Expression of various TGF-β isoforms and type I receptor in necrotizing human brain lesions

It is known that transforming growth factor beta (TGF-β) is involved in the modulation of cell growth, differentiation, and repair following injury. We performed an immunohistochemical study of human brain autopsy and biopsy material for the expression of TGF-β isoforms β1, β2 and β3, and TGF-β receptor (TβR) type I in different cells of necrotizing lesions such as infarction and abscess, and compared them with controls. Various cell types, both inside and in the proximity of lesions, showed immunoreactivity indicating the presence of all three isoforms. Significant values of immunoreaction for various TGF-βs and TβR-I were observed in cells such as astrocytes, macrophages, neurons, microvascular endothelial cells, and granulocytes. In the control cases, comprising biopsy material without necrotizing lesions, a prominent TGF-β2 immunoreactivity was observed in glial cells and neurons. TGF-β1 and TGF-β3 reactivity in controls, when compared with TGF-β2, was less. TβR-I antiserum showed clear and distinct signals in the same type of cells as for TGF-βs in the necrotizing lesions with varying values of significance. Our findings suggest that TGF-βs and their receptor type I are involved in reactive processes around necrotizing human brain lesions like glial and macrophage responses, angiogenesis, and deposition of extracellular matrix.