第 631 回生医研セミナー(多階層生体防御システム研究拠点)
免疫機構研究セミナー

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。

演題LAT signaling pathology: a T-cell dependent, B cell autoimmune condition without T cell self-reactivity

演者Bernard Malissen
Centre d’Immunologie de Marseille-Luminy,
Marseille, France.

日時平成24年9月24日(月)13時半より15時まで

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

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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