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The complement systemin systemic lupus erythematosus

Sturfelt, Gunnar LU (2002) In Scandinavian Journal of Rheumatology 31(3). p.129-132
Abstract
The etiology of SLE is multifactorial with an important genetic impact. Several genes involved in control of autoimmunity and inflammation appear to be important. Hereditary complement deficiency states are associated with increased risk of SLE, but contribute only marginally to the incidence of SLE in the population. However, these conditions have contributed considerably to the knowledge of pathogenetic mechanisms in this disease. Furthermore, acquired complement deficiency is a common finding in SLE. Complement has important protective functions but also contributes to tissue damage. Measurement of classical pathway complement components is important in the diagnosis of SLE and for monitoring of immune complex mediated manifestations,... (More)
The etiology of SLE is multifactorial with an important genetic impact. Several genes involved in control of autoimmunity and inflammation appear to be important. Hereditary complement deficiency states are associated with increased risk of SLE, but contribute only marginally to the incidence of SLE in the population. However, these conditions have contributed considerably to the knowledge of pathogenetic mechanisms in this disease. Furthermore, acquired complement deficiency is a common finding in SLE. Complement has important protective functions but also contributes to tissue damage. Measurement of classical pathway complement components is important in the diagnosis of SLE and for monitoring of immune complex mediated manifestations, especially proliferative glomerulonephritis. New complement activation tests, although promising in studies of selected patient groups, have not yet been proven to be of clinical value. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
complement, SLE, apoptosis
in
Scandinavian Journal of Rheumatology
volume
31
issue
3
pages
129 - 132
publisher
Taylor & Francis
external identifiers
  • wos:000176902300002
  • pmid:12195625
  • scopus:0036292073
ISSN
1502-7732
DOI
10.1080/rhe.31.3.129.132
language
English
LU publication?
yes
id
be176ec6-a825-410a-8baa-c0b3135074e2 (old id 332889)
date added to LUP
2007-11-14 15:01:26
date last changed
2017-01-01 04:30:08
@article{be176ec6-a825-410a-8baa-c0b3135074e2,
  abstract     = {The etiology of SLE is multifactorial with an important genetic impact. Several genes involved in control of autoimmunity and inflammation appear to be important. Hereditary complement deficiency states are associated with increased risk of SLE, but contribute only marginally to the incidence of SLE in the population. However, these conditions have contributed considerably to the knowledge of pathogenetic mechanisms in this disease. Furthermore, acquired complement deficiency is a common finding in SLE. Complement has important protective functions but also contributes to tissue damage. Measurement of classical pathway complement components is important in the diagnosis of SLE and for monitoring of immune complex mediated manifestations, especially proliferative glomerulonephritis. New complement activation tests, although promising in studies of selected patient groups, have not yet been proven to be of clinical value.},
  author       = {Sturfelt, Gunnar},
  issn         = {1502-7732},
  keyword      = {complement,SLE,apoptosis},
  language     = {eng},
  number       = {3},
  pages        = {129--132},
  publisher    = {Taylor & Francis},
  series       = {Scandinavian Journal of Rheumatology},
  title        = {The complement systemin systemic lupus erythematosus},
  url          = {http://dx.doi.org/10.1080/rhe.31.3.129.132},
  volume       = {31},
  year         = {2002},
}