A–J, In the absence of TGFβ1 (tgfβ1−/−), microglia proliferate (compare A, B) and express a panel of late-activation markers [MHC1 (C, D), αXβ2 (E, F), and B7.2 (I, J)] throughout the affected CNS, a response not observed in the uninjured, normal brain (tgfβ1+/+). A, B, Microglial proliferation in the cerebellar peduncle, double labeling using autoradiography for tritiated thymidine and immunoreactivity for αMβ2 integrin (3HT/αMβ2). C–J, Double immunofluorescence, with IBA1 in red. A subpopulation of activated microglia showed strong immunoreactivity for MHC1 (normal facial motor nucleus), αXβ2 (periventricular brainstem), B7.2 (cerebellar peduncle), and CD44 (spinal nucleus of the trigeminal nerve) in green. Note the changes in microglial morphology, with elaborate microglial branching in sections from TGFβ1+/+ animals. In the TGFβ1−/− mice, this branching is almost completely lost in MHC1+, αXβ2+, and B7.2+ microglia, and also strongly reduced in those that did not stain for these phagocytosis-associated markers. K, L, TGFβ1 deficiency had a stimulatory effect on the CD44/GFAP+ velate astrocytes in the CNS white matter, but some double-positive astrocytes were also present in the normal, TGFβ1+/+ mice (GFAP staining in red, CD44 staining in green). Scale bar: (in L) A, B, 75 μm; C–L, 25 μm.
