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Journal articles on the topic "ACKR4"
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Pacheco, Messias Oliveira, Fernanda Agostini Rocha, Thiago Pinheiro Arrais Aloia, and Luciana Cavalheiro Marti. "Evaluation of Atypical Chemokine Receptor Expression in T Cell Subsets." Cells 11, no. 24 (December 16, 2022): 4099. http://dx.doi.org/10.3390/cells11244099.
Full textAbstract:
Chemokines are molecules that pertain to a family of small cytokines and can generate cell chemotaxis through the interaction with their receptors. Chemokines can trigger signaling via conventional G-protein-coupled receptors or through atypical chemokine receptors. Currently, four atypical chemokine receptors have been are described (ACKR1, ACKR2, ACKR3 and ACKR4). ACKRs are expressed in various cells and tissues, including T lymphocytes. These receptors’ main function is related to the internalization and degradation of chemokines, as well as to the inflammation control. However, the expression of these receptors in human T lymphocytes is unclear in the literature. The objective of this study was to evaluate the expression of ACKRs in different subpopulations of T lymphocytes. For this, peripheral blood from healthy donors was used to analyze the expression of ACKR2, ACKR3 and ACKR4 by immunophenotyping CD4, CD8 T lymphocytes and, in their subsets, naive, transition and memory. Results obtained in this study demonstrated that ACKR2, ACKR3 and ACKR4 receptors were expressed by T lymphocytes subsets in different proportions. These receptors are highly expressed in the cytoplasmic milieu of all subsets of T lymphocytes, therefore suggesting that their expression in plasma membrane is regulated after transcription, and it must be dependent on a stimulus, which was not identified in our study. Thus, regarding ACKRs function as scavenger receptors, at least for the ACKR3, this function does not impair the chemotaxis exert for their ligand compared to the typical counterpart receptor.
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Pan, Li, Jianliang Lv, Zhongwang Zhang, and Yongguang Zhang. "Adaptation and Constraint in the Atypical Chemokine Receptor Family in Mammals." BioMed Research International 2018 (September 24, 2018): 1–9. http://dx.doi.org/10.1155/2018/9065181.
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Atypical chemokine receptors (ACKRs) are a subclass of G protein-coupled receptors characterized by promiscuity of ligand binding and an obvious inability to signal after ligand binding. Although some discoveries regarding this family in Homo sapiens and other species have been reported in some studies, the evolution and function of multiple ACKR in mammals have not yet been clearly understood. We performed an evolutionary analysis of ACKR genes (ACKR1, ACKR2, ACKR3, and ACKR4) in mammals. Ninety-two full-length ACKR genes from 27 mammal species were retrieved from the Genbank and Ensemble databases. Phylogenetic analysis showed that there were four well-conserved subfamilies in mammals. Synteny analysis revealed that ACKR genes formed conserved linkage groups with their adjacent genes across mammalian species, facilitating the identification of ACKRs in as yet unannotated genome datasets. Analysis of the site-specific profiles established by posterior probability revealed the positive-selection sites to be distributed mainly in the ligand binding region of ACKR1. This study highlights the molecular evolution of the ACKR gene family in mammals and identifies the critical amino acid residues likely to be relevant to ligand binding. Further experimental verification of these findings may provide valuable information regarding the ACKR’s biochemical and physiological functions.
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Lewandowska, Paulina, Jaroslaw Wierzbicki, Marek Zawadzki, Anil Agrawal, and Małgorzata Krzystek-Korpacka. "Biphasic Expression of Atypical Chemokine Receptor (ACKR) 2 and ACKR4 in Colorectal Neoplasms in Association with Histopathological Findings." Biomolecules 11, no. 1 (December 23, 2020): 8. http://dx.doi.org/10.3390/biom11010008.
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Facilitating resolution of inflammation using atypical chemokine receptors (ACKR) as an anticancer strategy is considered but requires a deeper understanding of receptor role in carcinogenesis. We aimed at transcriptional analysis (RTqPCR) of ACKR2 and ACKR4 expression in colorectal adenoma-adenocarcinoma sequence in paired normal-neoplastic tissues from 96 polyps and 51 cancers. On average, ACKR2 was downregulated in neoplastic as compared to non-affected tissue in polyp (by 2.7-fold) and cancer (by 3.1-fold) patients. The maximal downregulation (by 8.2-fold) was observed in adenomas with the highest potential for malignancy and was gradually lessening through cancer stages I-IV, owing to increased receptor expression in tumors. On average, ACKR4 was significantly downregulated solely in adenocarcinomas (by 1.5-fold), less so in patients with lymph node metastasis, owing to a gradual decrease in ACKR4 expression among N0-N1-N2 cancers in non-affected tissue without changes in tumors. In adenomas, ACKR4 downregulation in neoplastic tissue increased with increasing potential for malignancy and contribution of villous growth pattern. ACKR4 expression increased in non-affected tissue with a concomitant decrease in pathological mucosa. In conclusion, the changes in ACKRs expression occur already in precancerous colorectal lesions, culminating in the adenomas with the highest potential for malignancy. Therefore, chemoprevention by manipulating ACKRs’ expression is worth exploration.
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Wangmo, Dechen, Prem K. Premsrirut, Ce Yuan, William S. Morris, Xianda Zhao, and Subbaya Subramanian. "ACKR4 in Tumor Cells Regulates Dendritic Cell Migration to Tumor-Draining Lymph Nodes and T-Cell Priming." Cancers 13, no. 19 (October 7, 2021): 5021. http://dx.doi.org/10.3390/cancers13195021.
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Colorectal cancer (CRC) is one of the most common malignancies in both morbidity and mortality. Immune checkpoint blockade (ICB) treatments have been successful in a portion of mismatch repair-deficient (dMMR) CRC patients but have failed in mismatch repair-proficient (pMMR) CRC patients. Atypical Chemokine Receptor 4 (ACKR4) is implicated in regulating dendritic cell (DC) migration. However, the roles of ACKR4 in CRC development and anti-tumor immunoregulation are not known. By analyzing human CRC tissues, transgenic animals, and genetically modified CRC cells lines, our study revealed an important function of ACKR4 in maintaining CRC immune response. Loss of ACKR4 in CRC is associated with poor immune infiltration in the tumor microenvironment. More importantly, loss of ACKR4 in CRC tumor cells, rather than stromal cells, restrains the DC migration and antigen presentation to the tumor-draining lymph nodes (TdLNs). Moreover, tumors with ACKR4 knockdown become less sensitive to immune checkpoint blockade. Finally, we identified that microRNA miR-552 negatively regulates ACKR4 expression in human CRC. Taken together, our studies identified a novel and crucial mechanism for the maintenance of the DC-mediated T-cell priming in the TdLNs. These new findings demonstrate a novel mechanism leading to immunosuppression and ICB treatment resistance in CRC.
