Anti-BiP antibody levels in juvenile idiopathic arthritis (JIA)

Bodman‐Smith, Mark; Fife, M F; Wythe, Helena; Corrigal, V M; Panayi, G. S.; Wedderburn, Lucy R.; Woo, Patricia

doi:10.1093/rheumatology/keh186

Cited by 7 publications

(4 citation statements)

References 8 publications

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“…Another example of molecular mimcry which could contribute to the pathogenesis of JIA involves binding immunoglobulin protein (BiP), a member of the heat shock protein (HSP) 70 family, and another established autoantigen in inflammatory arthritis. Approximately 60% of adult patients with RA and 37% of pediatric patients with polyarticular-RF+ JIA have anti-BiP antibodies (128, 129). BiP appears to have immunomodulatory effects, including inducing the production of IL-10, IL-1 receptor antagonist, soluble TNFRII, and downregulation of CD86 and HLA-DR (130).…”

Section: Autoantibodies and Potential Examples Of Molecular Mimicry Imentioning

confidence: 99%

Autoantibodies in the Pathogenesis, Diagnosis, and Prognosis of Juvenile Idiopathic Arthritis

Mahmud

Binstadt

2019

Front. Immunol.

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Autoantibody production occurs in juvenile idiopathic arthritis (JIA) and numerous other autoimmune diseases. In some conditions, the autoantibodies are clearly pathogenic, whereas in others the roles are less defined. Here we review various autoantibodies associated with JIA, with a particular focus on antinuclear antibodies and antibodies recognizing citrullinated self-antigens. We explore potential mechanisms that lead to the development of autoantibodies and the use of autoantibody testing in diagnosis and prognosis. Finally, we compare and contrast JIA-associated autoantibodies with those found in adults with rheumatoid arthritis (RA).

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Section: Autoantibodies and Potential Examples Of Molecular Mimicry Imentioning

confidence: 99%

Autoantibodies in the Pathogenesis, Diagnosis, and Prognosis of Juvenile Idiopathic Arthritis

Mahmud

Binstadt

2019

Front. Immunol.

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“…Thus, ER chaperones released in the extracellular space induce (specific) immune responses. ( 17 , 21 , 40 – 44 ). The mechanism(s) by which such ER chaperones elicit immunity is not fully understood and may differ between respective chaperones.…”

Section: Extracellular Chaperones Can Act As Dampsmentioning

confidence: 99%

“…When proteins that normally reside intracellular become exposed to the immune system, this likely induces (auto)antibody responses. Indeed, early studies demonstrated that ER chaperones are target of autoimmunity in murine models ( 64 ) and patients ( 57 ), leading to the generation of autoantibodies against a number of chaperones in serum of patients with autoimmune diseases or malignancies ( 17 , 21 , 40 – 44 ) (Table 2 ). Thus, ER chaperones are being released and can trigger autoantibody formation.…”

Section: Appearance Of Extracellular Er Chaperones and Autoantibodiesmentioning

confidence: 99%

Mechanisms of Translocation of ER Chaperones to the Cell Surface and Immunomodulatory Roles in Cancer and Autoimmunity

et al. 2015

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Endoplasmic reticulum (ER) chaperones (e.g., calreticulin, heat shock proteins, and isomerases) perform a multitude of functions within the ER. However, many of these chaperones can translocate to the cytosol and eventually the surface of cells, particularly during ER stress induced by e.g., drugs, UV irradiation, and microbial stimuli. Once on the cell surface or in the extracellular space, the ER chaperones can take on immunogenic characteristics, as mostly described in the context of cancer, appearing as damage-associated molecular patterns recognized by the immune system. How ER chaperones relocate to the cell surface and interact with other intracellular proteins appears to influence whether a tumor cell is targeted for cell death. The relocation of ER proteins to the cell surface can be exploited to target cancer cells for elimination by immune mechanism. Here we evaluate the evidence for the different mechanisms of ER protein translocation and binding to the cell surface and how ER protein translocation can act as a signal for cancer cells to undergo killing by immunogenic cell death and other cell death pathways. The release of chaperones can also exacerbate underlying autoimmune conditions, such as rheumatoid arthritis and multiple sclerosis, and the immunomodulatory role of extracellular chaperones as potential cancer immunotherapies requires cautious monitoring, particularly in cancer patients with underlying autoimmune disease.

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“…In patients with limited cutaneous systemic sclerosis, the expression of ER stress markers BiP, ATF4, ATF6, and XBP1s were relatively increased in peripheral blood mononuclear cells (Lenna et al, ). Anti‐chaperone antibodies have been discovered in a number of autoimmune diseases, including inflammatory bowel disease, myasthenia gravis, RA, SLE, systemic sclerosis, primary biliary cirrhosis, juvenile autoimmune arthritis, and autoimmune hepatitis (Nagayama et al, ; Kreisel et al, ; Eggleton et al, ; Bodman‐Smith et al, ; Watanabe et al, ; Goeb et al, ; Komurasaki et al, ; Tarr et al, ; Weber et al, ). However, the precise mechanism of how these antibodies are generated and how they contribute to the progression of the disease are still being studied.…”

Section: Infection and Autoimmunitymentioning

confidence: 99%

Endoplasmic Reticulum Stress Interacts With Inflammation in Human Diseases

Cao

Luo

Shi

2015

Journal Cellular Physiology

125

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The endoplasmic reticulum is a critical organelle for normal cell function and homeostasis. Disturbed protein folding process in the ER, termed ER stress, leads to the activation of unfolded protein response (UPR) that encompasses a complex network of intracellular signaling pathways. The UPR can either restore ER homeostasis or activate pro-apoptotic pathways depending on specific insults, intensity and duration of the stress, and cell types. ER stress and the UPR have recently been linked to inflammation in a variety of human pathologies including autoimmune diseases, infection, neurodegenerative disease, and metabolic disorders. In the cell, ER stress and inflammatory signaling share extensive regulators and effectors in a broad spectrum of biological processes. In spite of different etiologies, the two signaling pathways were shown to form a vicious cycle in exacerbating cellular dysfunction and causing apoptosis in many cells and tissues. However, the interaction between ER stress and inflammation in many of these diseases remains elusive. Further understanding of those issues may enable the development of novel therapies that spontaneously target these pathogenic pathways.

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Anti-BiP antibody levels in juvenile idiopathic arthritis (JIA)

Cited by 7 publications

References 8 publications

Autoantibodies in the Pathogenesis, Diagnosis, and Prognosis of Juvenile Idiopathic Arthritis

Autoantibodies in the Pathogenesis, Diagnosis, and Prognosis of Juvenile Idiopathic Arthritis

Mechanisms of Translocation of ER Chaperones to the Cell Surface and Immunomodulatory Roles in Cancer and Autoimmunity

Endoplasmic Reticulum Stress Interacts With Inflammation in Human Diseases

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