UEA-I-binding to thymic medullary epithelial cells selectively reduces numbers of cortical TCRαβ+ thymocytes in FTOCs

Graziano, Monica; St‐Pierre, Yves; Potworowski, Édouard F.

doi:10.1016/s0165-2478(01)00218-8

Cited by 7 publications

(8 citation statements)

References 46 publications

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“…This selective UEA-1 labeling pattern was evidently ageregulated, inasmuch as a relative reduction of the area of reactive medullary tissue (both lymphoid and epithelial) was paralleled by a low-intensity labeling of epithelial cells in the subcapsular and outer cortical region selectively observed in the thymus of adult mice. In accordance with these observations, the age-regulated expression of UEA-1 fucosylated ligands in thymic medullary epithelial cells has been previously documented (Farr and Anderson, 1985;Domino et al, 1997;Graziano et al, 2001). Evidently, ultra-structural immuno-histochemistry has confirmed the selective association between UEA-1 + medullary epithelial cells and TCR gd + thymocytes in the neonatal thymus (Farr et al, 1990).…”

Section: Discussionsupporting

confidence: 58%

“…In lymphoid tissues, only the selective expression of UEA-I fucosylated targets has been immunohistochemically established among thymic medullary epithelial cells (Farr and Anderson, 1985;Domino et al, 1997;Graziano et al, 2001) and Peyer's patch M cells (Clark et al, 1995). In the present study, both UEA-I and AAA have been employed in probing the possible expression of their respective fucosylated ligands in murine lymphocyte subpopulations.…”

Section: Introductionmentioning

confidence: 87%

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The selective expression of distinct fucosylated glycoproteins on murine T and B lymphocyte subsets

2005

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Section: Discussionsupporting

confidence: 58%

Section: Introductionmentioning

confidence: 87%

The selective expression of distinct fucosylated glycoproteins on murine T and B lymphocyte subsets

2005

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“…Single cell suspensions of thymus, spleen, lymph node, and bone marrow were harvested and counted at various time points after surgery (days 8,30 [range, [28][29][30][31][32][33][34][35][36][37][38][39][40][41], 90 [range, 89-95], and 180 [range, 182-210]). Cells from the spleen, lymph node, and bone marrow were subjected to ammonium chloride potassium (ACK) lysis to remove red blood cells.…”

Section: Flow Cytometrymentioning

confidence: 99%

“…However, UEA ϩ TEC seem to be essential for initial thymocyte development and decrease with age. [38][39][40] Thus, it is likely that these UEA ϩ TEC play a role in early thymocyte development. Furthermore, our data suggest that cortical cells are likely proliferating at a higher rate postcastration as well, albeit slower than the UEA ϩ Figure 7.…”

mentioning

confidence: 99%

CCL25 increases thymopoiesis after androgen withdrawal

Williams

Lucas

Bare

et al. 2008

Blood

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Although studies have demonstrated that androgen withdrawal increases thymic size, molecular mechanisms underlying this expansion remain largely unknown. We show that decreased androgen signaling leads to enhanced immigration of bone marrow T-cell precursors, as manifested by both an early increase of early thymic progenitors (ETP) and improved uptake of adoptively transferred quantified precursors into congenic castrated hosts. We provide evidence that the ETP niche is enhanced after androgen withdrawal by proliferation of UEA ؉ thymic epithelial cells (TEC) and increased TEC production of CCL25, a ligand critical for ETP entry. Moreover, the greatest increase in CCL25 production is by UEA ؉ TEC, linking function of this subset with the increase in ETP immigration. Furthermore, blockade of CCL25 abrogated the effects of castration by impairing ETP entry, retarding immature thymocyte development, limiting increase of thymic size, and impairing increase of thymopoiesis. Taken together, these findings describe a cohesive mechanism underlying increased thymic productivity after androgen withdrawal. (Blood. 2008;112: 3255-3263) IntroductionImpaired thymopoiesis contributes to the immune deficiency after lymphopenia or allogeneic hematopoietic stem cell transplantation (HSCT). 1,2 The thymus is the primary site of new naive T-cell generation and the site of central tolerance induction where potentially autoreactive T cells are deleted. 3 Without thymic renewal during recovery from lymphopenia, an oligoclonal repertoire of T cells persists, leading to impaired clearance of infectious diseases and tumors, and increased rates of auto-or alloimmunity (graft-versus-host disease). [4][5][6][7][8] Thus, an understanding of the mechanisms underlying renewed thymopoiesis may be of critical importance to correcting thymic deficits after HSCT, AIDS therapies, and chemotherapeutic treatment for cancer.Androgen withdrawal presents a potential therapy to renew thymic function. Multiple studies have demonstrated that androgen withdrawal increases thymic size and thymocyte numbers in male mice. [9][10][11][12][13] These studies suggested that this enlargement represents enhanced thymic activity as evidenced by subsequent increases in naive T cells in peripheral organs. 12,14 Furthermore, transplant studies in mice and man have shown enhanced thymic recovery and increased peripheral recent thymic emigrants (RTE) after androgen withdrawal, consistent with overall augmented thymopoiesis. 12,15,16 However, the mechanism by which androgen withdrawal induces thymic recovery remains incompletely understood. Because thymic epithelial cells (TEC) and thymocytes possess functional androgen receptors, studies have focused on these cells as mediators of thymic enlargement associated with androgen withdrawal. 17,18 Initial studies into the thymic effects of androgen revealed rapid thymocyte apoptosis associated with thymic involution after androgen administration. 19,20 Conversely, androgen withdrawal has been shown to enhance proliferation of t...

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“…Is Ulex binding to the putative EPC a more specific endothelial marker than Ac-LDL uptake? Ulex is bound by many circulating blood cells and a variety of epithelial cells in addition to vascular endothelial cells (Graziano et al 2001;Holthofer et al 1982;Liu and Li 1996;Schwechheimer et al 1984). Thus, neither Ac-LDL uptake nor Ulex binding is specific markers for an EPC.…”

Section: Methods To Identify Human Epcmentioning

confidence: 99%

Defining Endothelial Progenitor Cells

Mund

Ingram

Yoder

2011

Regenerative Therapy Using Blood-Derived Stem Cells

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Human cord blood-derived endothelial progenitor cells (EPC) have been defined as circulating cells that express a panel of cell surface markers similar to those known to be expressed by vascular endothelial cells, that home to sites of hypoxia/ischemia upon infusion into experimental animal models, and participate in blood vessel formation (as analyzed by in vitro and in vivo methods). Although no specific marker for an EPC has been identified, a group of markers has been consistently utilized as a surrogate marker for cells purported to display vascular regenerative capacity. Since both hematopoietic and vascular endothelial subsets display many of the same cell surface antigens and both participate in new blood vessel formation, recent analyses have stressed the need to reconsider the use of the term EPC. This chapter reviews our current approaches to identifying human EPC and provides a brief summary statement for a new definition of an EPC.

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UEA-I-binding to thymic medullary epithelial cells selectively reduces numbers of cortical TCRαβ+ thymocytes in FTOCs

Cited by 7 publications

References 46 publications

The selective expression of distinct fucosylated glycoproteins on murine T and B lymphocyte subsets

The selective expression of distinct fucosylated glycoproteins on murine T and B lymphocyte subsets

CCL25 increases thymopoiesis after androgen withdrawal

Defining Endothelial Progenitor Cells

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