T cells and their partners: the chemokine dating agency

Viola, Antonella; Contento, Rita Lucia; Molon, Barbara

doi:10.1016/j.it.2006.07.004

Cited by 72 publications

(57 citation statements)

References 52 publications

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“…In previous studies, CD40/CD40L interactions and DC-derived IL-12 have been shown to be critical for the production of IFN-␥ by NKT cells (33,34), whereas CD28/B7 interactions are required for the generation of both IL-4 and IFN-␥ (33,36). The requirement for CXCR6 to obtain optimal NKT cell activation is consistent with the observation that chemokine receptor interactions help facilitate activation of T cells during Ag presentation (40,62). …”

Section: Discussionsupporting

confidence: 79%

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Critical Role for the Chemokine Receptor CXCR6 in Homeostasis and Activation of CD1d-Restricted NKT Cells

Germanov¹,

Veinotte²,

Cullen³

et al. 2008

The Journal of Immunology

103

109

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NK T (NKT) cells play important roles in the regulation of diverse immune responses. However, little is known about the mechanisms that regulate homeostasis and activation of these cells. Thymic NKT cells up-regulated the chemokine receptor CXCR6 following positive selection and migrated toward CXCL16 in vitro. However, CXCR6 was not essential for thymic development or maturation. In contrast, liver and lung NKT cells were depleted in CXCR6+/− and CXCR6−/− mice. The reduction in liver and lung NKT cells coincided with an increase in bone marrow NKT cells, suggesting a redistribution of NKT cells in CXCR6−/− animals. In wild-type mice, CXCL16 neutralization reduced accumulation of mature NK1.1+, but not immature NK1.1− NKT cell recent thymic emigrants in the liver. Given that thymic NKT cells are preferentially exported as NK1.1− cells, this suggests an additional role for CXCR6/CXCL16 in maturation or survival of immature liver NKT cells. CXCL16 blockade did not deplete resident NK1.1+ NKT cells, indicating that CXCR6/CXCL16 are not required to retain mature NKT cells in the liver. Cytokine production by liver and spleen NKT cells was impaired in CXCR6−/− mice following in vivo stimulation with α-galactosylceramide, implicating a novel role for CXCR6 in NKT cell activation. Reduced IFN-γ production was not due to an intrinsic defect as production was normal following PMA and ionomycin stimulation. Preformed transcripts for IL-4, but not IFN-γ, were reduced in CXCR6−/− liver NKT cells. These data identify critical roles for CXCR6/CXCL16 in NKT cell activation and the regulation of NKT cell homeostasis.

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Section: Discussionsupporting

confidence: 79%

“…However, chemokines also play important roles in lymphocyte development, differentiation, and effector functions including cytokine polarization (39,40). Human and mouse NKT cells express several chemokine receptors, including high levels of CXCR6 (41)(42)(43)(44).…”

mentioning

confidence: 99%

Critical Role for the Chemokine Receptor CXCR6 in Homeostasis and Activation of CD1d-Restricted NKT Cells

Germanov¹,

Veinotte²,

Cullen³

et al. 2008

The Journal of Immunology

103

109

View full text Add to dashboard Cite

show abstract

“…By controlling leukocyte influx to foci of infection as well as migration of antigen presenting cells and lymphocytes to secondary lymphoid tissue, chemokines initiate and guide host immune responses (7)(8)(9)(10)12). The directed migration induced by chemokine signaling requires the establishment of chemokine concentration gradients.…”

Section: Chemokine Signalingmentioning

confidence: 99%

The role of chemokines during herpes simplex virus-1 infection

Todd¹

2008

Front Biosci

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Herpes simplex virus-type 1 is among the most prevalent and successful humans pathogens. Although infection is largely uncomplicated in the immunocompetent human host, HSV-1 infection can cause blinding corneal disease, and individuals with defects in innate or adaptive immunity are susceptible to herpes simplex encephalitis. Chemokines regulate leukocyte trafficking to inflamed tissues and play a crucial role in orchestrating the immune response to HSV-1 infection. In this review we will focus on the pathways that induce chemokine expression during HSV-1 infection and the implications of chemokine signaling on control of viral replication.

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“…10,[13][14][15][16] Chemokines such as CCR7-ligands Ebstein-Barr-Virus-inducedmolecule-1-ligand-chemokine (ELC/CCL19) and secondary lymphoid-tissue chemokine (SLC/CCL21) are key regulators of innate and adaptive immune responses, since they orchestrate migration of DC and T cells into secondary lymphatic tissues, thereby organizing immune synapse formation. [17][18][19][20] CCL19 is constitutively expressed by cells distributed throughout the T-cell zones of lymph nodes, spleen and Peyer's patches. Additionally, recent studies suggest that DC themselves are able to secrete CCL19 during activation and migration.…”

Section: Introductionmentioning

confidence: 99%