Vasculitis is an inflammatory disease affecting blood vessels with an autoimmunological origin. Autoimmunity is an immune reaction against the organism’s own components produced by the existence of autoreacting clones which have not been destroyed during immuno-system maturation. Antibodies produced by this clones react against autoantigens. Some of these antibodies react against components of the blood vessel walls. These reactions produce damage in the vessel walls producing vasculitis. The clinical manifestations of vasculitis depend on the organ in which vessels are affected. The more commonly affected organs are lung and kidney. In the present work we have studied the immunoreactivity of the serum of a patient under no treatment, suffering from a vasculitis characterized by focal necrotizing glomerulonephritis with no immune deposits. We identified proteins that previously were unknown as autoantigens and that could be involved in the pathophysiology of this vasculitis.

With the immunoscreening method SEREX (serological identification of antigens by recombinant expression cloning), the patient’s serum was used as a probe to screen a brain cDNA expression library. Five positive clones were found and four of these were purified and sequenced. By comparing the sequences with those in the databases by Blast we found that two clones were cDNA sequences with no counterpart in the databases. The other two clones encoded proteins of known functions but which are unknown as autoantigens. These proteins are jos 302 (HDAC5), jos 304 (TFC4), jos 307 and jos 313. The recombinant proteins of the four clones were probed as antigens by Western blot with different sera from patients affected with known vasculitis (i.e. LES) as well as sera from controls. Only the serum from the patient origin of this study recognized the recombinant proteins.

Although we cannot determine the role of these proteins in the aetiopathology of this disease at this point, the results suggests that they could be used as markers in the diagnosis of subfamilies in immune diseases.