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Bastow, Cameron R., Mark D. Bunting, Ervin E. Kara, Duncan R. McKenzie, Adriana Caon, Sapna Devi, Lynn Tolley, et al. "Scavenging of soluble and immobilized CCL21 by ACKR4 regulates peripheral dendritic cell emigration." Proceedings of the National Academy of Sciences 118, no. 17 (April 19, 2021): e2025763118. http://dx.doi.org/10.1073/pnas.2025763118.
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Leukocyte homing driven by the chemokine CCL21 is pivotal for adaptive immunity because it controls dendritic cell (DC) and T cell migration through CCR7. ACKR4 scavenges CCL21 and has been shown to play an essential role in DC trafficking at the steady state and during immune responses to tumors and cutaneous inflammation. However, the mechanism by which ACKR4 regulates peripheral DC migration is unknown, and the extent to which it regulates CCL21 in steady-state skin and lymph nodes (LNs) is contested. Specifically, our previous findings that CCL21 levels are increased in LNs of ACKR4-deficient mice [I. Comerford et al., Blood 116, 4130–4140 (2010)] were refuted [M. H. Ulvmar et al., Nat. Immunol. 15, 623–630 (2014)], and no differences in CCL21 levels in steady-state skin of ACKR4-deficient mice were reported despite compromised CCR7-dependent DC egress in these animals [S. A. Bryce et al., J. Immunol. 196, 3341–3353 (2016)]. Here, we resolve these issues and reveal that two forms of CCL21, full-length immobilized and cleaved soluble CCL21, exist in steady-state barrier tissues, and both are regulated by ACKR4. Without ACKR4, extracellular CCL21 gradients in barrier sites are saturated and nonfunctional, DCs cannot home directly to lymphatic vessels, and excess soluble CCL21 from peripheral tissues pollutes downstream LNs. The results identify the mechanism by which ACKR4 controls DC migration in barrier tissues and reveal a complex mode of CCL21 regulation in vivo, which enhances understanding of functional chemokine gradient formation.
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Kara, Ervin E., Cameron R. Bastow, Duncan R. McKenzie, Carly E. Gregor, Kevin A. Fenix, Rachelle Babb, Todd S. Norton, et al. "Atypical chemokine receptor 4 shapes activated B cell fate." Journal of Experimental Medicine 215, no. 3 (January 31, 2018): 801–13. http://dx.doi.org/10.1084/jem.20171067.
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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.
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Bryce, Steven, Darren Asquith, Shannon Bromley, Andrew Luster, Gerard Graham, and Robert Nibbs. "The atypical chemokine receptor ACKR4 facilitates dendritic cell migration during inflammation by scavenging CCL19 (CCR3P.205)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 49.6. http://dx.doi.org/10.4049/jimmunol.194.supp.49.6.
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Abstract The migration of dendritic cells from tissues to draining lymph nodes is a critical step in the induction of peripheral tolerance and the initiation of adaptive immune responses. This is dependent on CCR7 expression by dendritic cells. In response to the chemokine CCL21, CCR7 directs dendritic cells into lymphatic vessels in the tissue, and permits their transit from the subcapsular sinus into the lymph node parenchyma. The CCR7 ligands CCL19 and CCL21 also bind ACKR4, an atypical chemokine receptor expressed by keratinocytes in the skin and lymphatic endothelial cells lining the subcapsular sinus. In mice, ACKR4 controls interfollicular CCL21 gradients, and enhances dendritic cell entry into the lymph node parenchyma from the subcapsular sinus. Here we report that Ackr4 deficiency disrupts CCR7-dependent dendritic cell arrival at skin-draining lymph nodes during cutaneous inflammation. We show that this, at least in part, is due to the defective departure of dendritic cells from inflamed skin, and is accompanied by dysregulation of bioavailable CCL19 and CCL21 in the skin. Strikingly, genetic deletion of CCL19 completely rescues the defective inflammation-driven trafficking of dendritic cells caused by Ackr4 deficiency. Thus, by regulating CCL19, ACKR4 helps maintain CCR7-dependent dendritic cell departure from inflamed tissues.
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Purvanov, Vladimir, Christoph Matti, Guerric P. B. Samson, Ilona Kindinger, and Daniel F. Legler. "Fluorescently Tagged CCL19 and CCL21 to Monitor CCR7 and ACKR4 Functions." International Journal of Molecular Sciences 19, no. 12 (December 4, 2018): 3876. http://dx.doi.org/10.3390/ijms19123876.
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Chemokines are essential guidance cues orchestrating cell migration in health and disease. Cognate chemokine receptors sense chemokine gradients over short distances to coordinate directional cell locomotion. The chemokines CCL19 and CCL21 are essential for recruiting CCR7-expressing dendritic cells bearing pathogen-derived antigens and lymphocytes to lymph nodes, where the two cell types meet to launch an adaptive immune response against the invading pathogen. CCR7-expressing cancer cells are also recruited by CCL19 and CCL21 to metastasize in lymphoid organs. In contrast, atypical chemokine receptors (ACKRs) do not transmit signals required for cell locomotion but scavenge chemokines. ACKR4 is crucial for internalizing and degrading CCL19 and CCL21 to establish local gradients, which are sensed by CCR7-expressing cells. Here, we describe the production of fluorescently tagged chemokines by fusing CCL19 and CCL21 to monomeric red fluorescent protein (mRFP). We show that purified CCL19-mRFP and CCL21-mRFP are versatile and powerful tools to study CCR7 and ACKR4 functions, such as receptor trafficking and chemokine scavenging, in a spatiotemporal fashion. We demonstrate that fluorescently tagged CCL19 and CCL21 permit the visualization and quantification of chemokine gradients in real time, while CCR7-expressing leukocytes and cancer cells sense the guidance cues and migrate along the chemokine gradients.
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Eckert, Nadine, Kathrin Werth, Stefanie Willenzon, Likai Tan, and Reinhold Förster. "B cell hyperactivation in an Ackr4 ‐deficient mouse strain is not caused by lack of ACKR4 expression." Journal of Leukocyte Biology 107, no. 6 (December 16, 2019): 1155–66. http://dx.doi.org/10.1002/jlb.2ma1119-300r.
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Mohammed, Mostafa M., Olfat Shaker, Maggie M. Ramzy, Shereen S. Gaber, Heba S. Kamel, and Mohamed F. Abed EL Baky. "The relation between ACKR4 and CCR7 genes expression and breast cancer metastasis." Life Sciences 279 (August 2021): 119691. http://dx.doi.org/10.1016/j.lfs.2021.119691.
