Role of SOCS2 in the Regulation of Immune Response and Development of the Experimental Autoimmune Encephalomyelitis

Figure 3

SOCS2 modulates inflammation in the CNS during EAE. Histology of brain (brainstem) and spinal cord sections from WT and SOCS2-deficient animals. Control mice with normal histological appearance. Brain, 14 days: EAE induced WT mice showing a locally extensive and intense infiltration of mononuclear cells (asterisk). EAE induced SOCS2^-/- mice with moderate perivascular inflammation (asterisk). Spinal cord, 14 days: EAE induced WT mice showing intense myelitis characterized by infiltration of mononuclear cells (asterisk). EAE induced SOCS2^-/- mice with mild to moderate myelitis (asterisk). Spinal cord at 28 days: EAE induced WT mice exhibiting mild to moderate meningomyelitis and EAE induced SOCS2^-/- mice showing locally extensive and intense meningomyelitis and demyelization (asterisks). Brain at 28 days: EAE induced WT mice exhibiting moderate encephalitis and induced SOCS2^-/- mice showing intense inflammatory infiltration (asterisks). Original magnification: ×200 ( animals per group). Data are representative of three independent experiments.