Experimental autoimmune encephalomyelitis (EAE) is an animal model commonly used to investigate the inflammatory response in organ-specific autoimmunity and a model of the early immune responses of multiple sclerosis.
This protocol outlines the methods used for the processing of peripheral immune tissues, the spleen and draining lymph nodes, as well as the site of inflammation, the central nervous system (CNS), for analyzing immune cell phenotype and function during murine EAE.
This is a preview of subscription content, log in to check access.
Springer Nature is developing a new tool to find and evaluate Protocols. Learn more
Work in the authors’ laboratory was supported by grants from the UK Medical Research Council and the Wellcome Trust.
McGeachy MJ, Stephens LA et al (2005) Natural recovery and protection from autoimmune encephalomyelitis: contribution of CD4+ CD25+ regulatory cells within the central nervous system. J Immunol 175(5):3025–3032PubMedCrossRefGoogle Scholar
Mildner A, Mack M et al (2009) CCR2+ Ly-6Chi monocytes are crucial for the effector phase of autoimmunity in the central nervous system. Brain 132(Pt 9):2487–2500PubMedCrossRefGoogle Scholar
Vainchtein ID, Vinet J et al (2014) In acute experimental autoimmune encephalomyelitis, infiltrating macrophages are immune activated, whereas microglia remain immune suppressed. Glia 62:1724–1735. doi:10.1002/glia.22711PubMedCrossRefGoogle Scholar
Gautier EL, Shay T et al (2012) Gene-expression profiles and transcriptional regulatory pathways that underlie the identity and diversity of mouse tissue macrophages. Nat Immunol 13(11):1118–1128PubMedCentralPubMedCrossRefGoogle Scholar
King IL, Dickendesher TL et al (2009) Circulating Ly-6C+ myeloid precursors migrate to the CNS and play a pathogenic role during autoimmune demyelinating disease. Blood 113(14):3190–3197PubMedCentralPubMedCrossRefGoogle Scholar
Drutman SB, Kendall JC et al (2012) Inflammatory spleen monocytes can upregulate CD11c expression without converting into dendritic cells. J Immunol 188(8):3603–3610PubMedCrossRefGoogle Scholar