Complement in Lupus Nephritis: New Perspectives
Author(s) -
Lihua Bao,
Patrick N. Cunningham,
Richard J. Quigg
Publication year - 2015
Publication title -
kidney diseases
Language(s) - English
Resource type - Journals
eISSN - 2296-9381
pISSN - 2296-9357
DOI - 10.1159/000431278
Subject(s) - complement system , immunology , lupus nephritis , decay accelerating factor , classical complement pathway , alternative complement pathway , pathogenesis , complement factor b , complement deficiency , immune complex , systemic lupus erythematosus , complement receptor , immune system , eculizumab , nephritis , complement factor i , complement component 5 , biology , medicine , disease , pathology
Systemic lupus erythematosus (SLE) is an autoimmune disorder caused by loss of tolerance to self-antigens, the production of autoantibodies and deposition of complement-fixing immune complexes (ICs) in injured tissues. SLE is characterized by a wide range of clinical manifestations and targeted organs, with lupus nephritis being one of the most serious complications. The complement system consists of three pathways and is tightly controlled by a set of regulatory proteins to prevent injudicious complement activation on host tissue. The involvement of the complement system in the pathogenesis of SLE is well accepted; yet, its exact role is still not clear.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom