Regulation of T-cell migration by co-stimulatory molecules

David, Rachel; Marelli‐Berg, Federica M.

doi:10.1042/bst0351114

Cited by 6 publications

(4 citation statements)

References 56 publications

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“…The present study suggests that CCR9 and CCR10, the respective chemokine receptors that recruit T and B cells to secondary lymphoid structures in the gut and skin, are not expressed in LF (23)(24)(25).…”

Section: Discussionmentioning

confidence: 67%

“…In the present study, we examined the expression of CXCR3 and its ligands by lymphoid follicle cells in the COPD lung and examined the effects of cigarette smoking on lymphoid follicle CXCR3 expression by comparing results obtained in subjects with COPD with smokers without COPD and never-smokers. Finally, because specific chemokine receptors mediate T-cell recruitment into lymphoid follicles in other parts of the body, we examined LF expression of CCR9 and CCR10, the chemokine receptors that mediate T-cell recruitment into lymphoid follicles in the skin (i.e., CCR9) and gut (i.e., CCR10) (23)(24)(25)(26).…”

Section: What This Study Adds To the Fieldmentioning

confidence: 99%

See 1 more Smart Citation

Lymphoid Follicle Cells in Chronic Obstructive Pulmonary Disease Overexpress the Chemokine Receptor CXCR3

Kelsen

Aksoy²,

Georgy³

et al. 2009

Am J Respir Crit Care Med

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Section: Discussionmentioning

confidence: 67%

Section: What This Study Adds To the Fieldmentioning

confidence: 99%

Lymphoid Follicle Cells in Chronic Obstructive Pulmonary Disease Overexpress the Chemokine Receptor CXCR3

Kelsen

Aksoy²,

Georgy³

et al. 2009

Am J Respir Crit Care Med

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“…Along these lines, a recent study demonstrate that recruitment of Treg to sites of inflammation is strongly favored by their ability to recognize self-Ags presented by endothelium ( 182 ). Of note, the specific expression patterns of costimulatory/coinhibitory molecules found on endothelium are thought to strongly influence the above processes ( 183 ).…”

Section: Potential Functions Of Endothelial Nhapcmentioning

confidence: 99%

T Lymphocyte–Endothelial Interactions: Emerging Understanding of Trafficking and Antigen-Specific Immunity

2015

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Antigen-specific immunity requires regulated trafficking of T cells in and out of diverse tissues in order to orchestrate lymphocyte development, immune surveillance, responses, and memory. The endothelium serves as a unique barrier, as well as a sentinel, between the blood and the tissues, and as such it plays an essential locally tuned role in regulating T cell migration and information exchange. While it is well established that chemoattractants and adhesion molecules are major determinants of T cell trafficking, emerging studies have now enumerated a large number of molecular players as well as a range of discrete cellular remodeling activities (e.g., transmigratory cups and invadosome-like protrusions) that participate in directed migration and pathfinding by T cells. In addition to providing trafficking cues, intimate cell–cell interaction between lymphocytes and endothelial cells provide instruction to T cells that influence their activation and differentiation states. Perhaps the most intriguing and underappreciated of these “sentinel” roles is the ability of the endothelium to act as a non-hematopoietic “semiprofessional” antigen-presenting cell. Close contacts between circulating T cells and antigen-presenting endothelium may play unique non-redundant roles in shaping adaptive immune responses within the periphery. A better understanding of the mechanisms directing T cell trafficking and the antigen-presenting role of the endothelium may not only increase our knowledge of the adaptive immune response but also empower the utility of emerging immunomodulatory therapeutics.

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“…Chemokines have been shown to be involved in lymphocyte chemotaxis (6,7), and cause cancer cells to home to specific secondary sites to promote organ-specific metastasis (8,9). It has recently been shown that CXCR4, CXCR7 and CCR7 are expressed by BrCa cells (10-13) and play an important role in metastatic spread of breast tumor cells to the lungs and lymph nodes (5,14).…”

Section: Discussionmentioning

confidence: 99%

CCL25 mediates migration, invasion and matrix metalloproteinase expression by breast cancer cells in a CCR9-dependent fashion

Johnson-Holiday

Singh²,

Johnson³

et al. 2011

Int J Oncol

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Breast cancer (BrCa) is one of the most frequently diagnosed cancers and the second leading cause of cancer-related deaths in North American women. Most deaths are caused by metastasis, and BrCa is characterized by a distinct metastatic pattern involving lymph nodes, bone marrow, lung, liver and brain. Migration of metastatic cells share many similarities with leukocyte trafficking, which are regulated by chemokines and their receptors. The current study evaluates the expression and functional role of CCR9, and its only known ligand, CCL25, in BrCa cell migration and invasion. Quantitative immunohistochemical analysis showed that both moderately and poorly differentiated BrCa tissue expressed significantly more (P<0.0001) CCR9 compared to non-neoplastic breast tissue. Interestingly, poorly differentiated BrCa tissue expressed significantly more (P<0.0001) CCR9 compared to moderately differentiated BrCa tissue. Similarly, CCR9 was highly expressed by the aggressive breast cancer cell line (MDA-MD-231) compared to the less aggressive MCF-7. Migration as well as invasion assays were used to evaluate the functional interaction between CCR9 and CCL25 in BrCa cell lines (MDA-MB-231 and MCF-7). Neutralizing CCR9-CCL25 interactions significantly impaired the migration and invasion of BrCa cells. Furthermore, CCL25 enhanced the expression of MMP-1, -9, -11 and -13 active proteins by BrCa cells in a CCR9-dependent fashion. These studies show CCR9 is functionally and significantly expressed by BrCa (poorly > moderately differentiated) tissue and cells as well as that CCL25 activation of this receptor promotes breast tumor cell migration, invasion and MMP expression, which are key components of BrCa metastasis.

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Regulation of T-cell migration by co-stimulatory molecules

Cited by 6 publications

References 56 publications

Lymphoid Follicle Cells in Chronic Obstructive Pulmonary Disease Overexpress the Chemokine Receptor CXCR3

Lymphoid Follicle Cells in Chronic Obstructive Pulmonary Disease Overexpress the Chemokine Receptor CXCR3

T Lymphocyte–Endothelial Interactions: Emerging Understanding of Trafficking and Antigen-Specific Immunity

CCL25 mediates migration, invasion and matrix metalloproteinase expression by breast cancer cells in a CCR9-dependent fashion

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