High serum concentrations of autoantibodies to HSP47 in nonspecific interstitial pneumonia compared with idiopathic pulmonary fibrosis

Kakugawa, Tomoyuki; Yokota, Shinichi; Mukae, Hiroshi; Sakamoto, Noriho; Mizunoe, Syunji; Matsuoka, Yoshikazu; Kadota, Jun‐ichi; Fujii, Nobuhiro; Nagata, Kazuhiro; Kohno, Shigeru

doi:10.1186/1471-2466-8-23

Cited by 18 publications

(21 citation statements)

References 27 publications

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“…In fact, we have shown that anti-Th/To autoantibodies facilitate the differentiation of patients with SSc without scleroderma from those with IPF [28]. Additional antibodies include those directed against HSP47, which are detected at higher levels in the serum of patients with idiopathic NSIP compared with IPF patients [29]. Antivimentin antibodies were also detected in sera of patients with IPF and NSIP [30].…”

Section: Autoantibodies and Other Serum Biomarkersmentioning

confidence: 87%

Pathogenesis of Pulmonary Fibrosis in Systemic Sclerosis: Lessons from Interstitial Lung Disease

2010

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Interstitial lung disease is a frequent complication of systemic sclerosis and currently is the leading cause of death. Our ability to predict which individuals are at greatest risk of developing clinically significant, progressive interstitial lung disease remains inadequate. Identification of circulating autoantibodies and other biomarkers, as well as genetic polymorphisms and aberrant gene expression, all hold promise as diagnostic and prognostic tools, as well as therapeutic targets. Many practice patterns for the diagnosis and monitoring of connective tissue disease-associated interstitial lung disease are based upon published experience with idiopathic interstitial lung diseases. Although there are likely commonalities in the pathophysiologic mechanisms and clinical progression among all fibrosing lung diseases, a better understanding of features unique to systemic sclerosis-associated interstitial lung disease is essential to the development of more effective monitoring and treatment strategies.

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Section: Autoantibodies and Other Serum Biomarkersmentioning

confidence: 87%

Pathogenesis of Pulmonary Fibrosis in Systemic Sclerosis: Lessons from Interstitial Lung Disease

2010

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“…Only very limited release was noted from cultured fibroblasts. Recently, highserum auto-antibodies to HSP47 or HSP47 itself have been reported under inflammatory conditions, such as interstitial pneumonia and mixed connective tissue disease (Yokota et al, 2003;Kakugawa et al, 2008). If HSP47 is released from cancers in patients with UC, its detection in serum would be helpful for the clinical detection of malignancy.…”

Section: Discussionmentioning

confidence: 99%

High expression of HSP47 in ulcerative colitis-associated carcinomas: proteomic approach

et al. 2009

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BACKGROUND: Ulcerative colitis (UC) is a chronic relapsing inflammatory bowel disease, known to be associated with a markedly increased risk of colorectal carcinoma development. METHODS: Using proteomic analysis with two-dimensional gel electrophoresis and mass spectrometry, differentially expressed proteins were assessed between UC-associated cancer and sporadic colon cancer cell lines. Western blot and immunostaining were performed for confirming the expression. RESULTS: Heat-shock protein of 47 kDa (HSP47) was identified as one of the proteins expressed more highly in UC-associated cancer cell lines, and an immunohistochemical examination confirmed significantly higher levels of HSP47 in UC-associated colon cancers than in sporadic counterparts, the expression increasing with a progression of neoplastic lesions. Heat-shock protein of 47 kDa was further found to be coexpressed with type I collagen in the cytoplasm, and both HSP47 and type I collagen were released from cultured cells into the culture medium. CONCLUSION: These results suggest that overexpression of HSP47 is a unique characteristic of UC-associated carcinoma related to type I collagen synthesis, with possible clinical applications.

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“…More direct evidence is derived from reports of autoantibody and T cell responses to a variety of ubiquitously expressed proteins in patients with ILD (8–10). However, these putative antigens are not tissue specific and so it is not clear how they could cause a disease process limited to the lung.…”

Section: Introductionmentioning

confidence: 99%

Identification of an Autoantigen Demonstrates a Link Between Interstitial Lung Disease and a Defect in Central Tolerance

et al. 2009

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Interstitial lung disease (ILD) is a common manifestation of systemic autoimmunity characterized by progressive inflammation or scarring of the lungs. Patients who develop these complications can exhibit significantly impaired gas exchange that may result in hypoxemia, pulmonary hypertension and even death. Unfortunately, little is understood about how these diseases arise, including the role of specific defects in immune tolerance. Another key question is whether autoimmune responses targeting the lung parenchyma are critical to ILD pathogenesis, including that of isolated, idiopathic forms. We show that a specific defect in central tolerance brought about by mutations in the autoimmune regulator gene (Aire) leads to an autoreactive T cell response to a lung antigen named vomeromodulin and the development of ILD. We found that a human patient and mice with defects in Aire develop lung pathology that is strikingly similar, demonstrating that the AIRE-deficient model of autoimmunity is a suitable translational system in which to unravel fundamental mechanisms of ILD pathogenesis.

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High serum concentrations of autoantibodies to HSP47 in nonspecific interstitial pneumonia compared with idiopathic pulmonary fibrosis

Cited by 18 publications

References 27 publications

Pathogenesis of Pulmonary Fibrosis in Systemic Sclerosis: Lessons from Interstitial Lung Disease

Pathogenesis of Pulmonary Fibrosis in Systemic Sclerosis: Lessons from Interstitial Lung Disease

High expression of HSP47 in ulcerative colitis-associated carcinomas: proteomic approach

Identification of an Autoantigen Demonstrates a Link Between Interstitial Lung Disease and a Defect in Central Tolerance

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