Full textDissertations / Theses on the topic "ACKR4"
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Garcia, Ibanez Laura. "Decision events in the germinal centre : the role of ACKR4." Thesis, University of Birmingham, 2017. http://etheses.bham.ac.uk//id/eprint/7365/.
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Murine atypical chemokine receptor 4, ACKR4, which binds to chemokines CCL19, CCL21 and CCL25, is expressed specifically in germinal centre (GC) B cells and in a layer of stromal cells surrounding the splenic marginal zone. Although ACKR4 is unable to signal as classical GPCRs, it creates gradients of its ligands. It is shown here that ACKR4 deficiency in the stroma causes infiltration of naïve B cells into the GC area. ACKR4 deficiency in the B cells causes dysregulation of the intragerminal centre distribution, with enlarged light zones and reduced dark zones when compared to ACKR4-competent mice. This skewed GC distribution is caused by the inability of ACKR4-deficient B cells to downregulate c-Myc, as they receive increased signalling though the CCR7- p-Akt - c-Myc signalling pathway. Moreover, ACKR4-deficient mice contain elevated numbers of memory B cells (MBC) in the distant lymphoid organs. MBCs are retained in the draining lymph node (drLN) by the presence of a CCL19/21 gradient towards the subcapsular sinus (SCS). When this gradient is absent, as occurs in ACKR4-deficient mice, MBCs escape the drLN easier through the SCS and appear in other sites in elevated numbers. Together, this shows a new role for ACKR4 in the GC response and in the migration of GC-derived MBCs out of the follicle and the drLN.
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Fumagalli, Amos. "Deciphering CXCR4 and ACKR3 interactomes reveals an influence of ACKR3 upon Gap junctional intercellular communication." Thesis, Montpellier, 2018. http://www.theses.fr/2018MONTT036.
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Le récepteur atypique ACKR3 et le récepteur CXCR4 sont des récepteurs couplés aux protéines G appartenant à la famille des récepteurs CXC des chimiokines. Ces deux récepteurs sont activés par la chimiokine CXCL12 et sont surexprimés dans de nombreux cancers comme les gliomes, dont ils favorisent la prolifération et le caractère invasif. Le récepteur CXCR4 active des voies de signalisation qui dépendent de la protéine Gi et des β-arrestines et s’associe à plusieurs protéines impliquées dans la transduction du signal, le trafic et la localisation cellulaire du récepteur. Par contre, les mécanismes de signalisation impliqués dans les effets d’ACKR3 restent mal connus. Le récepteur déclenche une signalisation dépendant des β-arrestines, mais son couplage aux protéines G dépend du type cellulaire ou se fait par un mécanisme indirect via son association au récepteur CXCR4. Le récepteur ACKR3 s’associe également au récepteur de l’EGF pour induire la prolifération cellulaire par un mécanisme indépendant de sa stimulation par un agoniste. Ces données illustrent l’intérêt de caractériser de façon systématique l’interactome de ces récepteurs pour comprendre leurs rôles physiologiques et pathologiques. Cette thèse a poursuivi cet objectif grâce à la mise en œuvre d’une approche protéomique combinant la purification des partenaires des deux récepteurs par affinité suivie de leur identification par spectrométrie de masse. J’ai ainsi identifié respectivement 19 et 151 partenaires protéiques potentiels des récepteurs CXCR4 et ACKR3 exprimés dans les cellules HEK-293T. Parmi les protéines recrutées par ACKR3, nous nous sommes focalisés sur la connexine 43 (Cx43, une des protéines constituant les jonctions Gap) du fait de la similitude des effets du récepteur et de la Cx43 dans la pénétration des leucocytes dans le parenchyme cérébral, la migration des interneurones et la progression des gliomes. J’ai confirmé par Western blot et par BRET l’association spécifique de la Cx43 à l’ACKR3 et non pas au CXCR4. De la même façon, j’ai montré une co-localisation de la Cx43 et de l’ACKR3 dans des cellules de gliome humain, ainsi que dans les astrocytes de la zone sous-ventriculaire et les pieds astrocytaires entourant les capillaires cérébraux chez la souris, suggérant que les deux protéines forment un complexe protéique dans un contexte biologique authentique. Des études fonctionnelles ont révélé que l’ACKR3 module les fonctions de la Cx43 par différents mécanismes. L’expression de l’ACKR3 dans les cellules HEK-293T (mimant la surexpression du récepteur dans les tumeurs), induit par elle-même une inhibition de l’activité jonctionnelle de la Cx43. De même, la stimulation du récepteur par un agoniste réduit l’activité jonctionnelle de la Cx43 par un mécanisme impliquant l’activation d’une protéine Gi, la β-arrestine2 et l’internalisation de la Cx43. Cette thèse établit donc pour la première fois un lien fonctionnel entre le système constitué par les chimiokines CXCL11, CXCL12 et leur récepteur ACKR3 d’une part et les jonctions Gap d’autre part qui pourrait jouer un rôle critique dans la progression des gliomesThe Atypical Chemokine Receptor 3 (ACKR3) and CXCR4 are two G protein-coupled receptors (GPCR) belonging to the CXC chemokine receptor family. Both receptors are activated upon CXCL12 binding and are over-expressed in various tumours, including glioma, where they have been found to promote proliferation and invasive behaviours. Upon CXCL12 binding, CXCR4 activates canonical GPCR signalling pathways involving Gαi protein and β-arrestins. In addition, CXCR4 was found to interact with several proteins able to modify its signalling, trafficking and localization. In contrast, the cellular pathways underlying ACKR3-dependent effects remain poorly characterized. Several reports show that ACKR3 engages β-arrestin-dependent signalling pathways, but its coupling to G proteins is restricted to either specific cellular populations, including astrocytes, or occurs indirectly via its interaction with CXCR4. ACKR3 also associates with the epidermal growth factor receptor to promote proliferation of tumour cells in an agonist-independent manner. These examples suggest that the extensive characterization of ACKR3 and CXCR4 interactomes might be a key step in understanding or clarifying their roles in physiological and pathological contexts. This thesis addressed this issue employing an affinity purification coupled to high-resolution mass spectrometry proteomic strategy that identified 19 and 151 potential protein partners of CXCR4 and ACKR3 transiently expressed in HEK-293T cells, respectively. Amongst ACKR3 interacting proteins identified, we paid particular attention on the gap junction protein Connexin-43 (Cx43), in line with its overlapping roles with the receptor in the control of leukocyte entry into the brain, interneuron migration and glioma progression. Western blotting and BRET confirmed the specific association of Cx43 with ACKR3 compared to CXCR4. Likewise, Cx43 is co-localized with ACKR3 but not CXCR4 in glioma initiating cell lines, and ACKR3 and Cx43 are co-expressed in astrocytes of the sub-ventricular zone and surrounding blood vessels in adult mouse brain, suggesting that both proteins form a complex in authentic cell or tissue contexts. Further functional studies showed that ACKR3 influences Cx43 trafficking and functionality at multiple levels. Transient expression of ACKR3 in HEK-293T cells to mimic ACKR3 overexpression detected in several cancer types, induces Gap Junctional Intercellular Communication (GJIC) inhibition in an agonist-independent manner. In addition, agonist stimulation of endogenously expressed ACKR3 in primary cultured astrocytes inhibits Cx43-mediated GJIC through a mechanism that requires activation of Gαi protein, and dynamin- and β-arrestin2-dependent Cx43 internalisation. Therefore, this thesis work provides the first functional link between the CXCL11/CXCL12/ACKR3 axis and gap junctions that might underlie their critical role in glioma progression
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Heuninck, Joyce. "Analysis of CXCR4 and ACKR3 oligomerisation." Thesis, Montpellier, 2019. http://www.theses.fr/2019MONTT018.
