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Article ; Online: CXCR5

Tyllis, Timona S / Fenix, Kevin A / Norton, Todd S / Kara, Ervin E / McKenzie, Duncan R / David, Shannon C / Alsharifi, Mohammed / Yu, Di / McColl, Shaun R / Comerford, Iain

Frontiers in immunology

2021 Volume 12, Page(s) 626199

Abstract: Crosstalk between T and B cells is crucial for generating high-affinity, class-switched antibody responses. The roles of ... ...

Abstract	Crosstalk between T and B cells is crucial for generating high-affinity, class-switched antibody responses. The roles of CD4
MeSH term(s)	Animals ; Antibody Formation ; B-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/immunology ; Humans ; Immunization ; Influenza A virus/physiology ; Influenza, Human/immunology ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Orthomyxoviridae Infections/immunology ; Ovalbumin/immunology ; Receptors, CXCR5/genetics ; Receptors, CXCR5/metabolism
Chemical Substances	CXCR5 protein, mouse ; Receptors, CXCR5 ; Ovalbumin (9006-59-1)
Language	English
Publishing date	2021-07-13
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.626199
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Article ; Online: ACKR4 restrains antitumor immunity by regulating CCL21.

Whyte, Carly E / Osman, Maleika / Kara, Ervin E / Abbott, Caitlin / Foeng, Jade / McKenzie, Duncan R / Fenix, Kevin A / Harata-Lee, Yuka / Foyle, Kerrie L / Boyle, Sarah T / Kochetkova, Marina / Aguilera, Amelia Roman / Hou, Jiajie / Li, Xian-Yang / Armstrong, Mark A / Pederson, Stephen M / Comerford, Iain / Smyth, Mark J / McColl, Shaun R

The Journal of experimental medicine

2020 Volume 217, Issue 6

Abstract: Current immunotherapies involving CD8+ T cell responses show remarkable promise, but their efficacy in many solid tumors is limited, in part due to the low frequency of tumor-specific T cells in the tumor microenvironment (TME). Here, we identified a ... ...

Abstract	Current immunotherapies involving CD8+ T cell responses show remarkable promise, but their efficacy in many solid tumors is limited, in part due to the low frequency of tumor-specific T cells in the tumor microenvironment (TME). Here, we identified a role for host atypical chemokine receptor 4 (ACKR4) in controlling intratumor T cell accumulation and activation. In the absence of ACKR4, an increase in intratumor CD8+ T cells inhibited tumor growth, and nonhematopoietic ACKR4 expression was critical. We show that ACKR4 inhibited CD103+ dendritic cell retention in tumors through regulation of the intratumor abundance of CCL21. In addition, preclinical studies indicate that ACKR4 and CCL21 are potential therapeutic targets to enhance responsiveness to immune checkpoint blockade or T cell costimulation.
MeSH term(s)	Animals ; Antigens, CD/metabolism ; CD8-Positive T-Lymphocytes/immunology ; Cell Proliferation ; Chemokine CCL21/metabolism ; Dendritic Cells/immunology ; Disease Models, Animal ; Humans ; Immune Checkpoint Inhibitors/pharmacology ; Immunity ; Integrin alpha Chains/metabolism ; Mice, Inbred C57BL ; Neoplasm Metastasis ; Neoplasms/genetics ; Neoplasms/immunology ; Receptors, CCR/metabolism ; Stromal Cells/metabolism ; Survival Analysis
Chemical Substances	Ackr4 protein, mouse ; Antigens, CD ; Chemokine CCL21 ; Immune Checkpoint Inhibitors ; Integrin alpha Chains ; Receptors, CCR ; alpha E integrins
Language	English
Publishing date	2020-04-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20190634
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Article ; Online: Tailored immune responses: novel effector helper T cell subsets in protective immunity.

Kara, Ervin E / Comerford, Iain / Fenix, Kevin A / Bastow, Cameron R / Gregor, Carly E / McKenzie, Duncan R / McColl, Shaun R

PLoS pathogens

2014 Volume 10, Issue 2, Page(s) e1003905

Abstract: Differentiation of naïve CD4⁺ cells into functionally distinct effector helper T cell subsets, characterised by distinct "cytokine signatures," is a cardinal strategy employed by the mammalian immune system to efficiently deal with the rapidly evolving ... ...

