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Antibody-induced arthritis: disease mechanisms and genes involved at the effector phase of arthritis.

Nandakumar, Kutty and Holmdahl, Rikard LU (2006) In Arthritis Research and Therapy 8(6). p.223-223
Abstract
During the development of rheumatoid arthritis (RA) autoantibodies to IgG-Fc, citrullinated proteins, collagen type II (CII), glucose 6 phosphoisomerase (G6PI) and some other self-antigens appear. Of these, a pathogenic effect of the anti-CII and anti-G6PI antibodies is well demonstrated using animal models. These new antibody mediated arthritis models have proven to be very useful for studies involved in understanding the molecular pathways of the induction of arthritis in joints. Both the complement and Fc(gamma)R systems have been found to play essential roles. Neutrophils and macrophages are important inflammatory cells and the secretion of tumour necrosis factor-alpha and IL-1 beta is pathogenic. The identification of the genetic... (More)
During the development of rheumatoid arthritis (RA) autoantibodies to IgG-Fc, citrullinated proteins, collagen type II (CII), glucose 6 phosphoisomerase (G6PI) and some other self-antigens appear. Of these, a pathogenic effect of the anti-CII and anti-G6PI antibodies is well demonstrated using animal models. These new antibody mediated arthritis models have proven to be very useful for studies involved in understanding the molecular pathways of the induction of arthritis in joints. Both the complement and Fc(gamma)R systems have been found to play essential roles. Neutrophils and macrophages are important inflammatory cells and the secretion of tumour necrosis factor-alpha and IL-1 beta is pathogenic. The identification of the genetic polymorphisms predisposing to arthritis is important for understanding the complexity of arthritis. Disease mechanisms and gene regions studied using the two antibody-induced arthritis mouse models (collagen antibody-induced arthritis and serum transfer-induced arthritis) are compared and discussed for their relevance in RA pathogenesis. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Arthritis Research and Therapy
volume
8
issue
6
pages
223 - 223
publisher
BioMed Central (BMC)
external identifiers
  • wos:000244927900004
  • scopus:84884236003
  • pmid:17254316
ISSN
1478-6362
DOI
10.1186/ar2089
language
English
LU publication?
yes
additional info
The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Department of Experimental Medical Science (013210000), Medical Inflammation Research (013212019)
id
c62a1a95-0e40-430b-9b5b-5c978f8330a0 (old id 164651)
date added to LUP
2016-04-01 12:11:51
date last changed
2021-08-18 01:47:31
@article{c62a1a95-0e40-430b-9b5b-5c978f8330a0,
  abstract     = {During the development of rheumatoid arthritis (RA) autoantibodies to IgG-Fc, citrullinated proteins, collagen type II (CII), glucose 6 phosphoisomerase (G6PI) and some other self-antigens appear. Of these, a pathogenic effect of the anti-CII and anti-G6PI antibodies is well demonstrated using animal models. These new antibody mediated arthritis models have proven to be very useful for studies involved in understanding the molecular pathways of the induction of arthritis in joints. Both the complement and Fc(gamma)R systems have been found to play essential roles. Neutrophils and macrophages are important inflammatory cells and the secretion of tumour necrosis factor-alpha and IL-1 beta is pathogenic. The identification of the genetic polymorphisms predisposing to arthritis is important for understanding the complexity of arthritis. Disease mechanisms and gene regions studied using the two antibody-induced arthritis mouse models (collagen antibody-induced arthritis and serum transfer-induced arthritis) are compared and discussed for their relevance in RA pathogenesis.},
  author       = {Nandakumar, Kutty and Holmdahl, Rikard},
  issn         = {1478-6362},
  language     = {eng},
  number       = {6},
  pages        = {223--223},
  publisher    = {BioMed Central (BMC)},
  series       = {Arthritis Research and Therapy},
  title        = {Antibody-induced arthritis: disease mechanisms and genes involved at the effector phase of arthritis.},
  url          = {https://lup.lub.lu.se/search/ws/files/2822862/625839.pdf},
  doi          = {10.1186/ar2089},
  volume       = {8},
  year         = {2006},
}