Adhesion between medullary thymic epithelial cells and thymocytes is regulated by miR-181b-5p and miR-30b*

Cotrim-Sousa, Larissa; Freire-Assis, Amanda; Pezzi, Nicole; Tanaka, Pedro Paranhos; Oliveira, Érika Arantes de; Passos, Geraldo A. S.

doi:10.1016/j.molimm.2019.09.010

Cited by 11 publications

(13 citation statements)

References 70 publications

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“…This suggests that the expansion of SP thymocytes occurring between D12 and D28 might have led to the increase in mTEC numbers. This is consistent with the fact that the development of the mTEC compartment during embryogenesis requires interaction between TECs and positively selected thymocytes (25)(26)(27)(28)(29)(30)(31), and suggests that a similar crosstalk is instrumental to the maintenance of mTECs in the adult thymus. Representative profiles of cTECs and mTECs at different time points during pregnancy and postpartum regeneration are shown in Supplementary Figure 1.…”

Section: Thymic Epithelium Does Not Suffer Cell Loss During Pregnancysupporting

confidence: 86%

Qualitative Changes in Cortical Thymic Epithelial Cells Drive Postpartum Thymic Regeneration

et al. 2020

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During gestation, sex hormones cause a significant thymic involution which enhances fertility. This thymic involution is rapidly corrected following parturition. As thymic epithelial cells (TECs) are responsible for the regulation of thymopoiesis, we analyzed the sequential phenotypic and transcriptomic changes in TECs during the postpartum period in order to identify mechanisms triggering postpartum thymic regeneration. In particular, we performed flow cytometry analyses and deep RNA-sequencing on purified TEC subsets at several time points before and after parturition. We report that pregnancy-induced involution is not caused by loss of TECs since their number does not change during or after pregnancy. However, during pregnancy, we observed a significant depletion of all thymocyte subsets downstream of the double-negative 1 (DN1) differentiation stage. Variations in thymocyte numbers correlated with conspicuous changes in the transcriptome of cortical TECs (cTECs). The transcriptomic changes affected predominantly cTEC expression of Foxn1, its targets and several genes that are essential for thymopoiesis. By contrast, medullary TECs (mTECs) showed very little transcriptomic changes in the early postpartum regenerative phase, but seemed to respond to the expansion of single-positive (SP) thymocytes in the late phase of regeneration. Together, these results show that postpartum thymic regeneration is orchestrated by variations in expression of a well-defined subset of cTEC genes, that occur very early after parturition.

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Section: Thymic Epithelium Does Not Suffer Cell Loss During Pregnancysupporting

confidence: 86%

Qualitative Changes in Cortical Thymic Epithelial Cells Drive Postpartum Thymic Regeneration

et al. 2020

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“…Tgfbr1 expression increases with age in mice, which is consistent with the decreased level of miR-181a in addition to the ability of TGF-β to decrease the proliferation of mTECs (44). Recently, Cotrim-Sousa et al suggest that miR181b and miR-30b modulate the expression of adhesion molecules involved in mTEC and thymocyte interactions (45).…”

Section: Mir-181amentioning

confidence: 62%

Role of miRNAs in Normal and Myasthenia Gravis Thymus

et al. 2020

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The thymus, a primary lymphoid organ, provides a complex environment essential for the generation of the T-cell repertoire. Thymic alterations occur during life either in the context of thymic involution upon aging or the pathophysiological context of Myasthenia Gravis (MG). These changes involve complicated regulatory networks, in which microRNAs (miRNAs) are key players. Here, we analyzed the role of miRNAs in thymocyte maturation and differentiation sustained by thymic epithelial cells. We compared data from the literature regarding the role of mouse thymic miRNAs and original data obtained from a human thymic miRnome study. We identified a set of highly expressed miRNAs defined as ThymiRs and investigated miRNA expression in infants as compared to adults to determine those associated with human thymic involution. Thymic changes are also frequently observed in MG, an autoimmune disease which results in the production of anti-acetylcholine receptor (AChR) antibodies that lead to muscle weaknesses. Alterations such as thymoma in late-onset MG patients and hyperplasia with ectopic germinal centers (GCs) in early-onset (EOMG) patients are found. Thymic miRNA expression has been studied in AChR-MG patients both in thymoma-associated MG (TAMG) and EOMG, and their function through their mRNA targets investigated. Most of the dysregulated thymic miRNAs in EOMG are associated with GC development, such as miR-7, miR-24, miR-139, miR-143, miR-145, miR-146, miR-150, miR-452, miR-548 or thymic inflammation, such as miR-125b, miR-146, or miR-29. Understanding these pathways may provide therapeutic targets or biomarkers of disease manifestations.

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“…In the study of the cell-cell interaction between mononuclear phagocyte and B plasma cell clusters after reperfusion, we found that the ligand-receptor pairs such as PLAUR_a4b1 complex and C5AR1_RPS19 were commonly enriched between mononuclear phagocyte and B plasma cell clusters. The interactions between MP and B cells were specifically enriched in LGALS9_CD47 and PTPRC_CD22 and other cell-cell/cell-matrix interactions related functions 47 , 48 . In addition, ligand-receptor pairs such as HLA − C_FAM3C , CD74_MIF, CD74_COPA , CD74_APP which play an important role in IRI, were enriched in the interaction between KC and B plasma cell clusters 41 – 43 .…”

Section: Resultsmentioning

confidence: 99%

Resolving the graft ischemia-reperfusion injury during liver transplantation at the single cell resolution

Wang

et al. 2021

Cell Death Dis

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Ischemia–reperfusion injury (IRI) remains the major reason for impaired donor graft function and increased mortality post-liver transplantation. The mechanism of IRI involves multiple pathophysiological processes and numerous types of cells. However, a systematic and comprehensive single-cell transcriptional profile of intrahepatic cells during liver transplantation is still unclear. We performed a single-cell transcriptome analysis of 14,313 cells from liver tissues collected from pre-procurement, at the end of preservation and 2 h post-reperfusion. We made detailed annotations of mononuclear phagocyte, endothelial cell, NK/T, B and plasma cell clusters, and we described the dynamic changes of the transcriptome of these clusters during IRI and the interaction between mononuclear phagocyte clusters and other cell clusters. In addition, we found that TNFAIP3 interacting protein 3 (TNIP3), specifically and highly expressed in Kupffer cell clusters post-reperfusion, may have a protective effect on IRI. In summary, our study provides the first dynamic transcriptome map of intrahepatic cell clusters during liver transplantation at single-cell resolution.

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Adhesion between medullary thymic epithelial cells and thymocytes is regulated by miR-181b-5p and miR-30b*

Cited by 11 publications

References 70 publications

Qualitative Changes in Cortical Thymic Epithelial Cells Drive Postpartum Thymic Regeneration

Qualitative Changes in Cortical Thymic Epithelial Cells Drive Postpartum Thymic Regeneration

Role of miRNAs in Normal and Myasthenia Gravis Thymus

Resolving the graft ischemia-reperfusion injury during liver transplantation at the single cell resolution

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