Abstract	Differentiation of naïve CD4⁺ cells into functionally distinct effector helper T cell subsets, characterised by distinct "cytokine signatures," is a cardinal strategy employed by the mammalian immune system to efficiently deal with the rapidly evolving array of pathogenic microorganisms encountered by the host. Since the T(H)1/T(H)2 paradigm was first described by Mosmann and Coffman, research in the field of helper T cell biology has grown exponentially with seven functionally unique subsets having now been described. In this review, recent insights into the molecular mechanisms that govern differentiation and function of effector helper T cell subsets will be discussed in the context of microbial infections, with a focus on how these different helper T cell subsets orchestrate immune responses tailored to combat the nature of the pathogenic threat encountered.
MeSH term(s)	Adaptive Immunity/immunology ; Animals ; Cell Differentiation/immunology ; Humans ; T-Lymphocyte Subsets/cytology ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes, Helper-Inducer/cytology ; T-Lymphocytes, Helper-Inducer/immunology
Language	English
Publishing date	2014-02-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7374
ISSN (online)	1553-7374
ISSN	1553-7374
DOI	10.1371/journal.ppat.1003905
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Article ; Online: Distinct chemokine receptor axes regulate Th9 cell trafficking to allergic and autoimmune inflammatory sites.

Kara, Ervin E / Comerford, Iain / Bastow, Cameron R / Fenix, Kevin A / Litchfield, Wendel / Handel, Tracy M / McColl, Shaun R

Journal of immunology (Baltimore, Md. : 1950)

2013 Volume 191, Issue 3, Page(s) 1110–1117

Abstract: Migration of Th cells to peripheral sites of inflammation is essential for execution of their effector function. The recently described Th9 subset characteristically produces IL-9 and has been implicated in both allergy and autoimmunity. Despite this, ... ...

Abstract	Migration of Th cells to peripheral sites of inflammation is essential for execution of their effector function. The recently described Th9 subset characteristically produces IL-9 and has been implicated in both allergy and autoimmunity. Despite this, the migratory properties of Th9 cells remain enigmatic. In this study, we examined chemokine receptor usage by Th9 cells and demonstrate, in models of allergy and autoimmunity, that these cells express functional CCR3, CCR6, and CXCR3, chemokine receptors commonly associated with other, functionally opposed effector Th subsets. Most Th9 cells that express CCR3 also express CXCR3 and CCR6, and expression of these receptors appears to account for the recruitment of Th9 cells to disparate inflammatory sites. During allergic inflammation, Th9 cells use CCR3 and CCR6, but not CXCR3, to home to the peritoneal cavity, whereas Th9 homing to the CNS during experimental autoimmune encephalomyelitis involves CXCR3 and CCR6 but not CCR3. To our knowledge, these data provide the first insights into regulation of Th9 cell trafficking in allergy and autoimmunity.
MeSH term(s)	Animals ; Autoimmunity/immunology ; Cell Movement/immunology ; Chemotaxis, Leukocyte/immunology ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Encephalomyelitis, Autoimmune, Experimental/metabolism ; Hypersensitivity/immunology ; Inflammation/immunology ; Interleukin-9 ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Receptors, CCR3/biosynthesis ; Receptors, CCR3/metabolism ; Receptors, CCR6/biosynthesis ; Receptors, CCR6/metabolism ; Receptors, CXCR3/biosynthesis ; Receptors, CXCR3/metabolism ; Receptors, Lymphocyte Homing/immunology ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism ; T-Lymphocytes, Helper-Inducer/immunology ; T-Lymphocytes, Helper-Inducer/metabolism
Chemical Substances	CCR6 protein, mouse ; Ccr3 protein, mouse ; Cxcr3 protein, mouse ; Interleukin-9 ; Receptors, CCR3 ; Receptors, CCR6 ; Receptors, CXCR3 ; Receptors, Lymphocyte Homing
Language	English
Publishing date	2013-06-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1203089
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Article ; Online: IL-17-producing γδ T cells switch migratory patterns between resting and activated states.

