Abstract: The present invention relates to an apheresis column loaded with a solid support comprising a composition comprising at least one peptide selected from the group consisting of: —the ?I7I-I85cit peptide of amino acid sequence VDIDIKIX1SCX2GSCS (SEQ ID NO: 8) wherein X1 and X2 each represent a citmllyl residue, —the ?62I-635Cit peptide of amino acid sequence X1GHAKSX2PVX3GIHTS (SEQ ID NO: 12) wherein X1, X2 and X3 each represent a citmllyl residue—the P60-74cit-NH2 peptide of amino acid sequence X1PAPPPISGGGYX2AX3 (SEQ ID NO: 15) wherein X1 and X2 each represent a citmllyl residue and X3 represents a citmllyl derivative with a carboxamide group and—the peptide, referred to as the Ac-a36-50crt peptide, having the amino acid sequence GPX1VVEX2HQSACKDS (SEQ ID NO: 6) wherein the residue G at the N-terminal is acetylated and wherein X1 and X2 each represent a citmllyl residue and/or the a36-50cit peptide of amino acid sequence GPX1VVEX2HQSACKDS (SEQ ID NO: 5) wherein X1 and X2 each represent a citmllyl residue.

Abstract: The present invention relates to field of treatment of rheumatoid arthritis. The inventors propose that PAD4, one of the enzymes which convert arginine into citrulline, is a target antigen for T cells that help the production of ACPA. They recently demonstrated that PAD immunization triggers anti-citrullinated fibrinogen antibody production in normal mice. Here, they demonstrate that the risk (OR) to develop RA associated with each of 12 HLA-DRB1 genotype correlates with the likelihood for the two HLA-DR molecules encoded by each genotype to bind at least one random peptide from PAD4, but not from citrullinated or native fibrinogen. PBLs from patients with RA, PsA and controls proliferate to PAD4 and they identify, notably, a peptide from PAD4, p8 (SEQ ID NO: 6), that stimulates T cells from RA patients and a few patients with PsA. Proliferative responses to p8 are associated with RA, shared epitope positive HLA-DR alleles and antibodies to PAD4.