NDLI: Protective role of the inflammatory CCR2/CCL2 chemokine pathway through recruitment of type 1 cytotoxic Î³Î´ T lymphocytes to tumor beds.

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Age-associated changes in the differentiation potentials of human circulating hematopoietic progenitors to T- or NK-lineage cells.

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Critical roles of a dendritic cell subset expressing a chemokine receptor, XCR1.

TLR3-triggered reactive oxygen species contribute to inflammatory responses by activating signal transducer and activator of transcription-1.

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Spontaneous miscarriages are explained by the stress/glucocorticoid/lipoxin A4 axis.

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Dipeptidyl peptidase IV is a human and murine neutrophil chemorepellent.

Pseudogout-associated inflammatory calcium pyrophosphate dihydrate microcrystals induce formation of neutrophil extracellular traps.

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Cross talk between follicular Th cells and tumor cells in human follicular lymphoma promotes immune evasion in the tumor microenvironment.

Protective role of the inflammatory CCR2/CCL2 chemokine pathway through recruitment of type 1 cytotoxic Î³Î´ T lymphocytes to tumor beds.

Reciprocal negative cross-talk between liver X receptors (LXRs) and STAT1: effects on IFN-Î³-induced inflammatory responses and LXR-dependent gene expression.

Recent thymic emigrants and mature naive T cells exhibit differential DNA methylation at key cytokine loci.

Helicobacter pylori infection inhibits phagocyte clearance of apoptotic gastric epithelial cells.

Antigen-specific effector CD4 T lymphocytes school lamina propria dendritic cells to transfer innate tolerance.

CD40 mediates downregulation of CD32B on specific memory B cell populations in rheumatoid arthritis.

GB virus C particles inhibit T cell activation via envelope E2 protein-mediated inhibition of TCR signaling.

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MicroRNA-155 confers encephalogenic potential to Th17 cells by promoting effector gene expression.

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Transglutaminase 2-specific autoantibodies in celiac disease target clustered, N-terminal epitopes not displayed on the surface of cells.

Superantigen-induced steroid resistance depends on activation of phospholipase Cß2.

T cell costimulation with anti-CD137 monoclonal antibodies is mediated by K63-polyubiquitin-dependent signals from endosomes.

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Comment on 'TLR9 provokes inflammation in response to fetal DNA: mechanism for fetal loss in preterm birth and preeclampsia'.

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Response to comment on 'Induced IL-17-producing invariant NKT cells require activation in presence of TGF-ß and IL-1ß'.

What is and what should always have been: long-lived plasma cells induced by T cell-independent antigens.

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Protective role of the inflammatory CCR2/CCL2 chemokine pathway through recruitment of type 1 cytotoxic Î³Î´ T lymphocytes to tumor beds.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Costa, Maria Fernanda Rei, Margarida Grosso, Ana Rita Silva-Santos, Bruno Lança, Telma Penido, Carmen Gonçalves-Sousa, Natacha
Description	Country affiliation: Portugal Author Affiliation: Lança T ( Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, 1649-028 Lisbon, Portugal.)
Abstract	Tumor-infiltrating lymphocytes (TILs) are important prognostic factors in cancer progression and key players in cancer immunotherapy. Although Î³Î´ T lymphocytes can target a diversity of tumor cell types, their clinical manipulation is hampered by our limited knowledge of the molecular cues that determine Î³Î´ T cell migration toward tumors in vivo. In this study we set out to identify the chemotactic signals that orchestrate tumor infiltration by Î³Î´ T cells. We have used the preclinical transplantable B16 melanoma model to profile chemokines in tumor lesions and assess their impact on Î³Î´ TIL recruitment in vivo. We show that the inflammatory chemokine CCL2 and its receptor CCR2 are necessary for the accumulation of Î³Î´ TILs in B16 lesions, where they produce IFN-Î³ and display potent cytotoxic functions. Moreover, CCL2 directed Î³Î´ T cell migration in vitro toward tumor extracts, which was abrogated by anti-CCL2 neutralizing Abs. Strikingly, the lack of Î³Î´ TILs in TCRÎ´-deficient but also in CCR2-deficient mice enhanced tumor growth in vivo, thus revealing an unanticipated protective role for CCR2/CCL2 through the recruitment of Î³Î´ T cells. Importantly, we demonstrate that human VÎ´1 T cells, but not their VÎ´2 counterparts, express CCR2 and migrate to CCL2, whose expression is strongly deregulated in multiple human tumors of diverse origin, such as lung, prostate, liver, or breast cancer. This work identifies a novel protective role for CCL2/CCR2 in the tumor microenvironment, while opening new perspectives for modulation of human VÎ´1 T cells in cancer immunotherapy.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	12
Volume Number	190
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-06-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Chemokine Ccl2 Immunology Lymphocytes, Tumor-infiltrating Neoplasms, Experimental Receptors, Ccr2 T-lymphocytes, Cytotoxic Animals Flow Cytometry Inflammation Mice Mice, Inbred C57bl Real-time Polymerase Chain Reaction Receptors, Antigen, T-cell, Gamma-delta Signal Transduction T-lymphocyte Subsets Tumor Microenvironment Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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