Fig. 5: Adipose tissue activation is associated with T cell mediated neuroinflammation in experimental model of multiple sclerosis.

a The cuprizone and EAE model involves treatment with cuprizone for 3 weeks followed by MOG immunization at week 5. Mice were imaged with [¹⁸F]F-AraG at baseline, at week 3 (lesions driven by innate immune cells) and at week 7 (lesions with T cell involvement). b Activation of BAT (white arrowhead) was observed only in mice with brain lesions with T cell involvement (yellow arrowhead). Mice treated with fingolimod, a drug that prevents intracerebral lymphocyte infiltration, did not show activation of BAT. Upper panels show sagittal slices, bottom panels show transverse slices with iBAT (white arrowhead). c [¹⁸F]F-AraG signal in the iBAT of CPZ-EAE mice was significantly higher than the baseline (p = 0.01), cuprizone treated mice (p = 0.005) and CPZ-EAE mice treated with fingolimod (p = 0.001). d Immunofluorescent CD3 staining confirmed presence of T lymphocytes in the corpus callosum. e CPZ-EAE mice showed high [¹⁸F]F-AraG signal in the bone marrow of the lumbar vertebrae (upper panel, white arrowhead) and proximal tibia and femur (bottom panel, yellow arrowheads). f [¹⁸F]F-AraG signal detected in the iBAT showed correlation with the signal observed in the brain. g [¹⁸F]F-AraG signal in the lumbar vertebrae strongly correlated with the signal in the brain. Data are shown as mean ± SD. (n = 10 for baseline, W7 CPZ-EAE and W7 CPZ-EAE + fingolimod, n = 5 for W3 CPZ) Each spot represents an individual animal. *p ≤ 0.05, **p ≤ 0.01.