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SLE Pathogenesis: From Apoptosis to Lymphocyte Activation

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Connective Tissue Disease

Part of the book series: Rare Diseases of the Immune System ((RDIS))

Abstract

Systemic lupus erythematosus (SLE) is considered a typical protean systemic autoimmune disease. It is characterized by multiorgan and multisystem involvement. Virtually, SLE may affect almost any organ during the disease course. Several pathogenic pathways have been reported to sustain inflammation in affected tissues in patients with SLE. Recently, the apoptotic process was thoroughly investigated. The link between apoptotic debris containing autoantigens and innate immunity activation has been also further elucidated. Indeed, as far as the role of lymphocytes in SLE pathogenesis is concerned, the “T-lymphocyte centric” SLE hypothesis has recently been counterbalanced with a newer “B-lymphocyte centric” theory, which was mainly supported by the emerging data arising from B-cell target therapy studies. In this chapter we provide an overview of both the traditional and the more recently discovered immunological pathways that drive inflammation and contribute to organ damage in SLE.

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Correspondence to Lorenzo Emmi .

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Squatrito, D., Emmi, G., Silvestri, E., Prisco, D., Emmi, L. (2016). SLE Pathogenesis: From Apoptosis to Lymphocyte Activation. In: Roccatello, D., Emmi, L. (eds) Connective Tissue Disease. Rare Diseases of the Immune System. Springer, Cham. https://doi.org/10.1007/978-3-319-24535-5_3

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  • DOI: https://doi.org/10.1007/978-3-319-24535-5_3

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