title: Subclass distribution of IgA and IgG antibodies against Clq in patients with rheumatic diseases.
abstract: To obtain insight into the immunoregulatory mechanisms in patients with different rheumatic diseases, the occurrence and the subclass distribution of IgA and IgG antibodies against Clq (anti-ClqAb) was determined. In patients with systemic lupus erythaematosus (SLE) the highest frequency of increased serum levels of IgG anti-ClqAb were found, whereas IgA anti-ClqAb were predominantly present in patients with ankylosing spondylitis (AS) and patients with rheumatoid arthritis complicated by vasculitis (RV). In all the IgA anti-ClqAb positive AS and RV patients the antibody reactivity involved the IgA1 subclass while the IgA2 subclass was found in 47% of the patients. Further characterization of the IgA anti-Clq binding activity in sera of AS patients revealed that both subclasses of IgA anti-ClqAb were predominantly polymeric; the binding of both IgA subclasses with solid phase Clq was inhibitable by aggregated fluid phase Clq; we found no detectable interference of rheumatoid factor in the test system for the measurement of IgA anti-ClqAb. In patients with SLE the IgG anti-ClqAb reactivity was mainly of the IgG2 and IgG3 subclass, whereas in the same patients the IgG anti-tetanus toxoid response was not restricted to these subclasses. The predominance of IgG2 and IgG3 subclass of anti-ClqAb in sera of SLE patients, suggests a skewing of the anti-ClqAb response. The observation that the IgA anti-ClqAb of both subclasses is predominantly polymeric in nature and the notion that polymeric IgA is associated with activation of inflammation cascades, suggests that IgA anti-ClqAb may contribute to tissue damage.
authors.affiliation: Department of Rheumatology, University Hospital Leiden, The Netherlands.
authors.forename: I E
authors.initials: IE
authors.lastname: Coremans
authors.forename: M R
authors.initials: MR
authors.lastname: Daha
authors.forename: E A
authors.initials: EA
authors.lastname: van der Voort
authors.forename: C E
authors.initials: CE
authors.lastname: Siegert
authors.forename: F C
authors.initials: FC
authors.lastname: Breedveld
mesh_terms: D000911:Antibodies, Monoclonal; D002850:Chromatography, Gel; D015922:Complement C1q / Q000276:immunology*; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D007070:Immunoglobulin A / Q000032:analysis / Q000145:classification*; D007074:Immunoglobulin G / Q000032:analysis / Q000145:classification*; D007132:Immunoglobulin Isotypes / Q000032:analysis*; D012216:Rheumatic Diseases / Q000276:immunology*
chemical_list: D000911:Antibodies, Monoclonal; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D007132:Immunoglobulin Isotypes; D015922:Complement C1q