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At least 217 records · Page 12Linked to original sources
PubMed1998

Correlation between chlamydial infection and autoimmune response: molecular mimicry between RNA polymerase major sigma subunit from Chlamydia trachomatis and human L7.

L7 is one of the ribosomal proteins frequently targeted by autoantibodies in rheumatic autoimmune diseases. A computer search revealed a region within the immunodominant epitope of L7 (peptide II) that is highly homologous to amino acid sequence 264-286 of the RNA polymerase major sigma factor of the eubacterium Chlamydia trachomatis. Anti-L7 autoantibodies affinity purified from the immunodominant epitope were able to recognize this sequence as they reacted with purified recombinant sigma factor. Immunofluorescence labeling experiments on C. trachomatis lysates revealed a punctate staining pattern of numerous spots when incubated with the affinity-purified anti-peptide II autoantibodies. Binding of autoantibodies to peptide II was inhibited by the homologous sigma peptide. This is the first demonstration of epitope mimicry between a human and a chlamydial protein on the level of B cells. Antibody screening revealed a significant correlation between the presence of anti-L7 autoantibodies and C. trachomatis infection in patients with systemic lupus erythematosus and mixed connective tissue disease. Our results suggest that molecular mimicry is involved in the initiation of anti-L7 autoantibody response and may represent a first glance into the immunopathology of Chlamydia with respect to systemic rheumatic diseases.

Amino Acid Sequence↗
PubMed1999

[Iodine responsive autoimmune thyroid diseases].

Iodine is an important element for the thyroid and regulates iodine accumulation, thyroid hormone synthesis and hormone release. As a result, dietary iodine deficiency is largely responsible for the production of T3 thyrotoxicosis. Supplemental iodine significantly elevated incidence of iodine induced hyperthyroidism in endemic goiter area. Even in normal iodine area, intake of iodine sometimes accelerates recurrence of hyperthyroid Graves' disease in antithyroid drug treated patients. In contrast, a possible role of iodine on Hashimoto's thyroiditis is not known. As a therapeutic means, excess iodide is used for rapid control of thyrotoxicosis and thyrotoxic crisis. Experimental studies indicated that excess iodide blocks thyroid hormone release by inhibiting thyroid stimulators. This blocking action is ascertained by measuring cAMP, colloid droplets formation and microscopic techniques. Excess iodide does induce hypothyroidism in Hashimoto's thyroiditis.

Animals↗
PubMed1997

The anti-erythrocyte autoimmune response of NZB mice. Identification of two distinct autoantigens.

With age, New Zealand black (NZB) mice spontaneously develop anti-mouse red blood cell (RBC) autoantibodies resulting in the development of autoimmune haemolytic anemia (AIHA). Previously, we characterized a panel of monoclonal autoantibodies derived from unimmunized, adult NZB mice. One of these antibodies (G8) was shown to be pathogenic, inducing AIHA in a non-autoimmune-prone mouse strain (BALB/c). Using G8, and two other antibodies from our panel, we have characterized two distinct autoantigens on the surface of mouse RBCs. The autoantigen, historically referred to as antigen X (AgX), was found to be partially hidden on the surface of the mouse RBC because glycosidase treatment or mild digestion with proteinase K resulted in increased reactivity with autoantibodies. One of the monoclonal antibodies (3H5G1) was found to immunoprecipitate a 110,000 MW protein identified as the erythrocyte anion transporter (band 3) whereas the pathogenic antibody (G8) as well as a third monoclonal antibody (2E6m) were shown to immunoprecipitate a 60,000 MW protein that was not reactive with the anti-band 3 serum. Finally, we show that the autoantigen recognized by G8 is expressed on differentiated mouse erythroleukaemia (MEL) cells. The results suggest that a protein distinct from band 3 can serve as a target for AIHA in NZB mice.

Anemia, Hemolytic, Autoimmune↗
PubMed1990

The autoimmune response of different mouse strains to T-cell epitopes of the human acetylcholine receptor alpha subunit.

The specific recognition of the acetylcholine receptor and its alpha-subunit by T cells derived from patients with myasthenia gravis or mice with experimental autoimmune myasthenia gravis raises the question of the role of autoreactive T cells in the myasthenic process. Sequences of the acetylcholine receptor alpha-subunit previously shown to be immunogenic in myasthenic patients were tested for their immunogenicity in various inbred mouse strains. High, intermediate and low T-cell proliferative responses could be observed to peptides representing sequences 195-212 and 259-271 of the human acetylcholine receptor alpha-subunit. Following immunization with the Torpedo acetylcholine receptor, lymphocytes of SJL mice proliferated efficiently to p 195-212 but not to p259-271. On the other hand, lymph node cells of BALB/c mice responded well to p259-271 but not to p195-212. Thus, the influence of the genetic make-up of the examined mice on the immune response to the two peptides could be clearly demonstrated by the existence of strain-dependent immunodominant and cryptic regions on the autoantigen. The differences between the strains were less pronounced when antibody responses were measured to these two T-cell epitopes, although a partial correlation with the proliferative responses could be observed. It can be concluded that epitopes specifically recognized by T lymphocytes of patients with myasthenia gravis also represent specific T-cell epitopes in the autoreactivity to the acetylcholine receptor in mice and that immune responsiveness to these peptides is influenced by the genetic make-up of the responding mouse strains.

