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- 1. 肥満細胞：表面受容体とシグナル伝達 mast cells surface receptors and signal transduction
- 2. T細胞受容体シグナル伝達 t cell receptor signaling
- 3. 免疫不全症を引き起こすCD3／T細胞受容体複合体疾患 cd3 t cell receptor complex disorders causing immunodeficiency
- 4. ホジキンリンパ腫におけるエプスタイン・バール・ウイルス the role of epstein barr virus in hodgkin lymphoma
- 5. NK細胞欠損症候群：臨床症状および診断 nk cell deficiency syndromes clinical manifestations and diagnosis
English Journal
- SAP Facilitates Recruitment and Activation of LCK at NTB-A Receptors during Restimulation-Induced Cell Death.
- Katz G1, Krummey SM, Larsen SE, Stinson JR, Snow AL.Author information 1Department of Pharmacology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814.AbstractUpon TCR restimulation, activated, cycling T cells can undergo a self-regulatory form of apoptosis known as restimulation-induced cell death (RICD). We previously demonstrated that RICD is impaired in T cells from patients with X-linked lymphoproliferative disease, which lack SLAM-associated protein (SAP) expression. Both SAP and the specific SLAM receptor NK, T, and B cell Ag (NTB-A) are required for RICD, but the mechanism by which these molecules promote a strong, proapoptotic signal through the TCR remains unclear. In this article, we show that the Src-family kinase LCK, but not FYN, associates with NTB-A in activated human T cells. This association increased after TCR restimulation in a SAP-dependent manner, requiring both immunoreceptor tyrosine-based switch motifs in the NTB-A cytoplasmic tail. Both NTB-A-associated LCK phosphorylation and kinase activity were enhanced in restimulated T cells, amplifying proximal TCR signaling. In contrast, TCR-induced LCK association with NTB-A, as well as phosphorylation and kinase activity, was reduced in T cells from patients with X-linked lymphoproliferative disease or normal T cells transfected with SAP-specific small interfering RNA, consistent with RICD resistance. Collectively, our data reveal how SAP nucleates a previously unknown signaling complex involving NTB-A and LCK to potentiate RICD of activated human T cells.
- Journal of immunology (Baltimore, Md. : 1950).J Immunol.2014 May 1;192(9):4202-9. doi: 10.4049/jimmunol.1303070. Epub 2014 Mar 31.
- Upon TCR restimulation, activated, cycling T cells can undergo a self-regulatory form of apoptosis known as restimulation-induced cell death (RICD). We previously demonstrated that RICD is impaired in T cells from patients with X-linked lymphoproliferative disease, which lack SLAM-associated protein
- PMID 24688028
- Role of the Immunoreceptor Tyrosine-Based Activation Motif of Latent Membrane Protein 2A (LMP2A) in Epstein-Barr Virus LMP2A-Induced Cell Transformation.
- Fukuda M1, Kawaguchi Y.Author information 1Division of Viral Infection, Department of Infectious Disease Control, International Research Center for Infectious Diseases, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.AbstractLatent membrane protein 2A (LMP2A) of Epstein-Barr virus (EBV) is widely expressed in EBV-associated malignancies. We demonstrate that LMP2A has a transformation ability. This study shows that LMP2A-induced transformation in several human nonhematopoietic cell lines was blocked in those cells expressing an immunoreceptor tyrosine-based activation motif (ITAM) LMP2A mutant. The Syk inhibitor or Syk-specific small interfering RNA (siRNA) inhibited LMP2A-induced transformation. These results indicate that the interaction of the LMP2A ITAM with Syk is a key step for LMP2A-mediated transformation.
- Journal of virology.J Virol.2014 May;88(9):5189-94. doi: 10.1128/JVI.03714-13. Epub 2014 Feb 19.
- Latent membrane protein 2A (LMP2A) of Epstein-Barr virus (EBV) is widely expressed in EBV-associated malignancies. We demonstrate that LMP2A has a transformation ability. This study shows that LMP2A-induced transformation in several human nonhematopoietic cell lines was blocked in those cells expres
- PMID 24554661
- The channel-kinase TRPM7, revealing the untold story of Mg2+ in cellular signaling.
