FoxP3+ T Cells Undergo Conventional First Switch to Lymphoid Tissue Homing Receptors in Thymus but Accelerated Second Switch to Nonlymphoid Tissue Homing Receptors in Secondary Lymphoid Tissues

Lee, Jee H.; Kang, Seung Goo; Kim, Chang H.

doi:10.4049/jimmunol.178.1.301

Cited by 113 publications

(134 citation statements)

References 63 publications

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“…Upon contact with cognate antigen, naive-like Treg become activated and change their homing receptor expression [11,34,38], comparable to what has previously been reported for conventional T cells [39,40]. We describe elsewhere that naive-like Treg harbor a high degree of plasticity for the induction of organselective homing receptors and respond to local factors of the tissue microenvironment [38].…”

Section: Discussionsupporting

confidence: 77%

“…Whereas CCR7-deficient naive-like Treg fail to recirculate through LN, resulting in an almost complete abolishment of their ability to inhibit the proliferation of naive T cells at this site, effector/memory-like Treg from CCR7 -/-mice display an increased accumulation in inflamed sites, which was accompanied by an enhanced suppression of the inflammatory reaction. CCR7 expression was predominantly observed on naive-like Treg [3,5,6,11,[31][32][33][34] and CCR7-expressing CD62L high CD25 + CD4 + Treg were found to be very efficient in preventing the development of autoimmunity [5] or in suppressing graft-versus-host disease [35,36]. It was suggested that Treg recirculation through LN mediated by CCR7 and CD62L is a prerequisite to suppress priming of autoreactive effector cells.…”

Section: Discussionmentioning

confidence: 99%

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Distinctive role of CCR7 in migration and functional activity of naive‐ and effector/memory‐like Treg subsets

et al. 2007

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Foxp3 + CD25 + CD4 + Treg play a fundamental role in the maintenance of self tolerance and the control of inflammatory reactions. Previous data demonstrated a division of labor between naive-and effector/memory-like Treg subsets, which is largely based on their lymph node-recirculating and inflammation-seeking migration behavior, respectively. The chemokine receptor CCR7 is expressed on both types of Treg subsets, albeit at different levels. Whether it fulfills similar or distinct roles in these subsets has not been studied so far. We here show that the recirculation of naive-like Treg through LN and, to some extent, the gut is dependent on CCR7. Lack of CCR7 not only prevents recirculation, but also almost completely abolishes the ability of naive-like Treg to control the priming phase of an immune response. In contrast, CCR7 deficiency in effector/memory-like Treg promotes their accumulation in inflamed sites, compatible with a role of CCR7 for exit from the tissue. Local Treg accumulation was accompanied by an enhanced suppression of inflammation. Together, our findings provide conclusive evidence that CCR7 expression on Treg differentially controls in vivo function of the naive-and effector/memory-like subsets.

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Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Distinctive role of CCR7 in migration and functional activity of naive‐ and effector/memory‐like Treg subsets

et al. 2007

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“…Differential expression of trafficking receptors, including CD62L, has been used to distinguish lymphoid homing T-regulatory cells [21]. The Tregulatory cells identified in follicles and clusters in the current study expressed CD62L, suggesting T-regulatory cell recruitment akin to that of secondary lymph nodes [21,22].…”

Section: Foxp3mentioning

confidence: 60%

“…+ T-cells [20,21]. Differential expression of trafficking receptors, including CD62L, has been used to distinguish lymphoid homing T-regulatory cells [21].…”

Section: Foxp3mentioning

confidence: 99%

Increased T-regulatory cells within lymphocyte follicles in moderate COPD

Plumb¹,

Smyth²,

Adams³

et al. 2009

Eur Respir J

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Lymphoid follicles in the lung parenchyma are a characteristic feature of chronic obstructive pulmonary disease (COPD). There are reports of altered CD4 T-regulatory cell numbers in COPD lungs, but the location of these cells within COPD lung tissue specific follicles has not been investigated.The presence of CD4 + FOXP3 + T-regulatory cells was assessed in surgically resected lung tissue from 12 COPD patients, 11 smokers with normal lung function and seven nonsmokers by combined immunofluorescence and immunohistochemistry. Organised lymphoid follicles were observed in all three groups of patients, as well as lymphoid clusters lacking organisation. The percentage of CD4 cells that were T-regulatory cells were significantly increased (p50.02) within COPD (16%) follicles compared with smokers (10%) and nonsmokers (8%). In contrast, there was no change (p.0.05) in the percentage of T-regulatory cells in clusters or the subepithelium between groups.Lymphoid follicles in COPD patients have increased T-regulatory cells. Therefore, T-regulatory activity may be altered within COPD lymphoid follicles.

