Fig. 1

IL-1β expression in brain tissue of rhesus macaques with EAE induced by rhMOG in IFA. Brain lesions were characterized based on the extent of myelin (PLP in brown, left panels) damage and activation of innate immune cells (MHC class II in brown, middle panels). In small perivascular lesions without signs of demyelination (a), IL-1β staining (in brown, right panels) was mainly localized in MHC class II⁺ cells at the edge of the lesion. In mid-sized MHC class II⁺ lesions with clear signs of demyelination (b), IL-1β staining was more pronounced. In large fulminating lesions with extensive demyelination and infiltration of MHC class II⁺ cells (c), IL-1β staining was less pronounced compared to the mid-sized lesions and observed at the edge of the demyelinated area. Double labeling of perivascular lesions for IL-1β (in green) and Iba-1 or MRP14 (in red) demonstrated that all IL-1β⁺ cells were Iba-1⁺ (d), whereas all IL-1β⁺ cells were MRP14⁻ or MRP14^low (e). Original magnifications ×10, scale bar represents 200 μm, insets ×100. Nuclei were counterstained with hematoxylin (blue)