Animals↗
PubMed2003

Regulation, counter-regulation, and immunotherapy of autoimmune responses to immunologically privileged retinal antigens.

Our interests revolve around the study of biological mechanisms regulating self-tolerance to immunologically privileged retinal proteins that serve as targets in sight-threatening autoimmune uveitic disease. These studies are aimed at understanding how selftolerance to these antigens develops during ontogeny and is maintained during adulthood, the processes involved in its pathological breakdown, the regulatory mechanisms that bring about remission and recovery, and, finally, how we can utilize knowledge of these processes for therapeutic restoration of tolerance. To answer these questions, we use the experimental autoimmune uveitis (EAU) model in rats and mice. Because of the commonality of underlying immunological mechanisms, lessons and concepts learned in experimental ocular models are applicable to other disease entities, and, conversely, data gleaned from other autoimmune diseases are applicable to the study of uveitis.

Animals↗
PubMed1997

Effects of HgCl2 on the expression of autoimmune responses and disease in diabetes-prone (DP) BB rats.

Repeated exposure of Brown Norway (BN) rats to relatively low doses of HgCl2 induces autoantibodies to renal antigens (e.g., laminin) and a membranous glomerulonephropathy characterized by proteinuria. In contrast, Lewis (LEW) rats are "resistant" to the autoimmune effects of mercury and, when exposed to this metal, are protected against experimental autoimmune encephalomyelitis (EAE) and Heymann's nephritis. To date, there is no information on "suppressive" effects of mercury in naturally occurring (so-called "spontaneous") rat models of autoimmune disease. Therefore, we have administered HgCl2 to diabetes-prone (DP) BB rats, animals that spontaneously develop both insulin-dependent diabetes mellitus (IDDM) and thyroiditis. We found that DP rats treated with mercury or water for a period of 40-125 days developed autoantibodies to thyroglobulin, with a higher incidence in HgCl2-injected animals (92% vs. 56% in H2O-injected controls). A novel finding of our study was the detection of autoantibodies to laminin in the same rats, again with an increased incidence after HgCl2 treatment (83% vs. 44%). IgG2a was the most frequently detected isotype of antibodies to laminin, followed by IgG1, IgG2b and IgG2c. The IgG isotype profile suggests that treatment with HgCl2 may activate both Th1 and Th2 lymphocytes in BB rats. In spite of these stimulatory effects on autoantibody responses, we found that there was no difference in the incidence of IDDM and thyroiditis between HgCl2-treated and control animals. We conclude that the suppressive effects of mercury previously observed in EAE and Heymann's nephritis of LEW rats do not occur in "spontaneous" autoimmune IDDM and thyroiditis of BB rats. Therefore, immune suppression caused by HgCl2 cannot be considered a common phenomenon, but may be a genetically determined characteristic of LEW rats, possibly related to a specific or unique cytokine profile of this particular rat strain. In contrast, while mercury does not seem to recruit, induce or rescue regulatory T cell function in DP rats, it does stimulate autoantibody responses in these animals.

Adrenal Glands↗
PubMed1977

[Effect of somatotropic hormone on autoimmune responses induced in mice of different genotypes by syngenous heated erythrocytes].

A single administration of 1 X 10(9) heated erythrocytes to C57BL and BALB/c mice caused on the 13th day the appearance of antierythrocytic autoantibodies, an increase in the weight of the lymphoid organs, and lymphoreticular hyperplasia. These changes were more pronounced in BALB/c mice. During the development of autoimmune reactions the changes in the number of E- and EAC-rosette-forming cells in the thymus and spleen and in the immune response to the sheep erythrocyte immunization and E. coli endotoxin were revealed; distinct strain differences were observed. Daily somatotropic hormone administration (5 mg/kg of body weight) for 10 days decreased the degree of the autoimmune reactions development in mice of both strains. Its action was more expressed in BALB/c mice.

Animals↗
PubMed2003

The magnitude and encephalogenic potential of autoimmune response to MOG is enhanced in MOG deficient mice.

Myelin oligodendrocyte glycoprotein (MOG) is a minor component of central nervous system myelin presumably implicated in the pathogenesis of Multiple Sclerosis (MS). Immunization with MOG leads to the development of Experimental Autoimmune Encephalomyelitis (EAE), the experimental model of MS. It has been suggested that its encephalitogenic potential may be due to the lack of MOG self-immune tolerance. To clarify this, we have generated a MOG deficient mouse (MOG(-/-)) strain. Surprisingly, MOG(35-55)specific proliferation and Th1-type cytokine production were markedly enhanced in MOG(-/-)mice compared to wild type control. Furthermore, adoptive transfer of MOG(35-55)specific T cells, isolated from MOG deficient mice, into wild-type recipients resulted in the development of a more severe disease, indicating a high capacity of MOG(-/-)T cells to initiate effector responses. Interestingly, T cell reactivity to overlapping MOG peptides in MOG(-/-)mice did not reveal new potential immunodominant epitopes in H-2(b)mice. Taken together, our data suggests that MOG self-tolerance modulates the encephalitogenic potential of autoreactive MOG T cells in the periphery.

Adoptive Transfer↗