Background and objectives Rheumatoid arthritis is a chronic autoimmune disease with a prevalence of 1%. The pathomechanism of the disease is not completely understood. Previous studies from our laboratory showed that phospholipase Cγ2 (PLCγ2) is a critical player of the effector phase of the autoantibody-mediated K/BxN serum transfer arthritis model. Prior studies also showed that myeloid cells such as neutrophils and macrophages are essential for arthritis development in this model. The aim of our experiments was to investigate the role of PLCγ2 expression within myeloid cells during K/BxN serum transfer arthritis.

Materials and methods Lineage-specific deletion of PLCγ2 was achieved by crossing LysM and MRP8 promoter-driven Cre recombinase (LysM^Cre/Cre and MRP8^Cre/Cre) transgenic mice with PLCγ2^flox/flox animals. PLCγ2 expression in bone marrow neutrophils and bone marrow-derived macrophages was tested by Western blot. Mice were injected with arithrogenic (K/BxN) or control serum intraperitoneally. The development of arthritis was assessed by clinical scoring of the visible signs of the inflammation, measuring ankle thickness and testing articular function by a hanging test.

Results As expected, LysM promoter-driven Cre recombinase deleted PLCγ2 from both neutrophils and macrophages whereas MRP8 promoter-driven Cre recombinase deleted PLCγ2 from neutrophils but not macrophages. Although wild type mice injected with arithrogenic serum develop severe arthritis, no sings of the disease was assessed in similarly treated LysM^Cre/CrePLCγ2^flox/floxanimals. MRP8^Cre/CrePLCγ2^flox/flox mice were also almost completely protected from arthritis development.

Conclusions Our results indicate that the expression of PLCγ2 in myeloid cells and in particular neutrophils indispensable for the development of autoantibody-induced arthritis in experimental mice.