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“…In addition, the surface levels of each of these markers were unchanged in FuT7 Ϫ / Ϫ mice (unpublished data). Finally, we compared the ability of WT-and FuT7 Ϫ / Ϫ -T reg cells T reg cells up-regulate cutaneous homing receptors after antigen-recognition in the peripheral LNs ( 12,19,20 ), and suggests that T reg cell activity in nonlymphoid tissues may be important for their ability to prevent fatal autoimmunity after transfer into neonatal sf mice.…”

Section: Resultsmentioning

confidence: 99%

Foxp3+ regulatory T cells maintain immune homeostasis in the skin

Dudda

Perdue²,

Bachtanian³

et al. 2008

The Journal of Experimental Medicine

165

133

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Tolerance against self-and harmless environmental antigens involves several levels of immune regulation. Whereas deletional mechanisms attempt to purge the B and T cell repertoire of self-reactive specifi cities, antigen-specifi c suppression of autoimmunity by CD4 + Foxp3 + regulatory (T reg) T cells also plays a critical role in maintaining self-tolerance. The importance of T reg cells is highlighted by the severe autoimmunity in humans and mice rendered T reg cell -defi cient because of lesions in the FOXP3 gene, which in mice can be prevented by adoptive transfer of purifi ed T reg cells ( 1 -3 ). In addition, neonatal or adult ablation of T reg cells, or adoptive transfer of T reg cell -depleted CD4 + T cells to immunodefi cient mice rapidly triggers severe autoimmune or infl ammatory disease ( 4 -6 ). Collectively, these data demonstrate that T reg cells are required for both the establishment and maintenance of self-tolerance in vivo.T reg cells can be subdivided based on expression of homing receptors thought to direct their migration to lymphoid versus nonlymphoid tissues ( 7 ). However, the relative contributions of the various T reg cell subsets to the maintenance of self-tolerance are not well defi ned. Several reports have demonstrated that T reg cells function within nonlymphoid sites to restrict T cell responses to foreign antigens during experimentally induced acute infl ammation or infection ( 8 -11 ). In addition, we have shown that mice whose T reg cells lack the chemokine receptor CCR4 develop spontaneous infl ammatory disease in skin and lungs ( 12 ). However, although CCR4 helps direct T cell migration to the skin and lung airways, it may also facilitate interactions between T reg cells and antigenpresenting cells within secondary lymphoid tissues. Thus, the infl ammatory disease in these animals is likely the result of impaired T reg cell function in both lymphoid and nonlymphoid organs, and the importance of nonlymphoid T reg cells in maintaining tolerance in the absence of a strong infl ammatory stimulus has not been adequately addressed.Surface expression of functional E-and Pselectin ligands (E-/P-lig) is required for optimal migration of eff ector T cells to infl amed skin ( 13 ). Interestingly, a high percentage of circulating human and mouse T reg cells express Eand/or P-lig, and Foxp3 + T reg cells make up a large fraction of the CD4 + T cells in normal skin from both humans and mice ( 12,14 ). This Cutaneous immune responses must be tightly controlled to prevent unwanted infl ammation in response to innocuous antigens, while maintaining the ability to combat skin-tropic pathogens. Foxp3 + regulatory T (T reg) cells are potent immune regulators and are found at high frequency in both human and mouse skin. Although T reg cells migrate to the skin and can dampen immune responses during experimentally induced infl ammation or infection, the importance of cutaneous T reg cells for maintaining normal immune homeostasis in the skin has not been addressed. To selectively block T reg cell...

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FoxP3+ T Cells Undergo Conventional First Switch to Lymphoid Tissue Homing Receptors in Thymus but Accelerated Second Switch to Nonlymphoid Tissue Homing Receptors in Secondary Lymphoid Tissues

Cited by 113 publications

References 63 publications

Distinctive role of CCR7 in migration and functional activity of naive‐ and effector/memory‐like Treg subsets

Distinctive role of CCR7 in migration and functional activity of naive‐ and effector/memory‐like Treg subsets

Increased T-regulatory cells within lymphocyte follicles in moderate COPD

Foxp3+ regulatory T cells maintain immune homeostasis in the skin

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