- Schmitz C1, Brandao K2, Perraud AL1.Author information 1Integrated Department of Immunology, University of Colorado Denver, Denver, CO, 80206, USA, National Jewish Health, 1400 Jackson Street, Denver, CO, 80206, USA.2Integrated Department of Immunology, University of Colorado Denver, Denver, CO, 80206, USA.AbstractIon homeostasis dysregulations have severe effects on human health, impairing the effectiveness and appropriateness of major cellular events, including immune responses. The adverse effects of Mg2+ deficiency on cellular physiology are well known and documented, but mechanistic insights into Mg2+ sensitive signal transduction are still lacking. TRPM7 and its sister channel TRPM6 stand out as the only known fusions of an ion pore with a Ser/Thr kinase domain. Both channels are permeable to divalent cations and are central regulators of Mg2+ homeostasis. One crucial aspect of TRPM7 function we have extensively studied is the relationship between its ion channel portion and its C-terminal Ser/Thr kinase domain. The modulation of ion channels by phosphorylation through exogenous kinases is common, however the covalent bound between the TRPM7 channel and its kinase suggests a novel kind of link between ion-entry and signal transduction events. Current knowledge supports a reciprocal "two-way street" model where TRPM7-kinase modulates ion transport function through Ser/Thr phosphorylation, and in turn, channel gating and ionic conditions in close proximity to the pore regulate TRPM7-kinase mediated signaling. We have shown that TRPM7 acts as a sensor of Mg2+-availability, adjusting key cellular functions such as the rate of cellular protein translation to the Mg2+ nutritional status. Since molecular mechanisms controlling rates of protein translation are critical for cell growth and division in response to nutrient availability, this could have relevance for example for therapies targeted at molecules shaping the cancerous translational apparatus. In our quest to understand the biology of Mg2+ in the context of immune responses, we found that TRPM7 associates with, and phosphorylates phospholipase C gamma 2 (PLCγ2), a pivotal molecule in the signaling pathway following B-cell receptor (BCR) activation. This contributes to the Mg2+-dependent modulation of the Ca2+ response elicited by BCR ligation, and provides the first molecular pathway underlying the Mg2+-sensitivity of immune responses. Expanding our knowledge about the modulation of immunoreceptor signaling in response to Mg2+ availability could allow for the development of unexplored strategies for therapeutic intervention in autoimmune diseases, immunodeficiencies, and lymphoma.
- Magnesium research : official organ of the International Society for the Development of Research on Magnesium.Magnes Res.2014 Apr 22. [Epub ahead of print]
- Ion homeostasis dysregulations have severe effects on human health, impairing the effectiveness and appropriateness of major cellular events, including immune responses. The adverse effects of Mg2+ deficiency on cellular physiology are well known and documented, but mechanistic insights into Mg2+ se
- PMID 24752033
Japanese Journal
- 破骨細胞Up-to-date : 骨吸収を調節するITAMシグナル (特集 骨免疫学と臨床応用)
- 高橋 直之
- 臨床免疫・アレルギー科 = Clinical immunology & allergology 64(2), 107-112, 2015-08
- NAID 40020562917
- マスト細胞鎮静化と組織恒常性維持 (特集 慢性炎症と疾病)
- 倉島 洋介,小暮 優太,福井 渉 [他]
- 臨床免疫・アレルギー科 = Clinical immunology & allergology 63(6), 551-557, 2015-06
- NAID 40020505003
- クラススイッチしたB細胞における新規な負の調節因子 (特集 免疫記憶と疾病)
- 藤堂 景史,疋田 正喜
- 臨床免疫・アレルギー科 = Clinical immunology & allergology 63(6), 532-537, 2015-06
- NAID 40020504928
Related Links
- 複数の免疫レセプターのリン酸化レベルを同時に検出 Human Phospho-Immunoreceptor Array Kit ITAM / ITIMを有するヒト免疫レセプターに対する抗体をスポットしたアレイです。59種類の免疫レセプターのリン酸化状態を同時に検出 ※ R＆D ...
- Definition of immunoreceptor in the Definitions.net dictionary. Meaning of immunoreceptor. What does immunoreceptor mean? Information and translations of immunoreceptor in the most comprehensive dictionary definitions resource ... ...
Related Pictures
★リンクテーブル★
| リンク元 | 「免疫受容体」「免疫レセプター」「immunologic receptor」 |
| 拡張検索 | 「immunoreceptor tyrosine-based activation motif」「immunoreceptor tyrosine based activation motif」「immunoreceptor tyrosine-based inhibitory motifs」 |
「免疫受容体」
「免疫レセプター」
「immunologic receptor」
「immunoreceptor tyrosine-based activation motif」
- 関
- ITAM
「immunoreceptor tyrosine based activation motif」
「immunoreceptor tyrosine-based inhibitory motifs」
- 同
- ITIMs
- 同
- ITIMs