MULTIREACTIVE PATTERN OF SERUM AUTOANTIBODIES IN ASYMPTOMATIC INDIVIDUALS WITH IMMUNOGLOBULIN-A DEFICIENCY

Citation
N. Barka et al., MULTIREACTIVE PATTERN OF SERUM AUTOANTIBODIES IN ASYMPTOMATIC INDIVIDUALS WITH IMMUNOGLOBULIN-A DEFICIENCY, Clinical and diagnostic laboratory immunology, 2(4), 1995, pp. 469-472
Citations number
60
Categorie Soggetti
Immunology,"Infectious Diseases","Medical Laboratory Technology",Microbiology
ISSN journal
1071412X
Volume
2
Issue
4
Year of publication
1995
Pages
469 - 472
Database
ISI
SICI code
1071-412X(1995)2:4<469:MPOSAI>2.0.ZU;2-S
Abstract
Selective immunoglobulin A (IgA) deficiency (sIgAD) is associated with certain autoimmune states. Increased production of autoantibodies and eventual development of overt autoimmune disease are related in part to genetic and environmental factors as well as to the immune deficien cy. We Surveyed serum specimens from 60 healthy subjects with sIgAD fo r the presence of 21 different autoantibodies by enzyme-linked immunos orbent assays. The frequencies of 16 autoantibodies were higher in slg AD patients than in normal healthy controls. Autoantibodies to Jo-1 (2 8%), cardiolipin (21%), phosphatidylserine (20%), Sm (15%), asialo-GM( 1) (21%), sulfatide (32%), Sulfoglucuronyl paragloboside (11%), and co llagen type I (10%) were detected at high frequencies in comparison to those of normal healthy controls, Many of the serum samples were mult ireactive (i.e., exhibited binding to more than two autoantigens). For ty percent (24 of 60) of sIgAD serum samples reacted against six or mo re autoantigens; 10% (6 of 60) of sIgAD serum samples were not reactiv e with any of the 21 autoantigens. Three percent (7 of 209) of consecu tive serum samples submitted for autoimmune antibody analysis that wer e positive for autoantibodies were from patients with. IgA deficiency. Our finding of an increased frequency of autoantibodies in sIgAD pati ents supports the notion of polyclonal stimulation by repeated environ mental stimuli as an etiologic mechanism. Alternatively, the increased frequency may be caused by a dysregulation of the immune response in such individuals. The mere detection of autoantibodies cannot predict whether a subject with sIgAD will develop an autoimmune disease or det ermine which specific disease will emerge.