TY - JOUR
T1 - Type I interferons have no major influence on humoral autoimmunity in rheumatoid arthritis
AU - Cantaert, Tineke
AU - van Baarsen, Lisa G.
AU - Wijbrandts, Carla A.
AU - Thurlings, Rogier M.
AU - van de Sande, Marleen G.
AU - Bos, Carina
AU - Kraan van der Pouw, Tineke
AU - Verweij, Cor L.
AU - Tak, Paul P.
AU - Baeten, Dominique L.
PY - 2010
Y1 - 2010
N2 - Objective. Type I IFNs have recently been implicated in autoantibody-mediated diseases such as SLE. As half the RA patients display a type I IFN high signature, we investigated in a pilot study if type I IFN determines the autoantibody response in RA. Methods. Serum and peripheral blood cells were obtained from 52 RA patients, with paired samples before and after infliximab treatment in 21 patients. Additional samples were collected from 8 anti-citrullinated protein antibody (ACPA)-positive individuals without arthritis and from 10 ACPA-negative healthy controls. The type I IFN signature was determined by peripheral blood cell gene expression analysis and quantitative RT-PCR. ACPA IgG and IgM, RF IgM, anti-nucleosome IgM and anti-dsDNA were measured by ELISA. Results. The type I IFN signature was not related to the presence and titers of ACPA and RF during active disease. TNF blockade induced a similar rise of ANAs, and a similar decrease in RF titers in both groups. ACPA IgG and IgM levels appeared to be down-modulated only in the type I IFN low group. These changes were independent of the changes in type I IFN response gene activity after TNF blockade. Furthermore, the ACPA response in individuals without arthritis and inflammation was not related to an increase of type I IFN. Conclusions. In this explorative study, type I IFN signature does not appear to have a major impact on the humoral autoimmune response in RA. Replication of these data remains warranted
AB - Objective. Type I IFNs have recently been implicated in autoantibody-mediated diseases such as SLE. As half the RA patients display a type I IFN high signature, we investigated in a pilot study if type I IFN determines the autoantibody response in RA. Methods. Serum and peripheral blood cells were obtained from 52 RA patients, with paired samples before and after infliximab treatment in 21 patients. Additional samples were collected from 8 anti-citrullinated protein antibody (ACPA)-positive individuals without arthritis and from 10 ACPA-negative healthy controls. The type I IFN signature was determined by peripheral blood cell gene expression analysis and quantitative RT-PCR. ACPA IgG and IgM, RF IgM, anti-nucleosome IgM and anti-dsDNA were measured by ELISA. Results. The type I IFN signature was not related to the presence and titers of ACPA and RF during active disease. TNF blockade induced a similar rise of ANAs, and a similar decrease in RF titers in both groups. ACPA IgG and IgM levels appeared to be down-modulated only in the type I IFN low group. These changes were independent of the changes in type I IFN response gene activity after TNF blockade. Furthermore, the ACPA response in individuals without arthritis and inflammation was not related to an increase of type I IFN. Conclusions. In this explorative study, type I IFN signature does not appear to have a major impact on the humoral autoimmune response in RA. Replication of these data remains warranted
U2 - https://doi.org/10.1093/rheumatology/kep345
DO - https://doi.org/10.1093/rheumatology/kep345
M3 - Article
C2 - 19933783
SN - 1462-0324
VL - 49
SP - 156
EP - 166
JO - Rheumatology (Oxford, England)
JF - Rheumatology (Oxford, England)
IS - 1
ER -