Integrating p38α MAPK immune signals in nonimmune cells.
A study by Huang et al. in this issue of Science Signaling highlights key roles for the mitogen-activated protein kinase p38α and the phosphatase MK1 in mediating interleukin-17-dependent pathology in experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis.
Division of Rheumatology and Clinical Immunology, University of Pittsburgh, Pittsburgh, PA 15261, USA. sarah.gaffen@pitt.edu.
Sarah L
SL
Gaffen
Division of Rheumatology and Clinical Immunology, University of Pittsburgh, Pittsburgh, PA 15261, USA.
Mandy J
MJ
McGeachy
D000818:Animals; D054638:Dual Specificity Phosphatase 1 / Q000276:immunology*; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology*; D006801:Humans; D020935:MAP Kinase Signaling System / Q000276:immunology*; D048308:Mitogen-Activated Protein Kinase 14 / Q000276:immunology*; D009103:Multiple Sclerosis / Q000276:immunology*; D053722:Receptors, Interleukin-17 / Q000276:immunology*
D053722:Receptors, Interleukin-17; D048308:Mitogen-Activated Protein Kinase 14; D054638:Dual Specificity Phosphatase 1