IL-2 Family Cytokines: New Insights into the Complex Roles of IL-2 as a Broad Regulator of T helper Cell Differentiation
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TLDR
This work focuses on the recently discovered complex roles of IL-2 in broadly modulating T cells for T helper cell differentiation, and how it can prime and potentially maintain Th1 and Th2 differentiation as well as expand such populations of cells.About:
This article is published in Current Opinion in Immunology.The article was published on 2011-10-01 and is currently open access. It has received 584 citations till now. The article focuses on the topics: Common gamma chain & Cytokine receptor.read more
Citations
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JAK and STAT Signaling Molecules in Immunoregulation and Immune-Mediated Disease
TL;DR: Not only have genome-wide association studies demonstrated that this pathway is highly relevant to human autoimmunity, but targeting JAKs is now a reality in immune-mediated disease.
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Combinatorial antigen recognition with balanced signaling promotes selective tumor eradication by engineered T cells
TL;DR: Co-transduced T cells destroy tumors that express both antigens but do not affect tumors expressing either antigen alone, and this 'tumor-sensing' strategy may help broaden the applicability and avoid some of the side effects of targeted T-cell therapies.
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Signaling and Function of Interleukin-2 in T Lymphocytes
Sarah H. Ross,Doreen A. Cantrell +1 more
TL;DR: It is increasingly clear that within each T cell subset, IL-2 will signal within a framework of other signal transduction networks that together will shape the transcriptional and metabolic programs that determine T cell fate.
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JAK/STAT signaling in hematological malignancies
William Vainchenker,William Vainchenker,William Vainchenker,Stefan N. Constantinescu,Stefan N. Constantinescu +4 more
TL;DR: The nature and respective contribution of mutations dysregulating the JAK/STAT pathway in hematological malignancies are discussed and examples in which such mutations drive the disease, contribute to the phenotype, or provide a survival and proliferative advantage are presented.
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InterleuKin-33 And Interferon-Γ Counter-Regulate Group 2 Innate Lymphoid Cell Activation During Immune Perturbation
Ari B. Molofsky,Frédéric Van Gool,Hong-Erh Liang,Steven J. Van Dyken,Jesse C. Nussbaum,Jinwoo Lee,Jeffrey A. Bluestone,Richard M. Locksley +7 more
TL;DR: Interleukin-33 mediates activation of ILC2s and Treg cells in resting adipose tissue, but also after helminth infection or treatment with IL-2, and IFN-γ suppresses this pathway, likely to promote inflammatory responses and divert metabolic resources necessary to protect the host.
References
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Differentiation of Effector CD4 T Cell Populations
TL;DR: This review summarizes the discovery, functions, and relationships among Th cells; the cytokine and signaling requirements for their development; the networks of transcription factors involved in their differentiation; the epigenetic regulation of their key cytokines and transcription factors; and human diseases involving defective CD4 T cell differentiation.
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Selective in vitro growth of T lymphocytes from normal human bone marrows
TL;DR: The T cells exhibited a strict growth dependence upon Phytohemagglutinin-stimulated normal human lymphocytes and were consistently negative for Epstein-Barr viral information.
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The biology of interleukin-6.
TL;DR: Human IL-6 (BSF2) was originally identified as a factor in the culture supernatants of mitogen or antigen-stimulated peripheral mononuclear cells, which induced immunoglobulin production in Epstein Barr virus transformed B-cell lines or in Staphylococcus aureus Cowan 1 stimulated normal B cells.
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CD4 T cells: fates, functions, and faults
Jinfang Zhu,William E. Paul +1 more
TL;DR: Much of what is known about the 4 CD4 T-cell subsets is summarized, including the history of their discovery, their unique cytokine products and related functions, their distinctive expression of cell surface receptors and their characteristic transcription factors, the regulation of their fate determination, and the consequences of their abnormal activation.