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Biochemical Society Transactions (2007) 35, (686–688) (Printed in Great Britain)

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Astrocyte–leucocyte interactions and the mechanisms regulating matrix degradation in CNS tuberculosis

J.A. Green and J.S. Friedland¹

Department of Infectious Diseases and Immunity, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0NN, U.K.

Key words: astrocyte, central nervous system, glial cell, metalloproteinase, monocyte, tuberculosis (TB).

Abbreviations used: BBB, blood–brain barrier; BCG, Bacille Calmette–Guérin; CNS, central nervous system; CoMTB, conditioned medium from Mycobacterium tuberculosis-infected monocytes; CSF, cerebrospinal fluid; IFN-g, interferon g; IL, interleukin; MAPK, mitogen-activated protein kinase; MMP, matrix metalloproteinase; NF-kB, nuclear factor kB; TB, tuberculosis; TBM, TB meningitis; TIMP, tissue inhibitor of metalloproteinases.

¹To whom correspondence should be addressed (email j.friedland@imperial.ac.uk).

Abstract

The CNS (central nervous system) has a unique pattern of immune response to infection. TB (tuberculosis) of the CNS is devastating with widespread tissue destruction. In TB, astrocyte–leucocyte interactions are key in regulating MMP (matrix metalloproteinase) activity and are regulated by complex signalling pathways. A synergistic interaction between interferon g and monocyte-derived mediators drives high-level astrocyte MMP-9 secretion; this and other networking effects are inhibited by steroids. Better understanding of regulatory mechanisms may identify potential switch points that could be future therapeutic targets.

Received 2 April 2007

© The Authors Journal compilation © 2007 Biochemical Society