McKenzie, Duncan R / Kara, Ervin E / Bastow, Cameron R / Tyllis, Timona S / Fenix, Kevin A / Gregor, Carly E / Wilson, Jasmine J / Babb, Rachelle / Paton, James C / Kallies, Axel / Nutt, Stephen L / Brüstle, Anne / Mack, Matthias / Comerford, Iain / McColl, Shaun R

Nature communications

2017 Volume 8, Page(s) 15632

Abstract: Interleukin 17-producing γδ T (γδT17) cells have unconventional trafficking characteristics, residing in mucocutaneous tissues but also homing into inflamed tissues via circulation. Despite being fundamental to γδT17-driven early protective immunity and ... ...

Abstract	Interleukin 17-producing γδ T (γδT17) cells have unconventional trafficking characteristics, residing in mucocutaneous tissues but also homing into inflamed tissues via circulation. Despite being fundamental to γδT17-driven early protective immunity and exacerbation of autoimmunity and cancer, migratory cues controlling γδT17 cell positioning in barrier tissues and recruitment to inflammatory sites are still unclear. Here we show that γδT17 cells constitutively express chemokine receptors CCR6 and CCR2. While CCR6 recruits resting γδT17 cells to the dermis, CCR2 drives rapid γδT17 cell recruitment to inflamed tissues during autoimmunity, cancer and infection. Downregulation of CCR6 by IRF4 and BATF upon γδT17 activation is required for optimal recruitment of γδT17 cells to inflamed tissue by preventing their sequestration into uninflamed dermis. These findings establish a lymphocyte trafficking model whereby a hierarchy of homing signals is prioritized by dynamic receptor expression to drive both tissue surveillance and rapid recruitment of γδT17 cells to inflammatory lesions.
MeSH term(s)	Animals ; Basic-Leucine Zipper Transcription Factors/metabolism ; Cell Movement ; Chemokines/metabolism ; Chemotaxis ; Down-Regulation ; Female ; Homeostasis ; Inflammation ; Interferon Regulatory Factors/metabolism ; Interleukin-17/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Receptors, Antigen, T-Cell, gamma-delta/immunology ; Receptors, CCR2/metabolism ; Receptors, CCR6/metabolism ; Spleen/cytology ; T-Lymphocyte Subsets/cytology
Chemical Substances	Basic-Leucine Zipper Transcription Factors ; Batf protein, mouse ; CCR6 protein, mouse ; Ccr2 protein, mouse ; Chemokines ; Interferon Regulatory Factors ; Interleukin-17 ; Receptors, Antigen, T-Cell, gamma-delta ; Receptors, CCR2 ; Receptors, CCR6 ; interferon regulatory factor-4
Language	English
Publishing date	2017-06-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2041-1723
ISSN (online)	2041-1723
DOI	10.1038/ncomms15632
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Article ; Online: Atypical chemokine receptor 4 shapes activated B cell fate.

The Journal of experimental medicine

2018 Volume 215, Issue 3, Page(s) 801–813

Abstract: Activated B cells can initially differentiate into three functionally distinct fates-early plasmablasts (PBs), germinal center (GC) B cells, or early memory B cells-by mechanisms that remain poorly understood. Here, we identify atypical chemokine ... ...

Abstract	Activated B cells can initially differentiate into three functionally distinct fates-early plasmablasts (PBs), germinal center (GC) B cells, or early memory B cells-by mechanisms that remain poorly understood. Here, we identify atypical chemokine receptor 4 (ACKR4), a decoy receptor that binds and degrades CCR7 ligands CCL19/CCL21, as a regulator of early activated B cell differentiation. By restricting initial access to splenic interfollicular zones (IFZs), ACKR4 limits the early proliferation of activated B cells, reducing the numbers available for subsequent differentiation. Consequently, ACKR4 deficiency enhanced early PB and GC B cell responses in a CCL19/CCL21-dependent and B cell-intrinsic manner. Conversely, aberrant localization of ACKR4-deficient activated B cells to the IFZ was associated with their preferential commitment to the early PB linage. Our results reveal a regulatory mechanism of B cell trafficking via an atypical chemokine receptor that shapes activated B cell fate.
MeSH term(s)	Animals ; Antigens/metabolism ; B-Lymphocytes/cytology ; B-Lymphocytes/metabolism ; Cell Lineage ; Cell Proliferation ; Germinal Center/metabolism ; Mice, Inbred C57BL ; Receptors, CCR/metabolism ; Spleen/cytology
Chemical Substances	Ackr4 protein, mouse ; Antigens ; Receptors, CCR
Language	English
Publishing date	2018-01-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20171067
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Article ; Online: CCR2 defines in vivo development and homing of IL-23-driven GM-CSF-producing Th17 cells.