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Mon travail de thèse s’est focalisé sur l’étude des récepteurs CXCR4 et ACKR3, deux récepteurs aux chimiokines. Ceux-ci jouent des rôles majeurs dans différentes fonctions physiologiques notamment le chimiotactisme des cellules immunitaires. Le dérèglement de leur activité est souvent associé à différents pathologies, notamment des cancers. Outre le fait que ces récepteurs lient tous les deux la même chimiokine, CXCL12, il a été montré qu’ils étaient capables d’exercer l’un sur l’autre des régulations croisées. Les mécanismes sous-tendant celles-ci sont très mal connus. Ils pourraient être liés à une compétition entre les récepteurs pour lier le même ligand CXCL12 ou à des régulations au niveau des voies de signalisation activées lors de la liaison d’une chimiokine. Ces régulations croisées pourraient également résulter de la formation de complexes de récepteurs appelés oligomères, complexes qui disposeraient de propriétés pharmacologiques particulières. De tels complexes ont été décrits dès les années 1990 dans des systèmes d’expression hétérologues mais leur existence et leurs rôles dans des systèmes natifs reste très largement débattus. Une des raisons est la difficulté à élaborer des outils moléculaires permettant l’étude de ces oligomères dans les tissus natifs.Le premier objectif de ma thèse a été l’élaboration d’outils permettant d’étudier l’existence de ces oligomères dans les systèmes natifs. En collaboration avec des laboratoires d’Amsterdam, j’ai développé des nanobodies fluorescents, petits anticorps produits par le lama, afin de marquer spécifiquement les récepteurs endogènes exprimés à la surface des cellules. Pour rendre fluorescent ces nanobodies, nous avons utilisé une technique originale permettant de greffer un fluorophore sur l’extrémité C-terminale de la molécule. Ces nanobodies conservent des propriétés pharmacologiques remarquables puisqu’ils conservent de hautes affinité et spécificité pour leur cible. J’ai ainsi pu utiliser ces molécules et démontrer l’existence des oligomères CXCR4 dans des lignées cellulaires exprimant de façon endogène le récepteur CXCR4. Des analyses similaires sont en cours sur le récepteur ACKR3.Le second objectif de ma thèse a été de définir les rôles potentiels de ces oligomères. J’ai pu montrer que les hétéro-oligomères CXCR4 /ACKR3, complexes associant les deux types de récepteurs, possèdent des propriétés de liaison particulière. Ceux-ci semblent ne lier la chimiokine CXCL12 que sur le récepteur ACKR3 au sein du complexe. Cette asymétrie de liaison est très étonnante car le récepteur CXCR4 est capable de lier CXCL12 avec une cinétique bien supérieure à celle de ACKR3 pour ce même ligand. J’ai étudié les conséquences d’une telle asymétrie de liaison sur les propriétés de signalisation de ces récepteurs. Une analyse des différentes voies de couplage activées lors de la liaison de CXCL12 a été réalisée sur les récepteurs exprimés de façon isolée ou co-exprimés au sein d’une même cellule. Les résultats ne montrent pas de modifications majeures de leur propriété de couplage.Nous avons par ailleurs analysé la capacité de ces récepteurs à internaliser en absence ou en présence de ligand CXCL12. J’ai pu observer que les hétéro-oligomères CXCR4 / ACKR3 restaient vraisemblablement bloquer à la surface des cellules.Ces travaux ouvrent des perspectives intéressantes dans la mesure où elles constituent la première démonstration de l’existence d’oligomères CXCR4 dans des systèmes natifs.Par ailleurs l’observation d’une régulation différente de l’internalisation des hétéro-oligomères constitue une première piste conférant à ces complexes un rôle particulier dans les régulations croisées de l’activité que ces récepteurs exercent l’un sur l’autreDuring my PhD, I focused on two chemokine receptors, CXCR4 and ACKR3. They have several important physiological functions, such as chemotaxis of immune cells. However, on the other hand, when their function is disturbed, they are involved in different immunological pathologies and cancer. Both receptors recognise the same chemokine, CXCL12 and many studies have reported a crosstalk between CXCR4 and ACKR3. However, the mechanisms behind this crosstalk are still poorly understood. This crosstalk can occur because both receptors are competing for CXCL12, at the level of signalling pathways or due to the formation of complexes between CXCR4 and ACKR3 receptors, called oligomers. The oligomers might have specific pharmacological properties different from the receptor monomers. Oligomeric complexes have been described since the nineties. Most of the studies on these oligomers were performed on heterologous expression systems, but still a lot of debate exists about their existence and their role in native tissues. One of the reasons behind this controversy is that studying oligomers in a native context is complicated, especially because we often lack the molecular tools for these studies.The first objective of my PhD was to generate efficient tools to study the existence of CXCR4 and ACKR3 oligomers in native systems. In collaboration with laboratories from Amsterdam and Ghent, we have developed fluorescent nanobodies, small antibodies produced by llamas. These specific tools allow the detection of receptors endogenously expressed at the cell surface. In order to fluorescently label these nanobodies, we have used an original strategy that can specifically attach the fluorophore to the C-terminus of the nanobody. Interestingly, the fluorescent nanobodies retain high affinity and specificity for their target. With these nanobodies, I have demonstrated the existence of CXCR4 oligomers in cell lines that endogenously express CXCR4. We are currently investigating the existence of ACKR3 oligomers.The second objective of my PhD consists of defining the functional roles of these oligomers. I have shown that CXCR4/ACKR3 hetero-oligomers have specific binding characteristics. It seems that CXCL12 is binding only to ACKR3 within this hetero-oligomer and that ACKR3 impairs the CXCL12 binding to CXCR4 within the hetero-oligomer. This is interesting, since we also have demonstrated that CXCL12 is binding much faster on CXCR4 than on ACKR3.In addition, I have studied the consequences of this negative cooperativity within the CXCR4/ACKR3 hetero-oligomer on different signalling pathways. We have compared conditions where the receptor was expressed alone or when receptors were co-expressed. No major modifications have been found on their signalling properties. However, when investigating the internalisation of CXCR4 and ACKR3, it seems that CXCR4/ACKR3 hetero-oligomers remain blocked on the cellular surface.This opens interesting perspectives, since it is the first time CXCR4 oligomers have been detected at an endogenous level. Moreover, the observation of a different internalisation pattern of the hetero-oligomer is a first step to further investigate the specific roles of these oligomers in the crosstalk between the receptors
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Pallas, Kenneth James. "The role of ACKR2 in inflammatory pathologies." Thesis, University of Glasgow, 2015. http://theses.gla.ac.uk/6807/.
