Antibodies against Pentraxins and Lupus Nephritis Activity
|Katarzyna Jakuszko*, Magdalena Krajewska and Marian Klinger|
|Department of Nephrology and Transplantation Medicine, Wroclaw Medical University, Poland|
|Corresponding Author :||Katarzyna Jakuszko
Department of Nephrology and Transplantation Medicine
Wroclaw Medical University, Borowska 213, 50-556 Wroclaw, Poland
E-mail: [email protected]
|Received: April 08, 2014; Accepted: August 06, 2014; Published: August 13, 2014|
|Citation: Jakuszko K, Krajewska M, Klinger M (2014) Antibodies against Pentraxins and Lupus Nephritis Activity. J Clin Cell Immunol 5:246. doi:10.4172/2155-9899.1000246|
|Copyright: © 2014 Jakuszko K, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.|
|Related article at
Pubmed Scholar Google
Impaired apoptosis and dysfunction of the immune cells are considered to be the most important pathogenic mechanisms of systemic lupus erythematosus. Pentraxins, which are natural opsonins, are directly involved in the removal of cellular material by binding to different antigens and initiating and enhancing phagocytosis of damaged cells. Therefore the deficiency of pentraxins is a crucial risk factor for the development and progression of systemic lupus erythematosus.
Despite the presence of elevated levels of interleukin-6, which under physiological conditions increases the expression of acute phase protein genes, in systemic lupus a deficiency of C reactive protein and other pentraxins is observed. Several mechanisms responsible for pentraxin deficiency have been postulated, including the impairment of pentraxin synthesis due to mutations in genes, gene inhibition by interferon-α, and removal of pentraxins by autoantibodies.
In this review, we summarize the significance of antibodies directed against pentraxins in assessing the activity and severity of systemic lupus erythematosus and lupus nephritis, as well as the usefulness of these antibodies as an additional marker of the response to treatment. The role of antibodies directed against monomeric C reactive protein in the pathogenesis of lupus nephritis is also discussed, as these antibodies are considered as a factor causing damage to the glomerular cells.