Modulating BTK-dependent inflammatory signalling in microglia

Using the cuprizone-induced toxicity model, the role of Bruton’s tyrosine kinase (BTK) signalling in modulating inflammation in microglial cells was assessed [1]. Results showed that BTK-dependent inflammatory signalling in these cells can be modulated using brain-penetrant BTK inhibitors in vivo. This treatment may suppress microglia-driven neuroinflammation in MS progression. BTK is expressed in B-lymphocytes and monocytes/macrophages as well as in microglia. It is assumed to modulate the activity of both adaptive and innate immune cells. In B cells, BTK is centrally involved in the B-cell receptor signalling pathway, regulating proliferation, maturation, antigen presentation, and production of secreted immunoglobulins. The research that was reported focused on the possible role of BTK in regulating microglial deleterious inflammatory signalling. This role was evaluated applying immunohistochemistry, Western blotting, and RNA sequencing i...

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Posted on 25 November, 2020