Systemic inflammatory response and downmodulation of peripheral CD25+Foxp3+ T-regulatory cells in patients undergoing radiofrequency thermal ablation for lung cancer

Fietta, A.; Morosini, Monica; Passadore, Ileana; Cascina, Alessandro; Draghi, P.; Dore, Roberto; Rossi, Sandro; Pozzi, Ernesto; Meloni, Federica

doi:10.1016/j.humimm.2009.03.012

Cited by 98 publications

(82 citation statements)

References 42 publications

(54 reference statements)

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“…However, none are Treg-specific, and all show only modest efficacy that may reflect co-targeting of activated effector T cells (Antony et al, 2005, Attia et al, 2005, Knutson et al, 2006). These various approaches also bring increased risks of autoimmunity (Dranoff, 2005) or inflammatory toxicity (Fietta et al, 2009), and have only transient effects (Powell et al, 2007). …”

Section: Introductionmentioning

confidence: 99%

Ubiquitin-specific Protease-7 Inhibition Impairs Tip60-dependent Foxp3 + T-regulatory Cell Function and Promotes Antitumor Immunity

et al. 2016

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Foxp3 + T-regulatory (Treg) cells are known to suppress protective host immune responses to a wide variety of solid tumors, but their therapeutic targeting is largely restricted to their transient depletion or “secondary” modulation, e.g. using anti-CTLA-4 monoclonal antibody. Our ongoing studies of the post-translational modifications that regulate Foxp3 demonstrated that the histone/protein acetyltransferase, Tip60, plays a dominant role in promoting acetylation, dimerization and function in Treg cells. We now show that the ubiquitin-specific protease, Usp7, controls Treg function largely by stabilizing the expression and promoting the multimerization of Tip60 and Foxp3. Genetic or pharmacologic targeting of Usp7 impairs Foxp3 + Treg suppressive functions, while conventional T cell responses remain intact. As a result, pharmacologic inhibitors of Usp7 can limit tumor growth in immunocompetent mice, and promote the efficacy of antitumor vaccines and immune checkpoint therapy with anti-PD1 monoclonal antibody in murine models. Hence, pharmacologic therapy with Usp7 inhibitors may have an important role in future cancer immunotherapy.

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Section: Introductionmentioning

confidence: 99%

Ubiquitin-specific Protease-7 Inhibition Impairs Tip60-dependent Foxp3 + T-regulatory Cell Function and Promotes Antitumor Immunity

et al. 2016

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“…Progression and recurrence of HNSCC and other malignancies are associated with severe immune dysfunction [3, 4]. Tumor-infiltrating FoxP3 + CD25 + CD4 + regulatory T (Treg) cells can promote local tumor growth through exerting immunosuppressive activities against tumor-associated antigen (TAA) T cell responses [3, 5–11]. Thus, tumor-infiltrating Treg cells are a major obstacle in cancer immunotherapy [9, 10, 12–14].…”

Section: Introductionmentioning

confidence: 99%

Blockade of MCP-1/CCR4 signaling-induced recruitment of activated regulatory cells evokes an antitumor immune response in head and neck squamous cell carcinoma

Sun

Wei

et al. 2016

Oncotarget

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FoxP3+ regulatory T (Treg) cells have diverse functions in the suppression of antitumor immunity. We show that FoxP3hiCD45RA−CD4+ Treg cells [activated Treg (aTreg) cells] are the predominant cell population among tumor-infiltrating FoxP3+ T cells, and that high aTreg cell-infiltrating content is associated with reduced survival in patients with head and neck squamous cell carcinoma (HNSCC). In vitro studies have demonstrated that aTreg cells can suppress tumor-associated antigen (TAA) effector T cell immune responses in HNSCC. Moreover, C-C chemokine receptor 4 (CCR4) was specifically expressed by aTreg cells in the peripheral blood of HNSCC patients. Using a RayBiotech human chemokine antibody array, we showed that monocyte chemoattractant protein-1 (MCP-1), an endogenous CCR4-binding ligand, was specifically upregulated in the HNSCC microenvironment compared to the other four CCR4-binding ligands. Blocking MCP-1/CCR4 signaling-induced aTreg cell recruitment using a CCR4 antagonist evoked antitumor immunity in mice, and lead to inhibition of tumor growth and prolonged survival. Therefore, blocking aTreg cell trafficking in tumors using CCR4-binding agents may be an effective immunotherapy for HNSCC.

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“…In both in vitro and in vivo studies, IL-34 directly modulates the number and function of monocytes and regulates myeloid cell growth and differentiation. We believe that the immunological effects of IL-34 candidate this interleukin as an immunotherapeutic agent for the treatment of several different diseases (20,(26)(27)(28)(29)(30)(31)(32)(33)(34). To discover the receptor for IL-34, a collection ofextracellular domains oftrans-membrane proteins has been used which is a known cytokine receptor called colony-stimulating factor 1 receptor or macrophage colony-stimulating factor receptor (35)(36)(37)(38).…”

mentioning

confidence: 99%

IL-34 a Newly Discovered Cytokine

et al. 2010

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In this study we describe some biological effects of IL-34, a newly discovered cytokine. We show that 11-34 stimulates monocyte cell viability and directly modulates the number and function of monocytes and regulates myeloid cell growth and differentiation. Moreover, since IL-34 in mice is involved in osteoporosis, an antagonist of this cytokine could be beneficial for the treatment of this disease.Cytokines are immune-regulatory proteins (1-4) and they induce inflammation in vivo, based on recruitment of white blood cell population (5-7). These cytokines include IL-2, IL-4, IL-7, IL-9, IL-ll, IL-12, IL-13, IL-15 ... .IL-35 and Colony Stimulating Factors (CSFs) and many others. They are multifunctional proteins which have a role in both innate and adaptive immune responses (8-13) with an effect on proliferation, differentiation, inhibition, apoptosis and chemoattraction (14-16). In addition, cytokines are involved in and mediate many different diseases (17-18).The newly-characterized Interleukin-34 (IL-34) plays a central role in innate immunity and adaptive immunity, and is an important molecule for the communication between cells, tissues, and organs.Recently it has been reported that interleukin-34 (lL-34) stimulates monocyte viability but does not affect responses in a wide spectrum ofother assays (20)(21)(22)(23)(24)(25). In both in vitro and in vivo studies, IL-34 directly modulates the number and function of monocytes and regulates myeloid cell growth and differentiation. We believe that the immunological effects of IL-34 candidate this interleukin as an immunotherapeutic agent for the treatment of several different diseases (20,(26)(27)(28)(29)(30)(31)(32)(33)(34). To discover the receptor for IL-34, a collection ofextracellular domains oftrans-membrane proteins has been used which is a known cytokine receptor called colony-stimulating factor 1 receptor or macrophage colony-stimulating factor receptor

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Systemic inflammatory response and downmodulation of peripheral CD25+Foxp3+ T-regulatory cells in patients undergoing radiofrequency thermal ablation for lung cancer

Cited by 98 publications

References 42 publications

Ubiquitin-specific Protease-7 Inhibition Impairs Tip60-dependent Foxp3 + T-regulatory Cell Function and Promotes Antitumor Immunity

Ubiquitin-specific Protease-7 Inhibition Impairs Tip60-dependent Foxp3 + T-regulatory Cell Function and Promotes Antitumor Immunity

Blockade of MCP-1/CCR4 signaling-induced recruitment of activated regulatory cells evokes an antitumor immune response in head and neck squamous cell carcinoma

IL-34 a Newly Discovered Cytokine

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