Specific recruitment of regulatory T cells in ovarian carcinoma fosters immune privilege and predicts reduced survival

By T. Curiel, George Coukos, L. Zou, Xavier Alvarez, P. Cheng, P. Mottram, Melina Evdemon-Hogan, J. Conejo-Garcia, Lin Zhang, M. Burow and 11 more. Nature Medicine, 2004

5,364 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/724c40d7c264d44301b1b73826864f49d46fbb46

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In Immunology

Citations in the corpus

Tumor angiogenesis and vascular normalization: alternative therapeutic targets (2017, background): “Furthermore, regulatory T cells (Treg), which are immune-suppressive lymphoid cells, are also preferentially recruited into tumors via the expression of chemotactic factors, such as CCL-22 and CCL-28 in hypoxic areas of the tumor [90].”
PD-L1 (B7-H1) and PD-1 Pathway Blockade for Cancer Therapy: Mechanisms, Response Biomarkers and Combinations (2016, background): “The study of different cancer-infiltrating immune cell subsets, including CD4Foxp3 regulatory T cells (Tregs) (4), antigen-presenting cells (APCs) (5, 6), myeloid-derived suppressor cells (MDSCs) (7), and effector T cell subsets (8–13), and immune signature networks (3) has defined the nature of imm”
T Regulatory Cells: Key Players in Tumor Immune Escape and Angiogenesis (2012, background): “cancer (7), gastric cancer (8), and ovarian cancer (6, 9).”
Regulatory T cells in tumor immunity (2010, background): “1).50 An inflammatory condition in tumors might also recruit Tregs.66 As a mechanism of Treg recruitment to tumors, it has been proposed that tumor cells and tumor infiltrating macrophages produce the chemokine CCL22, which chemoattracts and recruits CD25þCD4þTregs expressing CCR4.”
Regulatory T cells recruited through CCL22/CCR4 are selectively activated in lymphoid infiltrates surrounding primary breast tumors and lead to an adverse clinical outcome. (2009, background): “Blood Treg have been shown to express high CCR4 levels and to selectively migrate in response to CCR4 ligands produced in the tumor microenvironment (14, 31–34), with an in vivo demonstration in ovarian carcinoma of the crucial role of CCL22 in intratumoral Treg recruitment, using a xenograft tumor ”
Functional delineation and differentiation dynamics of human CD4+ T cells expressing the FoxP3 transcription factor. (2009, background): “They play crucial roles in human diseases, such as autoimmune disease, allergy, and cancer (Curiel et al., 2004; Ehrenstein et al., 2004; Kriegel et al., 2004; Miyara et al., 2005; Viglietta et al., 2004).”
B7-H4 expression identifies a novel suppressive macrophage population in human ovarian carcinoma (2006, methodology): “Human T reg cells (26, 47) disable TAA-specifi c T cell immunity (5, 27).”
Radiotherapy and immunotherapy promote tumoral lipid oxidation and ferroptosis via synergistic repression of SLC7A11 (2019, background): “The major immunosuppressive mechanisms in the tumor microenvironment include high PD-L1 expression (39, 40) and regulatory T-cell infiltration (41).”
Epigenetic Control of the foxp3 Locus in Regulatory T Cells (2007, background): “Most notably, presence of Tregs, as defined by gene expression of FOXP3, has been shown to constitute a significant predictive parameter for the clinical outcome in ovarian cancer patients [40,41].”
Radiation-induced CXCL16 release by breast cancer cells attracts effector T cells (2008, background): “Cancer cells produce several chemokines, largely to recruit leukocytes that promote tolerance and immune escape and to aid tumor growth by enhanced angiogenesis (16, 17).”
IFN-γ from lymphocytes induces PD-L1 expression and promotes progression of ovarian cancer (2015, background): “In ovarian cancer, multiple inhibitory mechanisms are present, including regulatory T cells (Curiel et al, 2004; Barnett et al, 2010), tumour-associated macrophages (Zhang et al, 2012), myeloidderived suppressor cells (MDSCs) (Godoy et al, 2013) and inhibitory molecules expressed on tumour cells…”
Immunosuppressive strategies that are mediated by tumor cells. (2007, background): “Interestingly, the authors advanced a step forward demonstrating that Tregs migrate into the tumor site under the influence of the chemokine CCL22, providing convincing evidence that Tregs create a favorable environment for tumor escape (117).”