Pathogenesis of systemic lupus erythematosus (SLE)

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Presentation transcript:

Pathogenesis of systemic lupus erythematosus (SLE) Pathogenesis of systemic lupus erythematosus (SLE). Environmental factors, such as infectious organisms, drugs, and chemicals, serve as triggering agents in genetically and hormonally susceptible individuals to induce a state of immune dysregulation. These abnormal immune responses lead to hyperactive T-helper type 2 lymphocyte and B-lymphocyte function. Suppressor T-lymphocyte function, cytokine production, faulty clearance mechanisms, and other immune regulatory mechanisms also are abnormal and fail to downregulate autoantibody formation from hyperactive B lymphocytes. The autoantibodies formed from this immune dysregulation become pathogenic, form immune complexes, and activate complement that leads to damage of host tissue. (APCs, antigen-presenting cells; TH2, T-helper type 2.) Source: Chapter 96. Systemic Lupus Erythematosus and Other Collagen-Vascular Diseases, Pharmacotherapy: A Pathophysiologic Approach, 8e Citation: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey L. Pharmacotherapy: A Pathophysiologic Approach, 8e; 2011 Available at: http://accesspharmacy.mhmedical.com/DownloadImage.aspx?image=/data/books/dipi8/dipi8_c096f001.gif&sec=41126449&BookID=462&ChapterSecID=41100875&imagename= Accessed: November 13, 2017 Copyright © 2017 McGraw-Hill Education. All rights reserved