Research and Reports in Immunology

All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.
Reach Us +1 (202) 780-3397

Short Communication - Research and Reports in Immunology (2022) Volume 5, Issue 1

Thymocyte adhesion in medullary thymic epithelial cells under the influence of incrnas.

Freddie Williams*

Department of Immunology, The Scripps Research Institute, Florida, USA

*Corresponding Author:
Freddie Williams
Department of Immunology
The Scripps Research Institute
Florida, USA

Received: 31-Jan-2022, Manuscript No. AARRI-22-56883;  Editor assigned 3-Feb-2022, PreQC No. AARRI-22-56883 (PQ); Reviewed:  15-Feb-2022, QC No AARRI-22-56883; Revised:  19-Feb-2022, Manuscript No. AARRI-22-56883 (R); Published:  26-Feb-2022, DOI: 10.35841/aarri-5.1.101

Citation: Williams F. Thymocyte adhesion in medullary thymic epithelial cells under the influence of IncRNAs. Res Rep Immunol. 2022;5(1):101


Thymus atrophy, Thymic epithelial cell, Epigenetic modification, Foxn1, EMT, Rejuvenation.

Visit for more related articles at Research and Reports in Immunology


Background: Thymic epithelial cells, cytokines, exosomes, surface chemicals, and hormones from the cells make up the thymic microenvironment, which is important for T lymphocyte formation, differentiation, maturation, and homeostasis. The thymus, on the other hand, begins to degrade in humans as early as the second year of life and continues to do so throughout life, resulting in a decreased output of naive T cells, limited TCR variety, and an expansion of monoclonal memory T cells in peripheral organs. These changes will diminish the adaptive immune response to cancers and new infectious diseases like COVID-19, as well as make it easier for older people to develop autoimmune diseases. It is critical to explore and clarify the issues of global ageing. Main body: Histone modification, DNA methylation, non-coding RNA impacts, and chromatin remodelling are all examples of epigenetics. We address how senescent thymic epithelial cells define and control age-related thymic atrophy, as well as how epigenetic alteration affects this process. The role of the thymus adipose in thymic epithelial cell dysfunction and the possibility of treating thymus atrophy by targeting thymic epithelial cells. Conclusion: Epigenetic changes are emerging as important regulators of thymic epithelial cell growth and senescence. In the aged, it is advantageous to re-establish functional thymopoiesis, find a suitable therapeutic strategy, and rejuvenate immunological function.


The thymus, which arises from the third endodermal pouch and the third ectodermal cleft, is the major lymphoid organ and supports T cell development. The thymic microenvironment is made up of non-lymphoid stromal cells that play a key role in the formation, differentiation, and maturation of T cells, as well as maintaining T cell-related central tolerance [1]. Thymic stromal cells make up only 1% of the thymus' total cellularity, which also includes thymic epithelial cells (TECs), dendritic cells, and endothelial cells and TECs, which are made up of cortical thymic epithelial cells (cTECs) and medullary thymic epithelial cells (mTECs), are responsible for supporting T cell production at various stages of thymopoiesis [2]. T-cell progenitors (pro-T) start off in the bone marrow and travel to the thymus outer cortex, where they undergo TCR gene rearrangement and eventually become T-cell precursors (pre-T). The interplay of Notch receptor, pre-T expression, and Notch ligands expressed on TECs and thymic dendritic cells caused T-cell lineage commitment.

DNA methylation patterns, particularly the 5-methylcytosine, vary as people get older [3]. The methylation state of his DNA can be used to calculate chronological age and the risk of developing age-related disorders. As a result, it's known as the 'epigenetic clock.' DNA methylation has a variety of effects on thymus growth and involution. Previous research has mostly focused on the epigenetic mechanisms involved in thymocyte formation and differentiation in healthy and pathologic circumstances. TEC gene expression is, however, subject to epigenetic control that is not well understood. The Aired gene's DNA methylation modification in mTECs may have a role in the mTECs' final differentiation stage [4]. DNA methylation has also been shown to decrease Foxn1 gene transcription. In the human TECs line, the C20 region is found near the foxn1 promoter in the first Foxn1 intron. The region is characterised by CpG hypermethylation, which inhibits Foxn1 expression; Foxn1 level fall marks age-related thymus involution. In this review, we identify the key molecule implicated in TEC ageing and senescence, as well as the features of thymic involution. Furthermore, to further understand the mechanism, the intimate ties between TEC senescence and an epigenetic modifying network linked to thymic involution are explored. Finally, we review therapy accomplishments and future possibilities in thymus atrophy [5].


Thymus crosstalk, or the interaction between growing thymocytes and TECs, is thought to have a role in thymus development. cTECs rely on signalling from DN and DP thymocytes for development and differentiation, whereas mTECs rely on SP thymocytes. The status of cTEC research isn't totally clear. As a result, we concentrate on the signalling route involved in the maturation of mTECs. To begin, activation of the Notch signalling pathway is required for the lineage specification of the early mTECs. During the embryonic phase, the deletion of Notch1 in TECs contributes to the depletion of mTEPCs and a considerable loss of mTECs. Second, the NF-B signalling pathway, which is regulated by multiple members of the TNF receptor family, including receptor activator of nuclear factor, is required for the specification and differentiation of mTECs. RANK and CD40 signals drive the formation of mTECs, whereas LTR drives the terminal differentiation of late-stage mTECs, emphasising the relevance of cross-talk between maturation thymocytes and thymic epithelial cells.


  1. Boraschi D, Italiani P Immunosenescence and vaccine failure in the elderly: strategies for improving response. Immunol Lett. 2014;162:346– 53.
  2. Indexed at, Google Scholar, Cross Ref

  3. Pera A, Campos C, Lopez N, et al.Immunosenescence: implications for response to infection and vaccination in older people. Maturitas. 2015;82:50–5.
  4. Indexed at, Google Scholar, Cross Ref

  5. Salminen A, Kaarniranta K, Hiltunen M, et al.Histone demethylase Jumonji D3 (JMJD3/KDM6B) at the nexus of epigenetic regulation of infammation and the aging process.. J Mol Med (Berl). 2014;92:1035– 43.
  6. Indexed at, Google Scholar, Cross Ref

  7. Zook EC, Krishack PA, Zhang S, et al.Overexpression of Foxn1 attenuates age-associated thymic involution and prevents the expansion of peripheral CD4 memory T cells. Blood. 2011;118:5723–31.
  8. Indexed at, Google Scholar, Cross Ref

  9. Gregory PA, Bert AG, Paterson EL, et al.The miR-200 family and miR-205 regulate epithelial to mesenchymal transition by targeting ZEB1 and SIP1. Nat Cell Biol. 2008;10:593–601.
  10. Indexed at, Google Scholar, Cross Ref

Get the App