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Critical Reviews™ in Immunology

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ISSN Печать: 1040-8401

ISSN Онлайн: 2162-6472

The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) IF: 1.3 To calculate the five year Impact Factor, citations are counted in 2017 to the previous five years and divided by the source items published in the previous five years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) 5-Year IF: 2.6 The Eigenfactor score, developed by Jevin West and Carl Bergstrom at the University of Washington, is a rating of the total importance of a scientific journal. Journals are rated according to the number of incoming citations, with citations from highly ranked journals weighted to make a larger contribution to the eigenfactor than those from poorly ranked journals. Eigenfactor: 0.00079 The Journal Citation Indicator (JCI) is a single measurement of the field-normalized citation impact of journals in the Web of Science Core Collection across disciplines. The key words here are that the metric is normalized and cross-disciplinary. JCI: 0.24 SJR: 0.429 SNIP: 0.287 CiteScore™:: 2.7 H-Index: 81

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Autoantigens and Immune Pathways in Rheumatoid Arthritis

Том 22, Выпуск 4, 2002, 13 pages
DOI: 10.1615/CritRevImmunol.v22.i4.30
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Краткое описание

Rheumatoid arthritis (RA) is a major systemic autoimmune disease. A plethora of putative autoantigens has been described by the reactivity of antibodies present in the sera of patients. Despite this there is little evidence implicating most of them in its pathogenesis. Autoantigens fall into two major groups: first, those that are associated with the joint, such as collagen type II, human chondrocyte glycoprotein 39, and proteoglycans, for which a pathogenic role is easily understood; and second, those proteins not associated with the joint. Of these there are three groups: (1) highly conserved foreign antigens with human homologues, such as heat shock proteins (HSPs), in which the initiating antigenic stimulus may be through infection; (2) post-translationally altered proteins, such as citrullinated filaggrin, to which autoantibodies show high specificity but low sensitivity for RA and immunoglobulin G; and (3) ubiquitous proteins, such as glucose-6-phosphate isomerase, p205, and HSPs secreted during stress, such as BiP. The mechanisms by which such ubiquitous antigens cause pathology predominantly in the joints are difficult to understand. Autoantibodies, such as rheumatoid factors, that form immune complexes resulting in activation of phagocytic cells or the complement system, may cause joint pathology by deposition in the joints. Such an explanation, however, is not available for all of these autoantigens. It is possible that pathology may be the outcome of disturbed immunoregulation.

ЦИТИРОВАНО В
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