Kara, Ervin E / McKenzie, Duncan R / Bastow, Cameron R / Gregor, Carly E / Fenix, Kevin A / Ogunniyi, Abiodun D / Paton, James C / Mack, Matthias / Pombal, Diana R / Seillet, Cyrill / Dubois, Bénédicte / Liston, Adrian / MacDonald, Kelli P A / Belz, Gabrielle T / Smyth, Mark J / Hill, Geoffrey R / Comerford, Iain / McColl, Shaun R

Nature communications

2015 Volume 6, Page(s) 8644

Abstract: IL-17-producing helper T (Th17) cells are critical for host defense against extracellular pathogens but also drive numerous autoimmune diseases. Th17 cells that differ in their inflammatory potential have been described including IL-10-producing Th17 ... ...

Abstract	IL-17-producing helper T (Th17) cells are critical for host defense against extracellular pathogens but also drive numerous autoimmune diseases. Th17 cells that differ in their inflammatory potential have been described including IL-10-producing Th17 cells that are weak inducers of inflammation and highly inflammatory, IL-23-driven, GM-CSF/IFNγ-producing Th17 cells. However, their distinct developmental requirements, functions and trafficking mechanisms in vivo remain poorly understood. Here we identify a temporally regulated IL-23-dependent switch from CCR6 to CCR2 usage by developing Th17 cells that is critical for pathogenic Th17 cell-driven inflammation in experimental autoimmune encephalomyelitis (EAE). This switch defines a unique in vivo cell surface signature (CCR6(-)CCR2(+)) of GM-CSF/IFNγ-producing Th17 cells in EAE and experimental persistent extracellular bacterial infection, and in humans. Using this signature, we identify an IL-23/IL-1/IFNγ/TNFα/T-bet/Eomesodermin-driven circuit driving GM-CSF/IFNγ-producing Th17 cell formation in vivo. Thus, our data identify a unique cell surface signature, trafficking mechanism and T-cell intrinsic regulators of GM-CSF/IFNγ-producing Th17 cells.
MeSH term(s)	Animals ; Cell Differentiation ; Encephalomyelitis, Autoimmune, Experimental/genetics ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Encephalomyelitis, Autoimmune, Experimental/physiopathology ; Granulocyte-Macrophage Colony-Stimulating Factor/immunology ; Humans ; Interferon-gamma/genetics ; Interferon-gamma/immunology ; Interleukin-23/genetics ; Interleukin-23/immunology ; Mice, Inbred C57BL ; Mice, Knockout ; Receptors, CCR2/genetics ; Receptors, CCR2/immunology ; Receptors, CCR6/genetics ; Receptors, CCR6/immunology ; T-Box Domain Proteins/genetics ; T-Box Domain Proteins/immunology ; Th17 Cells/cytology ; Th17 Cells/immunology ; Tumor Necrosis Factors/genetics ; Tumor Necrosis Factors/immunology
Chemical Substances	CCR6 protein, mouse ; Ccr2 protein, mouse ; Eomes protein, mouse ; Interleukin-23 ; Receptors, CCR2 ; Receptors, CCR6 ; T-Box Domain Proteins ; T-box transcription factor TBX21 ; Tumor Necrosis Factors ; Interferon-gamma (82115-62-6) ; Granulocyte-Macrophage Colony-Stimulating Factor (83869-56-1)
Language	English
Publishing date	2015-10-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/ncomms9644
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Article ; Online: CXCR5(+) follicular cytotoxic T cells control viral infection in B cell follicles.

