Multiple Autoantigen Mimotopes of Infectious Agents Induce Autoimmune Arthritis and Uveitis in Lewis Rats

Wildner, Gerhild; Diedrichs-Moehring, M.

doi:10.1128/cdli.12.5.677-679.2005

Cited by 14 publications

(12 citation statements)

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“…An accompanying infection may provide an adjuvant effect (although severe endophthalmitis, which quickly destroys the injured eye and eliminates the source of antigen, may actually lessen chances of developing the disease) (3). In uveitic disease that cannot be linked to a trauma, it is believed that T cells capable of recognizing retinal antigens are primed in the periphery by microbial stimuli that may be immunologically similar in structure to their cognate retinal antigen (antigenic mimicry) (48)(49)(50). Microbial components also interact with innate pattern recognition receptors on APCs, generating "danger" signals that are necessary to elicit inflammatory immune reactions.…”

Section: Figurementioning

confidence: 99%

A look at autoimmunity and inflammation in the eye

2010

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Autoimmune and inflammatory uveitis are a group of potentially blinding intraocular inflammatory diseases that arise without a known infectious trigger and are often associated with immunological responses to unique retinal proteins. In the United States, about 10% of the cases of severe visual handicap are attributed to this group of disorders. As I discuss here, experimental models of ocular autoimmunity targeting retinal proteins have brought about a better understanding of the basic immunological mechanisms involved in the pathogenesis of uveitis and are serving as templates for the development of novel therapies.

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Section: Figurementioning

confidence: 99%

A look at autoimmunity and inflammation in the eye

2010

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“…For example, despite the fact that it is very well accepted that injection of HgCL 2 can induce scleroderma and lupus in animal models (14,(39)(40), no attempt was made to measure antibodies against Hg-HSA or Hg-binding nucleoproteins, such as fibrillarin and chromatin, in human lupus (11). Similarly, in the case of infections with Mycoplasma, Chlamydia and Mycobacteria, their heat shock proteins or mimic peptides are considered as the most likely triggering factors for RA (9,32,41). To our knowledge, this is the first report showing elevation in antibodies against protein-modifying factors in clinical specimens from lupus and arthritis (see Tables IV, V, VI and Fig.…”

Section: Discussionmentioning

confidence: 88%

“…Serum antibodies specific for modified self proteins are a hallmark for many complex autoimmune disorders, including RA. These disease-specific antibodies predominantly react with modified self proteins such as IgG, citrullinated protein, collagen and mitochondrial dehydrogenase, and several mimic peptides (9,(29)(30). Antibodies against aggregated IgG, arthritis peptide, citrullinated peptide, collagen type 2 peptide, mitochondrial dehydrogenase, Mycobacterium avium, Mycoplasma arthritidis, Chlamydia pneumoniae and HSP-60, which are detected frequently in patients with RA are shown in Table V and Fig.…”

Section: Resultsmentioning

confidence: 99%

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Antibodies as Predictors of Complex Autoimmune Diseases

Vojdani

2008

Int J Immunopathol Pharmacol

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Emerging evidence has suggested environmental factors such as infections and xenobiotics and some dietary proteins and peptides in the pathogenesis of many autoimmune diseases. Considering the fact that autoantibodies can often be detected prior to the onset of a disease, in this study an enzyme immunoassay was used for measurement of antibodies against different highly purified antigens or synthetic peptides originating not only from human tissue, but also from cross-reactive epitopes of infectious agents, dietary proteins and xenobiotics. The measurement of antibodies against a panel of antigens allows for identification of patterns or antibody signatures, rather than just one or two markers of autoimmunity, thus establishing the premise for increased sensitivity and specificity of prediction, as well as positive predictive values. This panel of different autoantibodies was applied to 420 patients with different autoimmune diseases, including pernicious anemia, celiac disease, thyroiditis, lupus, rheumatoid arthritis, osteoarthritis, Addison's disease, type 1 diabetes, cardiovascular disease and autoimmunity, which are presented in this article. In all cases, the levels of these antibodies were significantly elevated in patients versus controls. Antibody patterns related to neuroautoimmune disorders, cancer, and patients with somatic hypermutation will be shown in a subsequent article. We believe that this novel 96 antigen-specific autoantibody or predictive antibody screen should be studied for its incorporation into routine medical examinations. Clinicians should be aware that the detection of antibodies should not automatically mean that a patient will definitely become ill, but would rather give a percentage of risk for autoimmune disease over subsequent months or years.

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“…An infection could facilitate the presentation of self-antigens to lymphocytes by the HLA-A29 molecule. Autoimmune responses could occur in relation to molecular mimicry of self-and nonself-determinants that could be responsible for the break of immunological tolerance [23][24][25][26] . Autoimmune uveitis shows different clinical manifestations.…”

Section: Discussionmentioning

confidence: 99%

Pathological Aspects of Spontaneous Uveitis and Retinopathy in HLA-A29 Transgenic Mice and in Animal Models of Retinal Autoimmunity: Relevance to Human Pathologies

2008

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Purpose: A major increased risk of developing birdshot chorioretinopathy is reported in humans who are HLA-A29-positive. To better characterize this disease, an animal model of HLA-A29-associated disease was developed and the pathology arising spontaneously in these transgenic mice was compared to animal models of autoimmune uveoretinitis and to human pathology. Materials and Methods: HLA-A2902 cDNA (A29c) was obtained from a patient suffering from birdshot retinochoroidopathy and used for transgene construct to generate HLA-A29 transgenic mice. Histopathological examination of the animal cohort was performed up to 15 months of age. It was compared with the ocular pathology developed in C57BL/6 mice and in Lewis rats immunized with retinal autoantigens. Results: Aging HLA-A29 transgenic mice spontaneously developed an ocular disease with resemblance to experimental retinal-Ag-induced autoimmune ocular disease and to human pathologies shown in birdshot retinochoroidopathy, Vogt-Koyanagi-Harada and sympathetic ophthalmia. Pathogenic mechanisms could possibly be shared by these conditions. Conclusion: Humanized models of ocular inflammation developed in HLA class I and class II transgenic mice will help better understand the mechanisms responsible for ocular inflammation. Local control of autoimmunity in HLA-A29-positive individuals would be an important option for new therapeutic strategies.

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Multiple Autoantigen Mimotopes of Infectious Agents Induce Autoimmune Arthritis and Uveitis in Lewis Rats

Cited by 14 publications

References 14 publications

A look at autoimmunity and inflammation in the eye

A look at autoimmunity and inflammation in the eye

Antibodies as Predictors of Complex Autoimmune Diseases

Pathological Aspects of Spontaneous Uveitis and Retinopathy in HLA-A29 Transgenic Mice and in Animal Models of Retinal Autoimmunity: Relevance to Human Pathologies

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