Full textAbstract:
Chemokines are a highly conserved family of chemoattractant cytokines that are key to the movement of cells around the body under both inflammatory and homeostatic conditions. Chemokines bind to seven transmembrane G protein coupled receptors that signal and induce cell movement upon ligand binding. As well as the ‘classical’ chemokine receptors, there also exists a family of atypical chemokine receptors that do not induce a canonical signalling response upon ligand binding. These atypical chemokine receptors (ACKR) have been shown to modify the chemokine response through processes such as the scavenging of inflammatory chemokines. One such receptor with this scavenging function is ACKR2 which has been shown to bind and internalise all of the inflammatory CC chemokines. The functional repertoire of ACKR2 continues to be expanded and it is now thought to have a role in inflammation, lymphatic drainage and lymphatic vessel development. It has been shown that the absence of this receptor results in impaired resolution of inflammation and, as a result, increased inflammatory pathologies in vivo. In models of skin inflammation a lack of ACKR2 has been shown to result in increased pathology and impaired inflammatory resolution. Multiple models of cutaneous inflammation, including excisional wound healing and chemically induced damage, were used to further investigate the role of ACKR2 in this context. Work on wound healing suggested that although ACKR2 appears to play no role in wound closure it does have a role in the formation of scar tissue in an excisional wound. Our data suggest that ACKR2 has a role in collagen deposition in developing and maturing scars. We also found that ACKR2 had a protective role in chemically-induced models of skin inflammation. We then looked at the role of ACKR2 in ocular inflammation. The main work performed in this section involved the use of the experimental autoimmune uveitis (EAU) model. Here we found that ACKR2 had a protective effective resulting in reduced pathology and infiltration of inflammatory leukocytes. This work also suggested, using in vitro analysis, that a human retinal pigmented epithelial cell line expresses functional ACKR2 protein and that our findings may be relevant to human disease. Finally we looked at the role of ACKR2 in the inflammatory autoimmune disease rheumatoid arthritis (RA). By taking samples of peripheral blood from RA patients we assessed the transcript levels of Ackr2 and correlated them with clinical measurements. Our findings suggested that, in patients with ‘well-controlled’ RA, there was an increase in the transcription of Ackr2 in peripheral blood leukocytes. Additional work using in vitro methods suggest that the hypoxic nature of the rheumatoid joint, and some of the drugs used to treat the disease, may increase the transcription of Ackr2. Overall the findings in this work suggest novel roles for ACKR2 in the skin and the eye. They also shed light on further environmental factors that may alter the local expression of ACKR2 in the rheumatoid joint. Taken together this work suggests that ACKR2 may have great therapeutic potential and, furthermore, this potential may be relevant to a wider range of tissues than previously thought.
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Gallego, Carmen. "Interactions hôte-virus : la chimiokine CXCL12 et ses récepteurs CXCR4 et ACKR3 dans le cycle de vie du papillomavirus humain et la carcinogènese associée." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS337.
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Membres épithéliotropes de notre virome, les papillomavirus humains (HPV) causent majoritairement des infections asymptomatiques ou bénignes, contrôlées par les mécanismes de défense de l'hôte à l’échelle épithélial et immunitaire. Néanmoins, l’infection persistante par certains HPV à haut risque (hrHPV) cancérogène peut conduire au développement de cancers. Ainsi, les hrHPV à tropisme muqueux causent 98% des cancers cervicaux, et sont impliqués dans un nombre croissant de cancers ano-génitaux et oropharyngés. Les vaccins prophylactiques sont efficaces pour prévenir les lésions associées aux hrHPV à tropisme muqueux, mais à l'heure actuelle, il n'existe aucun traitement antiviral pour une infection établie. Dans cette thèse de doctorat, nous avons cherché à étudier les facteurs de l’hôte impliqués dans le cycle de vie d’HPV et sa carcinogenèse à deux niveaux : ceux du kératinocyte infecté et du système immunitaire. Des études chez certains patients immunodéficients (syndrome de WHIM, WS) présentant une susceptibilité sélective à la pathogénèse HPV ont identifié la chimiokine CXCL12 et CXCR4, son récepteur couplé aux protéines G (dont les mutations causent le WS) comme facteurs de contrôle du cycle de vie de ces virus. CXCL12/CXCR4 ainsi que ACKR3, le récepteur-leurre de CXCL12, peuvent moduler à la fois les réponses antivirales épithéliales et immunitaires. Nous avons d'abord étudié la contribution d'ACKR3 au cycle de vie d’HPV dans des cultures 3D de cellules épithéliales humaines (3D-EpC), seul modèle permettant la réplication d’HPV. Nos résultats indiquent que l'activité accrue d'ACKR3 présente un potentiel pro-oncogène puisqu'elle déplace le cycle de vie productif d’HPV vers l'oncogenèse et que le blocage d'ACKR3 pourrait être une approche thérapeutique attrayante pour favoriser la réplication d’HPV. Par la suite, nous avons étudié les conséquences fonctionnelles du cycle de vie productif d’HPV dans la communication intercellulaire, en mettant en place la technique FLIP dans les 3D-EpC. Enfin, nous avons étudié l'impact d’une mutation de CXCR4 associée au WS au niveau des cellules immunitaires cutanées dans le contexte de la carcinogenèse induite par HPV. Nous avons ainsi mis en évidence le rôle de CXCR4 dans la distribution, l’activation et la migration des cellules dendritiques dermales et des cellules de Langerhans ; leur possible dérégulation dans le contexte du WS pouvant contribuer à la sensibilité sélective des patients à la pathogenèse HPV. En conclusion, ce travail fournit des clés mécanistiques sur les interactions HPV-hôte aux niveaux épithélial et immunitaire. Il révèle le rôle central d'ACKR3 dans la réponse intrinsèque des kératinocytes envers HPV et approfondit nos connaissances sur le rôle de l’axe