Objective: Patients with systemic lupus erythematosus (SLE) often develop multi-organ damages including heart and kidney complications. We sought to better define the underlying mechanisms with a focus on the chemokine receptor CXCR1.
Methods: We generated Cx3cr1-deficient MRL/lpr lupus-prone mice through backcrossing.
NLRP12 has dual roles in shaping inflammation. We hypothesized that NLRP12 would modulate myeloid cells and T cell function to control systemic autoimmunity. Contrary to our hypothesis, the deficiency of in autoimmune-prone B6.
View Article and Find Full Text PDFPhys Rev B Condens Matter
September 1996