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The New Frontiers in Bone Tissue Engineering
Published in Ugo Ripamonti, The Geometric Induction of Bone Formation, 2020
Our systematic studies in calvarial defects of Papio ursinus using the three mammalian hTGF-β isoforms (Ripamonti et al. 1997; Ripamonti et al. 2000; Ripamonti et al. 2008; Ripamonti et al. 2016) have suggested novel regulatory pathways through Id2 and Id3 expression (Ripamonti et al. 2016). The molecular data have also shown that when TGF-β3 expression decreases, Id2 and Id3 expression are upregulated (Ripamonti et al. 2016). This has suggested that TGF-β signalling to regulate Id2 and Id3 gene expression promotes or inhibits the induction of calvarial bone formation. Interplays of Id genes, TGF-βs, Notch and BMPs control endothelial cell migration and differentiation (Itoh et al. 2004). Upregulation of Id gene expression promotes endothelial cell migration, with molecular interplay between Notch and BMP receptor signalling pathways. This regulates endothelial cell migration via upregulation of Id1 (Itoh et al. 2004). Segregated calvarial defects showed the induction of bone formation with capillary sprouting and invasion, directly correlating to Id2 and Id3 upregulation (Ripamonti et al. 2016). The application of exogenous hTGF-β3 to defects segregated from the dura mater creates a microenvironment that is permissive for bone formation (Ripamonti et al. 2016).
Immunologic and functional differences among individual compartments of the mucosal immune system
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Hiroshi Kiyono, Kohtaro Fujihashi, Jiri Mestecky
Chronological examination of Peyer's patches, NALT, and TALT during development has revealed that organogenesis of most of the secondary lymphoid tissues, including Peyer's patches and peripheral lymph nodes, is initiated during the prenatal stage of development. In contrast, the genesis of NALT and TALT begins after birth. In addition to these differences, the requirement for essential organogenesis molecules also differs among the three MALTs. The critical molecules required for the organogenesis of Peyer's patches and other peripheral lymphoid tissues are dispensable for the development of NALT. In mice, the transcription factor retinoic orphan receptor RORγt is required for the development of Peyer's patches but not for NALT or TALT. Similarly, neither the IL-7/IL-7Rα cytokine family nor the LTα1β2–LTβR signaling pathways, which are involved in the genesis of Peyer's patches and peripheral lymph nodes, are essential for NALT and TALT organogenesis. Interestingly, even Id2, another well-known transcriptional molecule for lymphoid tissue genesis, is essential for the development of Peyer's patches, peripheral lymph nodes, and NALT but dispensable for TALT genesis. Thus, at least three distinct tissue genesis programs operate in the development of MALTs associated with the intestine, respiratory tract, and tear duct: the organogenesis of Peyer's patches during gestation and that of NALT and TALT beginning during the postnatal stage (see Figure 3.4).
Temporal Models
Published in Virgilio Gómez-Rubio, Bayesian Inference with INLA, 2020
A similar model can be fit using the group argument. In this case, variable ID.Year is created to index the year (from 1 to 19) used to define the group. Argument control. grouptakes a list with the model (ar1) and other arguments to define this effect could be added. Index ID2 is created as a copy of the ID index so that it can be used in another latent effect.
