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PubMedDate not supplied

Islet-cell antibodies (ICA) in diabetes mellitus (evidence of an autoantigen common to all cells in the islet of Langerhans).

Pancreatic islet-cell antibodies (ICA) are important markers for two subtypes of insulin-dependent diabetes mellitus and stain the entire islet in the standard immunofluorescence test. This could indicate either a mixture of antibodies each directed against one cell type, or a population of antibodies reacting with a single antigen common to the endocrine pancreas. In the present experiments such a common antigen was demonstrated visually by application of animal antisera raised to each of the 4 pancreatic hormones, together with ICA-positive sera in a four-layer double immunofluorescent technique employing green and red anti-Ig conjugates. Double exposure photographs demonstrated that the patients' sera reacted equally with the different endocrine cells. The ICA antigen did not cross-react with gastric glucagon- or somatostatin-cells. By contrast, human antibodies against glucagon-cells (GCA) or somatostatin-cells (SCA) reacted with discrete antigens specific to each cell type and in 50% of cases the antibodies also stained the respective endocrine cells in the gastrointestinal tract. These refined discriminatory properties of human autoantibodies may lead to a better understanding of the intracellular membrane systems in these important endocrine organs.

Antigens↗
PubMed1979

Contractile proteins as autoantigens.

Smooth muscle antoantibodies are found in high titre in some patients with chronic active hepatitis, and in lower titres in a number of other liver diseases and certain viral infections. They are directed at contractile proteins of the actomyosin group, and anti-actin activity appears to predominate. Whether occurring in disease affecting the liver or in other conditions, smooth muscle antibody production is thought to be stimulated when contractile proteins of non-muscle cells become immunogenic as a result of changes induced in the cells by viral infection or by other unknown causes of derangement of cytoskeletal structure.

Animals↗
PubMed1977

A human immunoglobulin in myeloma protein with anti-gastric parietal cell autoantigen activity.

A previously characterised IgA Kappa myeloma protein was isolated and purified. The (Fab) alpha fragments of this immunoglobulin were obtained. The IgA and Fab fragments reacted in vitro with gastric parietal cells (GPC) using animal gastric sections and with smooth cytoplasmic membranes obtained from rabbit fundus (gastric) mucosa. This was seen macroscopically and by light and electron microscopy. Evidence is thus provided which supports the concept that this homogeneous immunoglobulin is a typical monoclonal autoantibody.

Autoantibodies↗
PubMedDate not supplied

[Autoimmune aspermatogenetic orchiepididymitis in guinea pigs induced by water-soluble adjuvants].

Use was made of water-soluble adjuvant fractions with homologous sperm, sperm extract or sperm autoantigens to induce autoimmune aspermatogenic orchiepididymitis (AIAO) in guinea-pigs. Guinea-pigs were injected with soluble sperm extract or sperm purified autoantigen S emulsified in incomplete Freund adjvant (IFA) together with two synthetic watersoluble adjuvants, Mur-Nac-L-Ala-D-isoGlu et Mur-Nac-L-Ala-acide D-isoGlu. These animals developed lesions of AIAO, delayed hypersensitivity reactions and specific anti-spermatozoa antibodies. These lesions and reactions were comparable to the ones induced in a control group treated with the same spermatozoa extract or autoantigen S in complet Freund adjuvants. No lesion was observed in the absence of IFA, Other guinea-pigs received a mixture of spermatoza or purified sperm autoantigens, S, P, T. and of polyadenylicpolyuridylic complex either in saline or emulsified in IFA. The recipients of sperm or autoantigen T mixed with Poly A:U, with ou without IFA, displayed lsdions of AIAO; autoantigen S and Poly A:U in IFA, provoked AIAO but did not do it in the absenceof IFA.

Adjuvants, Immunologic↗
PubMed1978

Delineation of spontaneous erythrocyte autoantibody responses of NZB and other strains of mice.

Four anti-erythrocyte autoantibody responses (anti-X, anti-HB, anti-HOL, and anti-I) that occur spontaneously in mice have been characterized with regard to antigenic specificities, predominant immunoglobulin class, and pathogenetic importance. Each autoantibody response exhibits specificity for an independent erythrocyte membrane autoantigen (X, HB, HOL, or I) or a soluble analogue (SEA-X or SEA-HB) present in the plasma. The anti-X response, unique to NZB mice, is directed to a normally exposed murine erythrocyte autoantigen, whereas the anti-HB response is directed to a cryptic erythrocyte autoantigen exposed by limited enzymatic cleavage of the membrane. The anti-I response also is directed to a cryptic but distinct autoantigen, and anti-HOL autoantibodies react with an erythrocyte autoantigen located at the cytoplasmic surface of the membrane. Analysis of the predominant immunoglobulin class of each of the autoantibodies has demonstrated that anti-HB and anti-I antibodies are predominantly of IgM class, whereas anti-X and anti-HOL antibodies are IgG immunoblobulins. Only anti-X and anti-HB autoantibodies are recovered from Coombs' positive erythrocytes from NZB mice and erythrocytes with surface C3 are detected only in NZB mice greater than 9 months of age. These data suggest that only the anti-X and anti-HB responses are pathogenetically implicated in the autoimmune hemolytic anemia of NZB mice.

Animals↗
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↗