Autoimmune pre-disease

Bieber, Katja; Hundt, Jennifer E.; Yu, Xinhua; Ehlers, Marc; Petersen, Frank; Karsten, Christian M.; Köhl, Jörg; Kridin, Khalaf; Kalies, Kathrin; Kasprick, Anika; Goletz, Stephanie; Humrich, Jens Y; Manz, Rudolf A.; Künstner, Axel; Hammers, Christoph M.; Akbarzadeh, Reza; Busch, Hauke; Sadik, Christian D.; Lange, Tanja; Graßhoff, Hanna; Hackel, Alexander; Erdmann, J.; König, Inke R.; Raasch, Walter; Becker, Mareike; Kerstein-Stähle, Anja; Lamprecht, Peter; Riemekasten, Gabriela; Schmidt, Enno; Ludwig, Ralf J.

doi:10.1016/j.autrev.2022.103236

Cited by 35 publications

(14 citation statements)

References 338 publications

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“…In SLE, rheumatoid arthritis and type 1 diabetes (T1DM) the presence of disease-specific autoantibodies prior to clinical disease manifestation is well-established (6)(7)(8)(9)(10). This is less well characterized for autoantibodies targeting BP180 or BP230, which characterize and cause bullous pemphigoid (14).…”

Section: From Health To Autoimmunitymentioning

confidence: 99%

“…Autoimmune diseases develop over a long time, which at least spans over several years. This is maybe best demonstrated by the presence of disease-specific autoantibodies years prior to diagnosis of the corresponding autoimmune disease ( 6 – 10 ). The presence of disease-specific autoantibodies, does not, however, reliably predict if clinical manifestation of the corresponding autoimmune disease will occur in the future.…”

Section: Introductionmentioning

confidence: 99%

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Editorial: Autoimmune pre-disease

et al. 2023

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According to the revised Witebsky postulates, diseases are of an autoimmune nature if, (i) the clinical phenotype can be reproduced through the transfer of autoantibodies and/or lymphocytes; (ii) the disease can be reproduced in experimental animal models; (iii) autoreactive T cells or autoantibodies are identified; and/or (iv) distinctive clinical observations, such as an HLA association, are found (1). These postulates mostly still hold true despite they were made 3 decades ago. However, in psoriasis, lichen sclerosus and lichen planus, which are considered chronic, non-communicable inflammatory diseases, autoreactive T cells and/or autoantibodies that potentially contribute to disease pathogenesis are also detected (2-5). Thus, rather than a clear distinction between autoimmune and chronic non-communicable inflammatory diseases, categorization of a given distinct disease may be better placed in the continuum between the two. Hence, within this research topic, we cover both "classic" autoimmune diseases, such as systemic lupus erythematosus (SLE), as well as non-communicable, inflammatory diseases with detectable autoimmunity, e.g., psoriasis.Autoimmune diseases develop over a long time, which at least spans over several years. This is maybe best demonstrated by the presence of disease-specific autoantibodies years prior to diagnosis of the corresponding autoimmune disease (6-10). The presence of disease-specific autoantibodies, does not, however, reliably predict if clinical manifestation of the corresponding autoimmune disease will occur in the future. Therefore, definite biomarkers that define the transition (i) from health to autoimmunity, (ii) from autoimmunity to autoimmune disease, and (iii) to chronicity or resolution of inflammation (Figure 1) would allow to implement measures to slow or prevent disease progression. This would have a significant impact on affected individuals, as well as the healthcare system because the incidence of autoimmune and non-communicable inflammatory diseases is rising and there are still many unmet medical needs in the care of patients with these diagnoses (12, 13).

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Section: From Health To Autoimmunitymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Editorial: Autoimmune pre-disease

et al. 2023

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“…Suspected drivers of SADs include internal and external exposures throughout life, interacting with genetic predispositions 6,7 . Pathogen infection is believed to play a pivotal role in the development of SADs 8 .…”

Section: Introductionmentioning

confidence: 99%

Evaluation of serum Epstein–Barr virus envelope glycoproteins antibodies and their association with systemic autoimmune diseases

Li,

Zhong,

Kang

et al. 2024

Journal of Medical Virology

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Systemic autoimmune diseases (SADs) are a growing spectrum of autoimmune disorders that commonly affect multiple organs. The role of Epstein–Barr virus (EBV) infection or reactivation as a trigger for the initiation and progression of SADs has been established, while the relationship between EBV envelope glycoproteins and SADs remains unclear. Here, we assessed the levels of IgG, IgA, and IgM against EBV glycoproteins (including gp350, gp42, gHgL, and gB) in serum samples obtained from patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), and found that RA and SLE patients exhibited a statistically significant increase in the levels of 8 and 11 glycoprotein antibodies, respectively, compared to healthy controls (p < 0.05). The LASSO model identified four factors as significant diagnostic markers for RA: gp350 IgG, gp350 IgA, gHgL IgM, and gp42 IgA; whereas for SLE it included gp350 IgG, gp350 IgA, gHgL IgA, and gp42 IgM. Combining these selected biomarkers yielded an area under the curve (AUC) of 0.749 for RA and 0.843 for SLE. We subsequently quantified the levels of autoantibodies associated with SADs in mouse sera following immunization with gp350. Remarkably, none of the tested autoantibody levels exhibited statistically significant alterations. Elevation of glycoprotein antibody concentration suggests that Epstein–Barr virus reactivation and replication occurred in SADs patients, potentially serving as a promising biomarker for diagnosing SADs. Moreover, the absence of cross‐reactivity between gp350 antibodies and SADs‐associated autoantigens indicates the safety profile of a vaccine based on gp350 antigen.

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“…Autoimmune diseases (ADs) are a heterogeneous group of more than 100 pathological conditions that are characterized by an alteration in the regulation of inflammatory processes against one or multiple autoantigens [ 1 , 2 ].…”

Section: Introductionmentioning

confidence: 99%

Molecular Mechanisms in Autoimmune Thyroid Disease

Vargas‐Uricoechea

2023

Cells

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The most common cause of acquired thyroid dysfunction is autoimmune thyroid disease, which is an organ-specific autoimmune disease with two presentation phenotypes: hyperthyroidism (Graves-Basedow disease) and hypothyroidism (Hashimoto’s thyroiditis). Hashimoto’s thyroiditis is distinguished by the presence of autoantibodies against thyroid peroxidase and thyroglobulin. Meanwhile, autoantibodies against the TSH receptor have been found in Graves-Basedow disease. Numerous susceptibility genes, as well as epigenetic and environmental factors, contribute to the pathogenesis of both diseases. This review summarizes the most common genetic, epigenetic, and environmental mechanisms involved in autoimmune thyroid disease.

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Autoimmune pre-disease

Cited by 35 publications

References 338 publications

Editorial: Autoimmune pre-disease

Editorial: Autoimmune pre-disease

Evaluation of serum Epstein–Barr virus envelope glycoproteins antibodies and their association with systemic autoimmune diseases

Molecular Mechanisms in Autoimmune Thyroid Disease

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