Deletion of IL-4Rα in the BALB/c mouse is associated with altered lesion topography and susceptibility to experimental autoimmune encephalomyelitis.

Deletion of IL-4Rα in the BALB/c mouse is associated with altered lesion topography and susceptibility to experimental autoimmune encephalomyelitis. Autoimmunity. 2015 Jun;48(4):208-21 Authors: Orian JM, Keating P, Downs LL, Hale MW, Jiang X, Pham H, LaFlamme AC Abstract The regulation of cytokine expression by immune deviation from a pro-inflammatory to anti-inflammatory or "regulatory" milieu is crucial to the prevention of permanent central nervous system (CNS) damage in neuroinflammation. Earlier studies in the murine experimental autoimmune encephalomyelitis (EAE) model pointed to an anti-inflammatory role for the Th2 cytokine, IL-4, which was not confirmed in IL-4Rα-deficient mice (IL-4Rα(-/-)). To examine the pathological consequences of loss of responsiveness to Th2 cytokines, we compared lesion evolution in IL-4Rα(-/-) and wild type (WT) BALB/c mice immunized with PLP180-199 and investigated how altering the magnitude of the antigen-specific autoimmune response in this model affected the pathology. We found that while changing the magnitude of the peripheral antigen-specific response differentially affected the incidence of clinical disease in WT BALB/c relative to IL-4Rα(-/-) mice, the differences in incidence did not correlate to differences in pro-inflammatory cytokine production. Additionally, although only approximately 75% of WT mice developed clinical disease, lesions were observed in 100% of the mice, principall...
Source: Autoimmunity - Category: Allergy & Immunology Tags: Autoimmunity Source Type: research