CXCL12/CXCR4 dans l'immunité cutanée à l’homéostasie et dans la carcinogenèse HPVHuman papillomavirus (HPV) are part of our virome and infect cutaneous and mucosal sites. Most infections are asymptomatic or only cause benign lesions that are controlled by the host defence mechanisms, which take place both at the epithelial and the immune system levels. However, persistent infections with certain mucosal HPV types at high-risk for cancer development, cause virtually all cases of cervical cancers, a majority of anogenital cancers and an increasing proportion of oropharyngeal cancers. Prophylactic vaccines are efficient in preventing mucosal HPV types-associated lesions but currently, there is no antiviral treatment for an established HPV infection. In this doctoral thesis, we aimed at investigating host factors involved in HPV life cycle and carcinogenesis at two levels: the infected keratinocyte and the immune system. Studies in the context of certain immunodeficient patients (WHIM syndrome, WS) with selective susceptibility to HPV pathogenesis have identified the CXCL12 chemokine and its classical G protein-coupled receptor CXCR4 (whose mutations are causing the WS) as host susceptibility factors that act as gatekeepers of HPV life cycle. CXCL12/CXCR4 together with ACKR3, the second receptor of CXCL12 with an atypical decoy activity, can modulate both epithelial and immune cell anti-viral responses. Therefore, we first investigated the intrinsic contribution of ACKR3 to HPV life cycle in 3D human epithelial cell cultures (3D-EpC), the sole model allowing for HPV replication. Our results indicate that enhanced ACKR3 activity displays pro-oncogenic potential as it shifts HPV productive life cycle toward oncogenesis and that blocking ACKR3 could be an attractive therapeutic approach to favour HPV replication. In addition, we have studied the functional consequences of the productive HPV life cycle in cell-cell communication, being pioneers in setting up FLIP technique in 3D-EpC. Lastly, we investigated the impact of CXCR4 WS-mutation at the cutaneous immune cell level in the context of HPV-induced carcinogenesis. We have thus gained insights into the role of CXCR4 in dendritic cell and Langerhans cell distribution, phenotype and migration and how their deregulation in the context of the WS could account for the selective susceptibility of WS patients to HPV pathogenesis. In conclusion, this work provides new insights into HPV-host interactions at the epithelial and immune cell levels. We have unravelled the central role of ACKR3 in keratinocyte intrinsic response against HPV and deepen our knowledge on the role of CXCL12/CXCR4 in skin immunity in health and in HPV carcinogenesis
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Jannat-e-Zereen. "Characterization of the role of ACR4, a receptor like kinase, in Arabidopsis thaliana." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/13252.
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Cutolo, Pasquale. "Etude de l'interaction structurelle et fonctionnelle entre la chimiokine CXCL12 et ses récepteurs : CXCR4 et ACKR3/CXCR7." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS550/document.
Full textAbstract:
L'axe formé par la chimiokine CXCL12 et son récepteur CXCR4 est conservé chez les vertébrés où il joue un rôle important dans l'embryogenèse et la vie adulte, régule de nombreux processus des réponses immunitaires grâce à ses fonctions dans la migration cellulaire, la survie et la prolifération.En outre, cet axe est impliqué dans les processus pathologiques tels que les cancers (croissance et métastase) et immunodéficiences ainsi que des dysfonctionnements (par exemple l'expression dérégulée, polymorphismes ou mutations) et est également détourné par certains agents pathogènes (par exemple le virus de l'immunodéficience humaine, virus du papillome humain).Un grand groupe de travail est consacré à cette paire comme cible thérapeutique, mais seulement un composé (à savoir Plérixafor) a atteint l'approbation pour une utilisation clinique faisant le potentiel de cet axe comme cible de médicament encore inexploré.Bien que cet axe est l'objet d'un grand intérêt, des questions demeurent quant aux déterminants structurels impliqués dans l'interaction CXCL12/CXCR4.Cependant, la structure récemment résolue par diffraction de CXCR4 a donné quelque indice au sujet de ces questions, et au delà, la possible stoichiométrie entre CXCL12 et CXCR4.Plusieurs éléments de preuve appuient le concept que les formes CXCR4 homo- et hétéro- oligomères (qui peut contribuer à la diversité des fonctions de récepteur), telles que la structure de diffraction, le gain de fonction d'un récepteur CXCR4 mutant responsable du syndrome WHIM et la modulation allostérique des fonctions de CXCR4 par CXCR7 (ACKR3), le second récepteur de CXCL12. La possibilité de former des oligomères ouvre de nombreuses questions en matière de CXCL12 et ses interactions avec CXCR4 et CXCR7/ACKR3. La stoichiométrie de cette interaction reste une question ouverte, comme le récepteur est capable de former des oligomères avec le même récepteur ou autre récepteurs, en particulier CXCR7/ACKR3. Ce récepteur, connu comme scavenger, n'a pas de structure résolue et son mécanisme d'interaction avec CXCL12 reste inconnu.Afin d'étudier les interactions CXCL12/CXCR4/CXCR7, nous avons appliqué plusieurs techniques de modélisation moléculaire tels que peptid-peptide docking et simulations de dynamique moléculaire.Objets du projet ont étés : la résolution des possibles formes stoichiométriques de l'interaction CXCR4/CXCL12 (modélisation moléculaire, docking et dynamique); la modélisation de la structure du récepteur CXCR7/ACKR3 et son interaction avec CXCL12 (homology modeling), avec caractérisation des domaines et des résidus clef de l'activation des pathways de signalisation en aval du récepteur (mutants CXCR7/ACKR3); l'étude et la caractérisation de nouveaux outils innovants pour la détection de l'oligomerisation de ces récepteurs en conditions endogènes. (Nanobodies, HTRF)Les résultats du premier objectif ont été publiés en janvier 2016 : PMID 26813575.La modélisation de CXCR7/ACKR3 nous a permit de générer plusieurs mutants du récepteur pour tester nos hypothèses sur l’activation.Les nanobodies caractérisés pour CXCR4 seront utilisé dans une deuxième étude pour l’identification