Helios expression in FoxP3<sup>+</sup>T regulatory cells

Elkord, Eyad; al-Ramadi, Basel K.

doi:10.1517/14712598.2012.711310

Cited by 26 publications

(17 citation statements)

References 19 publications

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“…20,21 For example, Helios 1 Treg frequencies are increased in the peripheral blood of cancer patients, and most carcinoma-infiltrating Tregs are Helios positive. [8][9][10][11][12] In contrast, in premalignant tumors, such as nasal polyposis 13 and respiratory papillomas, 14 most infiltrating Tregs were shown to be Helios negative. Moreover, in type 2 diabetes mellitus, peripheral blood Helios 2 Treg numbers were decreased, although Helios 1 Treg counts were normal, 18 whereas in patients with myasthenia gravis, Helios 1 Treg frequency was lower.…”

Section: Introductionmentioning

confidence: 98%

“…6,7 In mice and man, Helios 1 Tregs represent about 70%, whereas Helios 2 Tregs constitute around 30% of Foxp3 1 T cells in the periphery. 5 However, these frequencies appear differently in malignancies, [8][9][10][11][12][13][14] autoimmunity, [15][16][17][18][19] and after infection. 20,21 For example, Helios 1 Treg frequencies are increased in the peripheral blood of cancer patients, and most carcinoma-infiltrating Tregs are Helios positive.…”

Section: Introductionmentioning

confidence: 99%

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Differential control of Helios+/− Treg development by monocyte subsets through disparate inflammatory cytokines

Zhong

Yazdanbakhsh

2013

Blood

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Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Differential control of Helios+/− Treg development by monocyte subsets through disparate inflammatory cytokines

Zhong

Yazdanbakhsh

2013

Blood

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“…At present, only HELIOS merits attention as a potentially specific marker for human FOXP3 + T cells [27]. Recent studies suggest that HELIOS defines Treg subsets with distinct phenotypic and functional characteristics [28,29].…”

Section: Measurements Of Human Tregmentioning

confidence: 99%

“…Recent studies suggest that HELIOS defines Treg subsets with distinct phenotypic and functional characteristics [28,29]. However, there is considerable controversy as to HELIOS expression on nTregs and iTregs [27], and additional studies are needed to verify its involvement in the Treg development and functions. inducible T-Cell co-stimulator (ICOS), a costimulatory molecule, is found to be overexpressed on the surface of strongly suppressive IL-10-producing Tregs in melanoma-infiltrating T cells [30].…”

Section: Measurements Of Human Tregmentioning

confidence: 99%

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Induced regulatory T cells in inhibitory microenvironments created by cancer

Whiteside

2014

Expert Opinion on Biological Therapy

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Introduction Regulatory T cells (Tregs) accumulating in the peripheral circulation and tumor sites of patients contribute to tumor escape from the host immune system. Tregs encompass subsets of immune cells with distinct phenotypic and functional properties. Whereas natural (n) or thymic-derived (t) Tregs regulate responses to self-antigens, inducible (i) or peripheral (p) Tregs generated and expanded in regulatory microenvironments control immune responses to a broad variety of antigens. Areas covered Tregs accumulating in the tumor microenvironment (TME) are contextually regulated. They acquire phenotypic and functional attributes imposed by the inhibitory molecular pathways operating in situ. Several molecular pathways active in human cancer are reviewed. The pathways may differ from one tumor to another, and environmentally induced Tregs may be functionally distinct. Potential therapeutic strategies for selective silencing of iTregs are considered in the light of the newly acquired understanding of their phenotypic and functional diversity. Expert opinion Human Tregs accumulating in cancer comprise ‘bad’ subsets, which inhibit antitumor immunity, and ‘good’ anti-inflammatory subsets, which maintain tolerance to self and benefit the host. Future therapeutic strategies targeting Tregs will need to discriminate between these Treg subsets and will need to consider reprogramming strategies instead of Treg elimination. Re-establishment of effective antitumor immune responses in cancer patients without disturbing a normal homeostatic T-cell balance will greatly benefit from insights into inhibitory pathways engaged by human tumors.

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Neuropilin 1: function and therapeutic potential in cancer

Chaudhary

Khaled

Ammori

et al. 2013

Cancer Immunol Immunother

190

175

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Neuropilin 1 (NRP1) is a transmembrane glycoprotein that acts as a co-receptor for a number of extracellular ligands including class III/IV semaphorins, certain isoforms of vascular endothelial growth factor and transforming growth factor beta. An exact understanding of the role of NRP1 in the immune system has been obscured by the differences in NRP1 expression observed between mice and humans. In mice, NRP1 is selectively expressed on thymic-derived Tregs and greatly enhances immunosuppressive function. In humans, NRP1 is expressed on plasmacytoid dendritic cells (pDCs) where it aids in priming immune responses and on a subset of T regulatory cells (Tregs) isolated from secondary lymph nodes. Preliminary studies that show NRP1 expression on T cells confers enhanced immunosuppressive activity. However, the mechanism by which this activity is mediated remains unclear. NRP1 expression has also been identified on activated T cells and Tregs isolated from inflammatory microenvironments, suggesting NRP1 might represent a novel T cell activation marker. Of clinical interest, NRP1 may enhance Treg tumour infiltration and a decrease in NRP1+ Tregs correlates with successful chemotherapy, suggesting a specific role for NRP1 in cancer pathology. As a therapeutic target, NRP1 allows simultaneous targeting of NRP1-expressing tumour vasculature, NRP1+ Tregs and pDCs. With the development of anti-NRP1 monoclonal antibodies and cell-penetrating peptides, NRP1 represents a promising new target for cancer therapies. This paper reviews current knowledge on the role and function of NRP1 in Tregs and pDCs, both in physiological and cancer settings, as well as its potential as a therapeutic target in cancer.

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Helios expression in FoxP3⁺T regulatory cells

Cited by 26 publications

References 19 publications

Differential control of Helios+/− Treg development by monocyte subsets through disparate inflammatory cytokines

Differential control of Helios+/− Treg development by monocyte subsets through disparate inflammatory cytokines

Induced regulatory T cells in inhibitory microenvironments created by cancer

Neuropilin 1: function and therapeutic potential in cancer

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Helios expression in FoxP3+T regulatory cells

Cited by 26 publications

References 19 publications

Differential control of Helios+/− Treg development by monocyte subsets through disparate inflammatory cytokines

Differential control of Helios+/− Treg development by monocyte subsets through disparate inflammatory cytokines

Induced regulatory T cells in inhibitory microenvironments created by cancer

Neuropilin 1: function and therapeutic potential in cancer

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Helios expression in FoxP3⁺T regulatory cells