases the amount of cholesterol-peptide complex, a mechanism which may be activated as a feedback process following binding of toxin to the cholesterol component of the complex. These complexes will thus supply a readily available means of binding bacterial toxins before antibody formation begins; Cholesterol-peptide complexes, either alone or modified by binding to toxin, may function as autoantigens. It is postulated that immune complexes so formed may be involved in atherosclerosis either by directly damaging vessels walls or by cross-reaction of antibody with cell-membrane-bound lipoproteins which equilibrate with plasma-lipoproteins.

Antibodies, Bacterial↗
PubMed1975

Humoral antibodies to acetylcholine receptor in patients with myasthenia gravis.

Sera from patients with myasthenia gravis (M.G.) were studied by the quantitative micro-scale complement-fixation assay for the presence of humoral antibodies against acetylcholine receptor (AChR). The purified receptor was extracted from the electrogenic tissue of the electric ray, Torpedo californica. A significant difference in the antibody titres was observed between myasthenic and non-myasthenic patients. Out of fifteen patients with myasthenia gravis, at least 12 (80%) had antibodies against AChR. Only one case out of twenty-four controls had an indication of anti-receptor antibodies. In view of observations on the role of AChR as the autoantigen in myasthenia gravis, such antibodies may have significance in producing the neuro-muscular block characteristic of the disease.

Acetylcholine↗
PubMed1977

Genetic control of immune responsiveness in man.

Interest in immunogenetics originated from two streams: (a) histocompatibility in mouse and man, and (b) inheritance of specific immune responses in the guinea pig and mouse. In the mouse, there are genes associated with the major histocompatibility complex (MHC) which (i) code for antigens determining allograft responses and mixed lymphocyte reactions, (ii) control responses to certain antigens (Ir genes), and (iii) code for cell-surface antigens which elicit specific antisera (anti-Ia). In man, there is genetic control, in part X-linked, over levels of immunoglobulins and immunoglobulin classes. Evidence for MHC-linked genetic control is derived from immune responses to (i) micro-organisms, (ii) pollen antigens, (iii) food antigens, (iv) vaccines, (v) inocuous test antigens, and (vi) autoantigens. Some evidence exists for allotype-linked genetic control. Practical aspects concern influences of the MHC on susceptibility to disease, within individuals and populations.

Antibody Formation↗
PubMed1979

Immunopathologic studies of renal glomerular change in liver cirrhosis with special reference to its pathogenesis.

The kidneys from 62 proven liver cirrhosis cases were examined by immunofluorescence (IF), and 94% of the cases were positive for some immune reactants deposition. Combined deposition of immunoglobulin(s), both or each one of C1q and C4, and further with C3 were observed in about 70% of all IF positive cases. The morphological alterations of the glomeruli correlated with the intensities of regional immune reactants depositions. Guinea pig C3 was frequently activated in vitro on the glomeruli of these cases. Immune reactants depositions in the glomeruli appeared to form immune complex locally. Smooth muscle and liver cell antigens in the immune complex at the glomeruli were examined by indirect method of IF using monospecific antibodies and positive cases concerning each antigen were found in about 1/3 of the kidneys from 21 liver cirrhosis cases. These facts suggest that the high rate of the occurrence of immune complex deposition type glomerulo-nephritis may be due to the glomerular deposition of some autoantigen-antibody complexes including smooth muscle and liver cell antigens.

Adolescent↗
PubMed1975

Characterization of spermatozoal auto-, iso- and allo-antigens.