Leong, Yew Ann / Chen, Yaping / Ong, Hong Sheng / Wu, Di / Man, Kevin / Deleage, Claire / Minnich, Martina / Meckiff, Benjamin J / Wei, Yunbo / Hou, Zhaohua / Zotos, Dimitra / Fenix, Kevin A / Atnerkar, Anurag / Preston, Simon / Chipman, Jeffrey G / Beilman, Greg J / Allison, Cody C / Sun, Lei / Wang, Peng /

Xu, Jiawei / Toe, Jesse G / Lu, Hao K / Tao, Yong / Palendira, Umaimainthan / Dent, Alexander L / Landay, Alan L / Pellegrini, Marc / Comerford, Iain / McColl, Shaun R / Schacker, Timothy W / Long, Heather M / Estes, Jacob D / Busslinger, Meinrad / Belz, Gabrielle T / Lewin, Sharon R / Kallies, Axel / Yu, Di

Nature immunology

2016 Volume 17, Issue 10, Page(s) 1187–1196

Abstract: During unresolved infections, some viruses escape immunological control and establish a persistant reservoir in certain cell types, such as human immunodeficiency virus (HIV), which persists in follicular helper T cells (TFH cells), and Epstein-Barr ... ...

Abstract	During unresolved infections, some viruses escape immunological control and establish a persistant reservoir in certain cell types, such as human immunodeficiency virus (HIV), which persists in follicular helper T cells (TFH cells), and Epstein-Barr virus (EBV), which persists in B cells. Here we identified a specialized group of cytotoxic T cells (TC cells) that expressed the chemokine receptor CXCR5, selectively entered B cell follicles and eradicated infected TFH cells and B cells. The differentiation of these cells, which we have called 'follicular cytotoxic T cells' (TFC cells), required the transcription factors Bcl6, E2A and TCF-1 but was inhibited by the transcriptional regulators Blimp1, Id2 and Id3. Blimp1 and E2A directly regulated Cxcr5 expression and, together with Bcl6 and TCF-1, formed a transcriptional circuit that guided TFC cell development. The identification of TFC cells has far-reaching implications for the development of strategies to control infections that target B cells and TFH cells and to treat B cell-derived malignancies.
MeSH term(s)	Animals ; Arenaviridae Infections/immunology ; B-Lymphocytes/immunology ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Cell Differentiation ; Cells, Cultured ; Epstein-Barr Virus Infections/immunology ; Gene Expression Regulation ; Germinal Center/pathology ; Germinal Center/virology ; HIV/immunology ; Hepatocyte Nuclear Factor 1-alpha/genetics ; Hepatocyte Nuclear Factor 1-alpha/metabolism ; Humans ; Lymphocytic choriomeningitis virus/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Positive Regulatory Domain I-Binding Factor 1 ; Proto-Oncogene Proteins c-bcl-6/genetics ; Proto-Oncogene Proteins c-bcl-6/metabolism ; Receptors, CXCR5/genetics ; Receptors, CXCR5/metabolism ; T-Lymphocytes, Cytotoxic/immunology ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	Basic Helix-Loop-Helix Transcription Factors ; Bcl6 protein, mouse ; CXCR5 protein, human ; Hepatocyte Nuclear Factor 1-alpha ; Hnf1a protein, mouse ; Prdm1 protein, mouse ; Proto-Oncogene Proteins c-bcl-6 ; Receptors, CXCR5 ; Tcf3 protein, mouse ; Transcription Factors ; Positive Regulatory Domain I-Binding Factor 1 (EC 2.1.1.-)
Language	English
Publishing date	2016-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/ni.3543
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Article ; Online: CXCR5

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Article ; Online: ACKR4 restrains antitumor immunity by regulating CCL21.

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Article ; Online: Tailored immune responses: novel effector helper T cell subsets in protective immunity.

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Article ; Online: Distinct chemokine receptor axes regulate Th9 cell trafficking to allergic and autoimmune inflammatory sites.

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Article ; Online: IL-17-producing γδ T cells switch migratory patterns between resting and activated states.

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Article ; Online: Atypical chemokine receptor 4 shapes activated B cell fate.

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Article ; Online: CCR2 defines in vivo development and homing of IL-23-driven GM-CSF-producing Th17 cells.

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Article ; Online: CXCR5(+) follicular cytotoxic T cells control viral infection in B cell follicles.

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