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ISSN 打印: 1040-8401

ISSN 在线: 2162-6472

The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) IF: 1.3 To calculate the five year Impact Factor, citations are counted in 2017 to the previous five years and divided by the source items published in the previous five years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) 5-Year IF: 2.6 The Eigenfactor score, developed by Jevin West and Carl Bergstrom at the University of Washington, is a rating of the total importance of a scientific journal. Journals are rated according to the number of incoming citations, with citations from highly ranked journals weighted to make a larger contribution to the eigenfactor than those from poorly ranked journals. Eigenfactor: 0.00079 The Journal Citation Indicator (JCI) is a single measurement of the field-normalized citation impact of journals in the Web of Science Core Collection across disciplines. The key words here are that the metric is normalized and cross-disciplinary. JCI: 0.24 SJR: 0.429 SNIP: 0.287 CiteScore™:: 2.7 H-Index: 81

Indexed in

Orchestration of Invariant Natural Killer T Cell Development by E and Id Proteins

卷 35, 册 1, 2015, pp. 33-48
DOI: 10.1615/CritRevImmunol.2015012207
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摘要

Natural killer T (NKT) cells are αβ T cells that express a semi-invariant T-cell receptor (TCR) along with natural killer (NK) cell markers and have an innate cell-like ability to produce a myriad of cytokines very quickly upon antigen exposure and subsequent activation. These cells are diverted from conventional single positive (SP) T-cell fate at the double positive (DP) stage, where TCR-mediated recognition of a lipid antigen presented on a CD1d molecule promotes their selection into the NKT lineage. Although many key regulatory molecules have been shown to play important roles in the development of NKT cells, the mechanism of lineage specification and acquisition of effector functions in these cells still remain to be fully addressed. In this review, we specifically discuss the role of a family of class-I helix-loop-helix proteins known as E proteins, and their antagonists Id proteins in NKT celldevelopment. Recent work has shown that these proteins play key roles in invariant NKT (iNKT) development, from the invariant TCR rearrangement to terminal differentiation and maturation. Elucidating these roles provides an opportunity to uncover the transcriptional network that separates NKT cells from concurrently developed conventional αβ T cells.

对本文的引用
  1. Li Jia, Roy Sumedha, Kim Young-Mi, Li Shibo, Zhang Baojun, Love Cassandra, Reddy Anupama, Rajagopalan Deepthi, Dave Sandeep, Diehl Anna Mae, Zhuang Yuan, Id2 Collaborates with Id3 To Suppress Invariant NKT and Innate-like Tumors, The Journal of Immunology, 198, 8, 2017. Crossref

  2. Roy Sumedha, Moore Amanda J., Love Cassandra, Reddy Anupama, Rajagopalan Deepthi, Dave Sandeep S., Li Leping, Murre Cornelis, Zhuang Yuan, Id Proteins Suppress E2A-Driven Invariant Natural Killer T Cell Development prior to TCR Selection, Frontiers in Immunology, 9, 2018. Crossref

  3. Baraibar Iosune, Roman Marta, Rodríguez-Remírez María, López Inés, Vilalta Anna, Guruceaga Elisabeth, Ecay Margarita, Collantes María, Lozano Teresa, Alignani Diego, Puyalto Ander, Oliver Ana, Ortiz-Espinosa Sergio, Moreno Haritz, Torregrosa María, Rolfo Christian, Caglevic Christian, García-Ros David, Villalba-Esparza María, De Andrea Carlos, Vicent Silvestre, Pío Rubén, Lasarte Juan José, Calvo Alfonso, Ajona Daniel, Gil-Bazo Ignacio, Id1 and PD-1 Combined Blockade Impairs Tumor Growth and Survival of KRAS-mutant Lung Cancer by Stimulating PD-L1 Expression and Tumor Infiltrating CD8+ T Cells, Cancers, 12, 11, 2020. Crossref

  4. Nagel Stefan, Pommerenke Claudia, Quentmeier Hilmar, Meyer Corinna, Kaufmann Maren, MacLeod Roderick A. F., Genomic Aberrations Generate Fusion Gene FOXK2::TP63 and Activate NFKB1 in Cutaneous T-Cell Lymphoma, Biomedicines, 10, 8, 2022. Crossref

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