CD8+ suppressor T cells resurrected

Kapp, Judith A.; Bucy, R. Pat

doi:10.1016/j.humimm.2008.07.018

Cited by 46 publications

(35 citation statements)

References 82 publications

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“…[65][66][67][68][69] Since first defining T cells Ϸ4 decades ago, the classification of these cells has dramatically changed. Today, not only surface …”

Section: No Easy History: T-cell Discovery and Lessons Learned From Imentioning

confidence: 99%

Endothelial-Regenerating Cells

2010

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Abstract-Atherosclerosis is the most common cause for cardiovascular diseases and is based on endothelial dysfunction.A growing body of evidence suggests the contribution of bone marrow-derived endothelial progenitor cells, monocytic cells, and mature endothelial cells to vessel formation and endothelial rejuvenation. To this day, various subsets of these endothelial-regenerating cells have been identified according to cellular origin, phenotype, and properties in vivo and in vitro. However, the definition and biology, especially of endothelial progenitor cells, is complex and under heavy debate. In this review, we focus on current definitions of endothelial progenitor cells, highlight the clinical relevance of endothelial-regenerating cells, and provide new insights into cell-cell interactions involved in endothelial cell rejuvenation. (Hypertension. 2010;55:593-599.)

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“…[65][66][67][68][69] Since first defining T cells Ϸ4 decades ago, the classification of these cells has dramatically changed. Today, not only surface …”

Section: No Easy History: T-cell Discovery and Lessons Learned From Imentioning

confidence: 99%

Endothelial-Regenerating Cells

2010

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“…Such animals develop a severe systemic inflammatory disorder leading to early lethality. However, in addition to its suppressive effects on "conventional" α/β T cell receptor CD4 + and CD8 + T cells, TGF-β, in concert with specific combinations of cytokines, can also promote the development of specific types of both pro-and antiinflammatory T cells, including Th17, Tc17, Tregs, and certain T suppressor (Ts) cell subsets (11)(12)(13)(14)(15)(16). The Th17 subset, a population that normally resides in the lining of the gut, can also originate from activated T cell populations upon exposure to specific combinations of cytokines (11).…”

Section: Introductionmentioning

confidence: 99%

Smad4 deficiency in T cells leads to the Th17-associated development of premalignant gastroduodenal lesions in mice

Hahn¹,

Falck²,

Jirik³

2011

J. Clin. Invest.

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While there is evidence that specific T cell populations can promote the growth of established tumors, instances where T cell activity causes neoplasms to arise de novo are infrequent. Here, we employed two conditional mutagenesis systems to delete the TGF-β signaling pathway component Smad4 in T cells and observed the spontaneous development of massive polyps within the gastroduodenal regions of mice. The epithelial lesions contained increased levels of transcripts encoding IL-11, IL-6, TGF-β, IL-1β, and TNF-α, and lamina propria cells isolated from lesions contained abundant IL-17A + CD4 + T cells. Furthermore, we found that Smad4 deficiency attenuated TGF-β-mediated in vitro polarization of FoxP3 + CD4 + T cells, but not IL-17A + CD4 + T cells, suggesting that the epithelial lesions may have arisen as a consequence of unchecked Th17 cell activity. Proinflammatory cytokine production likely accounted for the raised levels of IL-11, a cytokine known to promote gastric epithelial cell survival and hyperplasia. Consistent with IL-11 having a pathogenic role in this model, we found evidence of Stat3 activation in the gastric polyps. Thus, our data indicate that a chronic increase in gut Th17 cell activity can be associated with the development of premalignant lesions of the gastroduodenal region.

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“…Although CD8 C T suppressor cells (CD8 C Ts, also called CD8 C Tregs) were first described decades ago, the study of these cells has attracted less attention, 43,46,47 Several phenotypic markers of CD8 C Tregs are found in different systems and include CD28 -, CD25…”

Section: Cd8mentioning

confidence: 99%

Mutual interaction between BCL6 and microRNAs in T cell differentiation

Wei

Gao

et al. 2015

RNA Biology

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y Contributed equally to this work T he transcription factor B-cell CLL/ lymphoma 6 (BCL6) and the regulatory factor microRNAs (miRNAs) are of great importance in the differentiation of T cell subsets. An increasing body of evidence has demonstrated that BCL6 and miRNAs can target one another and mutually adjust their expression in T cell subsets, such as T helper (Th)-2, Th17, CD8C regulatory T (CD8CTreg) and T follicular helper (Tfh) cells. Here, we discuss the most recent advances and emerging concepts in how BCL6 and miRNAs regulate one another, and the effects of such mutual regulations on T cell subset differentiation.

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CD8+ suppressor T cells resurrected

Cited by 46 publications

References 82 publications

Endothelial-Regenerating Cells

Endothelial-Regenerating Cells

Smad4 deficiency in T cells leads to the Th17-associated development of premalignant gastroduodenal lesions in mice

Mutual interaction between BCL6 and microRNAs in T cell differentiation

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