Please use this identifier to cite or link to this item: http://hdl.handle.net/123456789/1710
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dc.contributor.authorChadha S-
dc.contributor.authorBehl T-
dc.contributor.authorBungau S-
dc.contributor.authorKumar A-
dc.contributor.authorKaur R-
dc.contributor.authorVenkatachalam T-
dc.contributor.authorGupta A-
dc.contributor.authorKandhwal M-
dc.contributor.authorChandel D-
dc.date.accessioned2021-05-12T15:10:05Z-
dc.date.available2021-05-12T15:10:05Z-
dc.date.issued2021-
dc.identifier.uri10.1007/s10753-020-01324-8-
dc.identifier.urihttp://hdl.handle.net/123456789/1710-
dc.description.abstractAutophagy exerts its dual role in eukaryotic cells and exerts its cytoprotective action through degradation mechanism and by regulating catabolic processes which results in elimination of pathogens. Under suitable conditions, autophagy is associated with recycling of cytoplasmic components which causes regeneration of energy whereas deregulated autophagy exerts its implicated role in development and pathogenesis of auto-immune diseases such as rheumatoid arthritis. The immune, innate, and adaptive responses are regulated through the development, proliferation, and growth of lymphocytes. Such innate and adaptive responses can act as mediator of arthritis; along with this, stimulation of osteoclast-mediated bone resorption takes place via transferring citrullinated peptides towards MHC (major histocompatibility complex) compartments, thereby resulting in degradation of bone. Processes such as apoptosis resistance are also regulated through autophagy. In this review, the current knowledge based on role of autophagy in pathogenesis of rheumatoid arthritis is summarized along with proteins associated.en_US
dc.language.isoenen_US
dc.publisherInflammationen_US
dc.subjectAuto-immuneen_US
dc.subjectautophagyen_US
dc.subjectimmune responseen_US
dc.subjectrheumatoid arthritis.en_US
dc.titleFocus on the Multimodal Role of Autophagy in Rheumatoid Arthritisen_US
dc.typeArticleen_US
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