Three approaches are utilized to study and characterize spermatozoal antigens. An immunological approach has demonstrated the presence of spermatozoal auto-, iso- and allo-antigens. Spermatozoal auto-antigens studies by several authors are able to induce the whole spectrum of immune reactions (delayed hypersensitivity, complement-fixing antibodies and anaphylactic antibodies0 as well as of autoimmune aspermatogenic orchiepididymitis (AIAO). Different extraction procedures result in various preparations and even in different independent autoantigens (at least four), one protein, one membrane-linked antigen and at least two glyco-proteins. Spermatozoal iso-antigens stricto sensu are determined by the Y chromosome and present on at least 50% of the spermatozoa. Spermatozoal allo-antigens are also present at the surface of spermatozoa, especially blood group antigens (ABO and MNS systems), transplantation antigens (HL-A, H-2) and also some other unidentified ones. A biochemical approach has mainly been directed towards spermatozoal enzymes that have been directed towards spermatozoal enzymes that have been shown to be antigenic even in the species of origin. This is the case for lactic dehydrogenase LDH-X (a mid-piece enzyme) and for acrosomal enzymes, e.g., hyaluronidase, possibly sorbitol dehydrogenase and trypsin-like acrosomal proteinase (the auto- and allo-antigenicity of the latter having not been established). At least three of these enzymes are known or supposed to play a role in the process of fertilization. A clinical approach has described the presence of spermatozoal-coating antigen(s), such as transferrin or blood group substances from secretors obtained following the admixture of the secretions of the seminal vesicles. Indications were also obtained for the existence of antibodies directed against defined antigens. Several types of localization of antibodies on spermatozoa were described: acrosome (front part), equatorial segment, post-nuclear region, mid-piece and tail. Attempts at fractionation of human psermatozoal antigens are still at a preliminary stage. Whatever the approach, the main interest of these antigens is that they are able to induce, in the species of origin or in a related species antibodies capable of interfering with the normal process of reproduction, especially fertilization..

Alcohol Oxidoreductases↗
PubMedDate not supplied

The influence of homologous pulmonary proteins on the lung tissue reactivity: an experimental analysis.

The influence of homologous pulmonary proteins on the lung tissue reactivity was experimentally and immunomorphologically analysed in rabbits: a. in the development of specific sensitized substrate; b. by the challenge of hypersensitivity reactions: and c. by the evaluation of the development of an experimental lung tuberculosis at the level of the sensitized lung. Morphometrical methods were used. The immunomorphological analysis pointed out the importance of the increase of pyroninophilic and plasma cells and of eosinocytes in the lung tissue sensitized to homologous proteins included in the complete Freund adjuvant, the specificity and peculiarities (frequency of plasmocytosis and necrosis) of hypersensitivity reactions intratracheally and intravenously challenged with the homologous pulmonary proteins at the level of the sensitized lung, as well as the severe evolution of the experimental lung tuberculosis by comparison with that developing in a lung substrate sensitized without homologous pulmonary proteins or unsensitized. These results provided data for the influence exerted on the lung substrate by the pulmonary proteins which are released during the evolution of lugn processes and could act as autoantigens in the framework of an autoaggressive pathogenic component of chronic diseases.

Anaphylaxis↗
PubMed1978

Demonstration of antibodies in patients' sera, directed against nonspecific cross-reacting antigen.

Nonspecific cross-reacting antigen (NCA), which strongly cross-reacts with carcinoembryonic antigen, was demonstrated to be an autoantigen. Antibodies directed against NCA were shown in different groups of patients, but high titers (greater than 1/64) were found only in cancer patients. A correlation between tumor mass, antigen load, and antibody titer apparently existed. Sera obtained from patients preoperatively and postoperatively differed significantly (P greater than 0.01) in the sense that titers were high only in sera sampled after the patients were treated. Nevertheless, the formation of these antibodies cannot be considered a cancer-specific phenomenon because of their existence also in patients with nonmalignant diseases.

Adult↗
PubMed1979

Myasthenia gravis and lymphoma. A clinical and immunological association.

Myasthenia gravis and lymphoma rarely coexist, but the occurrence of myasthenia shortly after the treatment of a patient with poorly differentiated nodular lymphoma suggested that an immunological disorder may have contributed to the development of both diseases; the fundamental defects in this association may be impaired immunological surveillance and impaired regulation of immune responses to autoantigens. The finding of T-cell immunodeificiency, including profound T-cell lymphopenia, impaired delayed hypersensitivity responses, and failure to a thymus-dependent antibody response to Salmonella adelaide flagellin, is consistent with this hypothesis.

Autoantibodies↗