scRNA-seq reveals ATPIF1 activity in control of T cell antitumor activity
Published in OncoImmunology, 2022
Genshen Zhong, Qi Wang, Ying Wang, Ying Guo, Meiqi Xu, Yaya Guan, Xiaoying Zhang, Minna Wu, Zhishan Xu, Weidong Zhao, Hongkai Lian, Hui Wang, Jianping Ye
The conclusion is supported by scRNA-seq analysis of TILs, in which the decreased T cell activities in KO mice were observed with an increased expression of exhaustion markers and decreased expression of IFN-γ. scRNA-seq was employed to determine the subpopulation of CD8+ T cells in TILs, which led to the characterization of eight major subsets of T cells. In these subclusters, mRNA expression of exhaustion markers, such as PD-1, LAG-3, and TIGIT, were significantly increased in the CD8+ T proliferative and effector-memory subcluster, indicating that ATPIF1 inactivation led to the exhaustion of CD8+ T cells for the decreased antitumor efficacy. The increased PD1 and LAG-3 were confirmed at the protein levels with flow cytometry in the T cells isolated from TILs, spleen, and lymph nodes. The heatmap, KEGG pathway, and GSEA analysis based on the RNA-seq data suggest that the decreased expression of cytokine genes (such as IFN-γ and Gzmb) was associated with the significant changes in ribosome or ribosome biogenesis-related genes. This indicates that ATPIF1 knockout reduced the protein synthesis, which may count for the decreased IFN-γ expression in the KO cells. Id2 (inhibitor of differentiation-2) expression was decreased significantly in the KO cells as shown in the heatmap of RNA-seq, which may be a reason for decreased proliferation and antitumor activity of KO T cells. It was reported that Id2 was closely related to CD8+ T cell function and differentiation.31,32
Plasmacytoid dendritic cells and asthma: a review of current knowledge
Published in Expert Review of Respiratory Medicine, 2020
The development of pDC is highly dependent on the Flt3L signaling and coordinated action of many transcription factors such as GATA2, PU.1, GFI1, IKZF1 and IRF8, and mutations in any of these can result in aberrant development and functionality of pDC [65]. E2-2 is an indispensable lineage-determining factor during the development of pDC, promoting many factors critical to the function of pDC including IRF7, IRF8, Runt-related transcription factor 2 (RUNX2), and Class II Major Histocompatibility complex transactivator (CIITA). E2-2 can be negatively regulated by ID2 (inhibitor of DNA binding 2). The regulation of E2-2 and ID2 can influence the relative production of pDC and conventional DC (cDC). Repressing ID2 was shown to increase pDC production, whereas greater ID2 expression leads to enhanced cDC synthesis. Loss of E2-2 can leads to a reduction in numbers of IFN-α producing pDC [2,65,74,75]. Following bone marrow release, mature pDC migrate into the periphery where they reside or recirculate through lymphoid organs to monitor and rapidly recognize pathogens (e.g. HRV) and produce large amount of IFN-I to eliminate infections.
Radiation-induced augmentation in dendritic cell function is mediated by apoptotic bodies/STAT5/Zbtb46 signaling
Published in International Journal of Radiation Biology, 2020
Vipul K. Pandey, Bhavani S. Shankar
STAT–dependent pathways and transcription factors play an important role in DC development and control DC lineage diversification. DC-IP was characterized by increased STAT5 and decreased STAT3 phosphorylation. STAT5 has been shown to be required for generation of classical DC (cDC) expressing transcription factor Id2 and Zbtb46 as well as suppression of plasmacytoid DC (pDC) in steady state Li et al. 2012. In contrast, pDCs, are dependent on STAT3 signaling and transcription factor Tcf4 (E2-2) (Esashi et al. 2008; Li et al. 2012). Since DC-IP had increased STAT5 signaling, we evaluated the expression of different transcription factors which play important roles in DC differentiation like E2-2, Zbtb46, Id2, Bcl6 and ATF3 in DC from IP as compared to BMDC from control progenitors (Murphy 2013). Expression of Zbtb46 and Id2 was significantly upregulated in DC IP (0.5 and 1.0 Gy). Both these transcription factors are important in DC differentiation, especially classic DC lineage. Id2 transcription factor works as repressor to inhibit transcription factor E2-2 and pDC lineage (Becker-Herman et al. 2002). Id2−/− mice has also been shown to be deficient in CD8α+ DCs (Hacker et al. 2003). Similarly, Zbtb46 is shown to be expressed by DC and committed dendritic cell precursors and its over expression in bone marrow progenitor cells has been shown to inhibit granulocyte potential and promote cDC development (Satpathy et al. 2012). Reversal of this STAT5/Zbtb46 signaling when ABs were depleted from IP further confirmed that the ICD signaling operated through STAT5/Zbtb46 pathway in DC.