By Frederick W. Alt
Advances in Immunology, a common and hugely revered book, provides present advancements in addition to complete reports in immunology. Articles handle the big variety of themes that contain immunology, together with molecular and mobile activation mechanisms, phylogeny and molecular evolution, and scientific modalities. Edited and authored by means of the major scientists within the box, each one quantity presents updated details and instructions for the future.
* Contributions from top experts * Informs and updates on all of the most modern advancements within the box
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Extra resources for Advances in Immunology, Volume 121
1999). The erythropoietin receptor: Structure, activation and intracellular signal transduction. Trends in Endocrinology and Metabolism, 10, 18–23. Constantinescu, S. , Huang, L. , & Lodish, H. F. (2001). The erythropoietin receptor cytosolic juxtamembrane domain contains an essential, precisely oriented, hydrophobic motif. Molecular Cell, 7, 377–385. Constantinescu, S. , Henis, Y. , & Lodish, H. F. (2001). Ligand-independent oligomerization of cell-surface erythropoietin receptor is mediated by the transmembrane domain.
Bazan, J. F. (1989). A novel family of growth factor receptors: A common binding domain in the growth hormone, prolactin, erythropoietin and IL-6 receptors, and the p75 IL-2 receptor beta-chain. Biochemical and Biophysical Research Communications, 164, 788–795. Bazan, J. F. (1990). Haemopoietic receptors and helical cytokines. Immunology Today, 11, 350–354. , et al. (2010). Covering a broad dynamic range: Information processing at the erythropoietin receptor. Science, 328, 1404–1408. , Ullmann, G.
With these two mutants in hand, we explored the relative contributions of type I versus type II receptors to different IL-4-induced bioactivities. Super-4 induces stronger activation of STAT6 in naı¨ve CD4 þ T cells (which express only the type I receptor) compared to wt IL-4 and promotes their differentiation into Th9 cells. However, Super-4 28 Ignacio Moraga et al. is unable to support the differentiation of monocytes into DCs despite activating STAT6 in monocytes to the same extent as IL-4, suggesting that type II receptor-induced pathways are required for monocyte differentiation into DCs.