下記のとおり、Bernard Malissen先生のセミナーを開催致します。 皆様のご来聴を歓迎いたします。
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演題 | LAT signaling pathology: a T-cell dependent, B cell autoimmune condition without T cell self-reactivity
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演者 | Bernard Malissen Centre d’Immunologie de Marseille-Luminy,
Marseille, France.
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日時 | 平成24年9月24日(月)13時半より15時まで
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場所 | 馬出医学系キャンパス内 生体防御医学研究所 本館1階 会議室
以下の地図の21番になります。 (http://www.kyushu-u.ac.jp/access/map/hospital/hospital.html)
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要旨 |
When the T-cell receptor (TCR) recognizes antigens, the CD3 chains of the TCR complex are phosphorylated by the Src family kinase Lck. This allows the recruitment of the protein tyrosine kinase ZAP-70 that in turn phosphorylates several intracellular substrates, including the LAT adaptor. Upon tyrosine phosphorylation, LAT nucleates the assembly of a multiprotein complex – the LAT signalosome – that bridges the T cell-specific and the ubiquitous components of the signaling pathways that control many aspects of T cell development and function. Partial loss-of-function mutations in several molecules involved in TCR signaling (ZAP-70, LAT) result in inflammation and autoimmunity. How can mutations that reduce TCR signaling output paradoxically lead to immune pathologies? We will present recent data demonstrating that mutations in LAT predispose toward aberrant T cell responses to antigen in the presence of normal thymic selection. In the absence of LAT, the activity of the Lck kinase appears sustained without the need for TCR engagement. As a consequence, in the absence of LAT, antigen-specific T cell responses evolve into pro-inflammatory responses that unfold in a TCR-independent manner and induce the production of autoantibodies in a “quasi-mitogenic” mode. Therefore, some pathological conditions called "autoimmune" might not result from the presence of self-reactive T cells but from defect in mechanisms that normally keep protein tyrosine kinase activity in check. |
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連絡先 | 生体防御医学研究所 分子免疫学分野 山崎 晶 電話:092-642-4531
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