des formes oligomériques du récepteur sur tissus et cellulesThe axis formed by the chemokine CXCL12 and its receptor CXCR4 is conserved in vertebrates where it plays an important role in embryogenesis and adult life, regulates many processes of immune responses through its functions in cell migration, survival and proliferation.In addition, this axis is involved in pathological processes such as cancers (growth and metastasis) and immune deficiencies and malfunctions (eg deregulated expression, mutations or polymorphisms) and is also hijacked by certain pathogens (eg HIV, human papilloma virus).A large working group is dedicated to this pair as a therapeutic target, but only a compound (ie Plerixafor) achieved approval for clinical use by the potential of this area as a drug target unexplored.Although this axis is the subject of great interest, questions remain about the structural determinants involved in CXCL12 / CXCR4 interaction.However, the recently resolved diffraction structure of CXCR4 gave some clue about these questions, and beyond possible stoichiometry between CXCL12 and CXCR4.Several lines of evidence support the concept that forms CXCR4 homo- and hetero-oligomers (which can contribute to the diversity of the receptor functions), as shown in the diffraction structure, the gain function of a mutant CXCR4 receptor responsible for the syndrome WHIM and allosteric modulation of CXCR4 functions by CXCR7 (ACKR3), the second receptor of the chemokine CXCL12. The ability to form oligomers opens many issues of CXCL12 and its interaction with CXCR4 and CXCR7 / ACKR3.The stoichiometry of this interaction still remains an open question, as the receptor is capable to form oligomers with the same receptor or other receptors, particularly CXCR7 / ACKR3. This receptor, known as scavenger, has not solved structure and the mechanism of interaction with CXCL12 is unknown.To study the interactions CXCL12 / CXCR4 / CXCR7, we applied several molecular modeling techniques such as peptide-peptide docking and molecular dynamics simulations.Objectives of this project were: the resolution of the different stoichiometric forms for the interaction of CXCR4 and CXCL12 (molecular modeling, docking and dynamic); modeling the CXCR7 / ACKR3 receptor structure and its interaction with CXCL12 (homology modeling), with the characterization of domains and residues key in the activation of downstream signaling pathways of the receptor (CXCR7 / ACKR3 mutants); the study and characterization of new innovative tools for the detection of oligomerization of these receptors in endogenous conditions. (Nanobodies, HTRF)The results of the first objective were published in January 2016: PMID 26813575.Modeling of CXCR7 / ACKR3 allowed us to generate several mutants of the receptor to test our hypothesis about the activation pathways.Nanobodies were fully characterized for CXCR4 to be used in a second study to identify oligomeric forms of the receptor in tissues and cells
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Woodcock, Thomas M., Tony Frugier, Tan Thanh Nguyen, Bridgette Deanne Semple, Nicole Bye, Matteo Massara, Benedetta Savino, et al. "The scavenging chemokine receptor ACKR2 has a significant impact on acute mortality rate and early lesion development after traumatic brain injury." PUBLIC LIBRARY SCIENCE, 2017. http://hdl.handle.net/10150/626472.
Full textAbstract:
The atypical chemokine receptor ACKR2 promotes resolution of acute inflammation by operating as a scavenger receptor for inflammatory CC chemokines in several experimental models of inflammatory disorders, however its role in the brain remains unclear. Based on our previous reports of increased expression of inflammatory chemokines and their corresponding receptors following traumatic brain injury (TBI), we hypothesised that ACKR2 modulates neuroinflammation following brain trauma and that its deletion exacerbates cellular inflammation and chemokine production. We demonstrate increased CCL2 and ACKR2 mRNA expression in post-mortem human brain, whereby ACKR2 mRNA levels correlated with later times post-TBI. This data is consistent with the transient upregulation of ACKR2 observed in mouse brain after closed head injury (CHI). As compared to WT animals, ACKR2(-/-) mice showed a higher mortality rate after CHI, while the neurological outcome in surviving mice was similar. At day 1 post-injury, ACKR2(-/-) mice displayed aggravated lesion volume and no differences in CCL2 expression and macrophage recruitment relative to WT mice. Reciprocal regulation of ACKR2 and CCL2 expression was explored in cultured astrocytes, which are recognized as the major source of CCL2 and also express ACKR2. ACKR2 mRNA increased as early as 2 hours after an inflammatory challenge in WT astrocytes. As expected, CCL2 expression also dramatically increased at 4 hours in WT astrocytes but was significantly lower in ACKR2(-/-) astrocytes, possibly indicating a co-regulation of CCL2 and ACKR2 in these cells. Conversely, in vivo, CCL2 mRNA/ protein levels were increased similarly in ACKR2(-/-) and WT brains at 4 and 12 hours after CHI, in line with the lack of differences in cerebral macrophage recruitment and neurological recovery. In conclusion, ACKR2 is induced after TBI and has a significant impact on mortality and lesion development acutely following CHI, while its role in chemokine expression, macrophage activation, brain pathology, and neurological recovery at later time-points is minor. Concordant to evidence in multiple sclerosis experimental models, our data corroborate a distinct role for ACKR2 in cerebral inflammatory processes compared to its reported functions in peripheral tissues.
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Perpiñá, Viciano Cristina [Verfasser], Carsten [Gutachter] Hoffmann, Martin J. [Gutachter] Lohse, and Elke [Gutachter] Butt-Dörje. "Study of the activation mechanisms of the CXC chemokine receptor 4 (CXCR4) and the atypical chemokine receptor 3 (ACKR3) / Cristina Perpiñá Viciano ; Gutachter: Carsten Hoffmann, Martin J. Lohse, Elke Butt-Dörje." Würzburg : Universität Würzburg, 2020. http://d-nb.info/1222910365/34.
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Whyte, Carly Ellyse. "Chemokine-mediated control of immunity to tumours and infectious pathogens." Thesis, 2018. http://hdl.handle.net/2440/128467.
