SEMINAR: Mechanisms of T cell extravasation into the brain in murine experimental autoimmune encephalomyelitis
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Mechanisms of T cell extravasation into the brain in murine experimental autoimmune encephalomyelitis : School of Anatomy & Human Biology Seminar Series |
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The Speaker: Prof Lydia Sorokin studied at UWA majoring in Physiology, Biochemistry and Zoology, and completed her PhD with Prof Evan Morgan and Dr George Yeoh on iron and transferrin in muscle in 1988. In March 1988, she started her first post doctoral appointment at the Max-Planck Institute for Developmental Biology in Tuebingen in Germany, where she worked on the role of extracellular matrix molecules and integrin receptors in kidney development with Dr Peter Ekblom. After three year in Tuebingen, Lydia moved to the Max-Planck Institute for Rheumatology in Erlangen, Germany, headed by Prof Klaus von der Mark, where she started her own group. From 1995 she and her group were at the Institute for Experimental Medicine, Connective Tissue Research, at the University of Erlangen-Nurnberg. From 2002 to 2005 she was the Professor of Tissue Biology, Head of Experimental Pathology in the Medical Faculty of the University of Lund, Sweden. She has been in her current position since 2005.
The Seminar: Specific inhibition of the entry of encephalitogenic T lymphocytes into the CNS in multiple sclerosis would provide a means of inhibiting disease without compromising unspecific acute immune responses. We show here that targeting lymphocyte interactions with endothelial basement membrane laminins provides such a possibility. In murine experimental autoimmune encephalomyelitis (EAE) T lymphocyte extravasation correlates with sites exclusively expressing laminin 4 and devoid of laminin 5. In mice lacking laminin 4, laminin 5 is ubiquitously expressed along the vascular tree, resulting in dramatic and selective reduction of T lymphocyte infiltration into the brain, and reduced disease susceptibility and severity. Vessel phenotype and immune response were not affected. Rather, laminin 5 directly inhibits integrin 61-mediated migration of T lymphocytes through laminin 4. The data demonstrate that T lymphocytes employ mechanisms distinct to other immune cells to penetrate the endothelial basement membrane barrier, permiting specific targetting of this immune cell population.
Speaker(s) |
Prof Lydia Sorokin, C4 Professor (Chair) of Physiological Chemistry and Pathobiochemisty, M�nster University, M�nster, Germany
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Location |
School of Anatomy & Human Biology, 1st Floor, Room 1.81
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Contact |
Debbie Hull
<[email protected]>
: 6488 3290
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Start |
Wed, 17 Feb 2010 12:00
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End |
Wed, 17 Feb 2010 13:00
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Submitted by |
Debbie Hull <[email protected]>
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Last Updated |
Mon, 08 Feb 2010 11:18
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