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Could antibodies against Serum Amyloid A function as physiological regulators in humans?

Authors :
Lakota, Katja
Thallinger, Gerhard G.
Cucnik, Sasa
Bozic, Borut
Mrak-Poljsak, Katjusa
Ambrozic, Ales
Rozman, Blaž
Blinc, Ales
Tomsic, Matija
Sodin-Semrl, Snezna
Source :
Autoimmunity; Mar2011, Vol. 44 Issue 2, p149-158, 10p
Publication Year :
2011

Abstract

The natural structuring of the immune system is responsible for the functional physiological state of the body. The development of natural autoantibodies involved in homeostasis relies on the ability to distinguish between exposed/masked and altered/non-altered self antigens. The objectives of this article were to address the relationships between antigen and autoantibodies against serum amyloid A (SAA), define SAA protein concentrations in 219 blood donor (BD) sera and determine their autoantibody levels and search for possible clinical associations with autoimmune and thrombotic diseases. Just recently, an increasing number of reports have indicated significantly decreased levels of autoantibodies against pro-inflammatory molecules, such as anti-TNF-alpha, anti-IL-6, or anti-CRP found in diseased conditions, as compared to healthy donors, or even to less severe disease conditions. In accord with this line of thought, our data indicate a predominant presence of anti-SAA autoantibodies in healthy BDs (above 95% as tested by the immunoblot analysis, n  ==  41). Using ELISA, high levels of anti-SAA antibodies were confirmed with a median OD  ==  0.996 for the BD group ( n  ==  219). This suggests that anti-SAA antibodies might have a physiological role in homeostasis and/or the innate immune system and could actually be a part of the natural antibody repertoire. Significantly, lower median levels were found in patients with arterial thrombosis. Based on 219 BD sera, we could establish a new median value of 20  μμg/ml for SAA antigen and a cut-off value of 114.7  μμg/ml (97.5th percentile). Significantly, higher concentrations of SAA were observed for antiphospholipid syndrome, rheumatoid arthritic, and SLE patients. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
08916934
Volume :
44
Issue :
2
Database :
Complementary Index
Journal :
Autoimmunity
Publication Type :
Academic Journal
Accession number :
57656395
Full Text :
https://doi.org/10.3109/08916934.2010.487504