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The ability of immune cells to migrate to distinct niches and peripheral sites is critical for their appropriate differentiation and for execution of their effector functions. This migration is facilitated to a large degree by the expression of chemokine receptors, which allow for migration in a spatiotemporally-controlled manner. The work presented in this thesis addresses two distinct issues regarding how regulation of immune cell migration affects development of anti-tumour immunity and infectious immunity. In the first part of this thesis, a novel role for the atypical chemokine receptor ACKR4 in controlling anti-tumour immune responses was identified. As a scavenging receptor, ACKR4 regulates the bioavailability of the CCR7 ligands, CCL19 and CCL21, and the CCR9 ligand, CCL25. These ligands have previously been shown to be critical for many aspects of immune homeostasis, as well as contributing to tumour cell growth and metastasis. However, the contribution of ACKR4 in regulating tumour-specific responses has been unclear. Using multiple orthotopic, transgenic and chemically-induced models of cancer, loss of ACKR4 resulted in inhibited tumour growth. In the absence of ACKR4, enhanced CCL21 levels were associated with enhanced tumour infiltration of IFNy+ CD8+ T cells. The reduced tumour growth seen was dependent on the enhanced CD8+ response, with depletion of CD8+ T cells restoring growth of Ackr4–/– tumours to wildtype levels. The enhanced CD8+ T cell response was not a result of altered priming in draining lymph nodes, although there was increased intratumoural proliferation of CD8+ T cells. Furthermore, ACKR4-deficient tumours showed increased retention of CD103+ DCs, with these cells previously being shown to be critical for effective recruitment of CD8+ T cells to tumours. Moreover, intratumoural administration of CCL21 into wildtype tumours also enhanced the accumulation of DCs, suggesting a direct role for the scavenging ability of ACKR4. These data support the notion that ACKR4, through its regulation of CCL21 bioavailability, controls DC migration in tumours thus regulating the development of anti-tumour immune responses. Furthermore, multiple immunotherapies show increased efficacy in the absence of ACKR4, suggesting ACKR4 may be useful as a potential novel target for immunotherapy. In the second part of this thesis, the role of CCR2 on memory CD4+ T cells was explored. Relatively little is understood about the generation, maintenance and effector functions of memory CD4+ T cells, despite correlations with improved disease outcomes. Furthermore, how these cells migrate to inflammatory sites is still largely unknown. In this project, CCR2 was identified as being enriched on antigen-specific memory CD4+ T cells in response to infection with the extracellular bacteria Streptococcus pneumoniae and infection with influenza A virus. Competitive co-transfer of wildtype and CCR2- deficient TCR-transgenic CD4+ T cells showed enhanced contraction of Ccr2–/– cells, suggesting a cell-intrinsic role for CCR2 in CD4+ T cell maintenance. CCR2-deficient effector cells were unaffected in their ability to secrete cytokines or enter into effector sites. Moreover, despite being numerically reduced at memory timepoints compared with CCR2-sufficent cells, they were equally capable of expanding upon secondary challenge. These data highlight CCR2 as an important regulator of CD4+ T cell memory maintenance. Taken together, this project has furthered our understanding of the complexity of cell migration in dictating immune responses. The identification of CCR2 as a mediator of memory CD4+ T cell generation may allow further investigation into how these cells are induced and maintained. In ACKR4, a novel level of post-transcriptional regulation of intratumoural DC trafficking has been identified, with this having the potential to be a tractable target for therapeutic manipulation in malignant disease.Thesis (Ph.D.) -- University of Adelaide, School of Biological Sciences, 2018
Book chapters on the topic "ACKR4"
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Thelen, Marcus. "ACKR3." In Compendium of Inflammatory Diseases, 1–5. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_222.
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Thelen, Marcus. "ACKR3." In Encyclopedia of Inflammatory Diseases, 1–5. Basel: Springer Basel, 2015. http://dx.doi.org/10.1007/978-3-0348-0620-6_222-1.
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Kleist, Andrew B., Francis Peterson, Robert C. Tyler, Martin Gustavsson, Tracy M. Handel, and Brian F. Volkman. "Solution NMR spectroscopy of GPCRs: Residue-specific labeling strategies with a focus on 13C-methyl methionine labeling of the atypical chemokine receptor ACKR3." In Methods in Cell Biology, 259–88. Elsevier, 2019. http://dx.doi.org/10.1016/bs.mcb.2018.09.004.
Full textConference papers on the topic "ACKR4"
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Song, S., B. Liu, H. Habibie, J. Van Den Bor, M. J. Smit, R. Gosens, X. Wu, et al. "D-dopachrome tautomerase contributes to lung epithelial repair via ACKR3-dependent Akt signalling." In ERS Lung Science Conference 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/23120541.lsc-2021.85.
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Song, Shanshan, Bin Liu, Habibie Habibie, Jelle Van Den Bor, Martine J. Smit, Reinoud Gosens, Xinhui Wu, et al. "D-dopachrome tautomerase contributes to lung epithelial repair via ACKR3-dependent Akt signaling." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.oa2700.
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Martini, Rachel, Brittany Jenkins, and Melissa Davis. "Abstract 1283: Mutations in theDuffy Antigen Receptor for Chemokines (DARC/ACKR1)gene result in population-private variants." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1283.
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Jenkins, Brittany D., Rachel N. Martini, Inasia Brown, and Melissa B. Davis. "Abstract 5071: The functional relevance of Atypical Chemokine Receptor 1 (ACKR1/DARC) genetic isoforms in breast cancer." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5071.
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Kim, Nayoung, Seung-Woo Baek, Hyewon Ryu, Yoon Seok Choi, Ik Chan Song, Hwan Jung Yun, Deog Yeon Jo, Samyong Kim, and Hyo Jin Lee. "Abstract 3947: Atypical chemokine receptor ACKR3 expression is associated with aggressive behavior and poor prognosis in gastric cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3947.
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Martini, Rachel N., Brittany D. Jenkins, Lisa A. Newman, Nancy Manley, and Melissa B. Davis. "Abstract 4630:In vivocharacterization of the Duffy antigen receptor for chemokines (DARC/ACKR1) in breast cancer tumor progression." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4630.
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Martini, Rachel N., Brittany D. Jenkins, Lisa A. Newman, Nancy Manley, and Melissa B. Davis. "Abstract 4630:In vivocharacterization of the Duffy antigen receptor for chemokines (DARC/ACKR1) in breast cancer tumor progression." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4630.
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Jenkins, Brittany D., Talina Fleifel, Rachel Martini, Haythem Ali, Lisa Newman, and Melissa Davis. "Abstract A081: Tumors expressing ACKR1 exhibit a unique signature of tumor-infiltrating immune cells in women with breast cancer." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-a081.
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Kim, Nayoung, Solbi Kim, Mina Joo, Heung Jin Jeon, Myung-Won Lee, Hyewon Ryu, and Hyo Jin Lee. "Abstract 2861: ACKR3 promotes cell metastasis via activating TGF-beta 1/Smad signaling in head and neck squamous cell carcinoma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2861.
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Kim, Nayoung, Solbi Kim, Mina Joo, Heung Jin Jeon, Myung-Won Lee, Hyewon Ryu, and Hyo Jin Lee. "Abstract 2861: ACKR3 promotes cell metastasis via activating TGF-beta 1/Smad signaling in head and neck squamous cell carcinoma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2861.
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