scholarly journals Dendritic Cell Immunization Route Determines CD8+T Cell Trafficking to Inflamed Skin: Role for Tissue Microenvironment and Dendritic Cells in Establishment of T Cell-Homing Subsets

2004 ◽  
Vol 172 (2) ◽  
pp. 857-863 ◽  
Author(s):  
Jan C. Dudda ◽  
Jan C. Simon ◽  
Stefan Martin
2005 ◽  
Vol 73 (7) ◽  
pp. 3896-3902 ◽  
Author(s):  
Tricia L. Humphreys ◽  
Lee Ann Baldridge ◽  
Steven D. Billings ◽  
James J. Campbell ◽  
Stanley M. Spinola

ABSTRACT T-cell homing to infected skin is not well studied in humans. We examined sites experimentally infected with Haemophilus ducreyi by immunohistochemistry and flow cytometry for expression of receptors and ligands involved in cutaneous T-cell homing and determined the phenotypes of the T cells that trafficked to skin. Endothelial cells expressed E-selectin in infected but not uninfected skin, while peripheral node addressin (PNAd) was minimally expressed in all samples. CC chemokine ligand 27 (CCL27) was expressed in the epidermis and endothelium of both infected and uninfected skin. Interestingly, CCL21, a chemokine thought to be associated principally with T-cell trafficking in the lymphatic compartment, was highly expressed on the endothelium of infected skin. Few naive cells were present in experimental lesions, emphasizing the combined role of PNAd and CCL21 in trafficking of this subset. Memory cells (CD45RA−) dominated both CD4 and CD8 T-cell populations at the site of infection. Effector memory (CD45RA− CD27−) CD4+ and CD8+ T cells were enriched in lesions. Although the CC chemokine receptor 7-positive (CCR7+) population of both central memory (CD45RA− CD27+) and effector memory cells was not enriched in the skin compared to peripheral blood, CCR7+ cells were not precluded from entering infected skin. Taken together with our previous work (D. Soler, T. L. Humphreys, S. M. Spinola, and J. J. Campbell, Blood 101:1677-1683, 2003), these studies led us to propose a model of memory T-cell trafficking to skin in response to experimental H. ducreyi infection.


Immunity ◽  
2006 ◽  
Vol 25 (3) ◽  
pp. 511-520 ◽  
Author(s):  
Luzheng Liu ◽  
Robert C. Fuhlbrigge ◽  
Kara Karibian ◽  
Tian Tian ◽  
Thomas S. Kupper

2017 ◽  
Vol 152 (5) ◽  
pp. S614
Author(s):  
Sebastian Zundler ◽  
Daniela Schillinger ◽  
Anika Fischer ◽  
Raja Atreya ◽  
Rocío López-Posadas ◽  
...  

2006 ◽  
Vol 36 (3) ◽  
pp. 613-622 ◽  
Author(s):  
Linda N. Stiles ◽  
Martin P. Hosking ◽  
Robert A. Edwards ◽  
Robert M. Strieter ◽  
Thomas E. Lane

2013 ◽  
Vol 210 (9) ◽  
pp. 1855-1869 ◽  
Author(s):  
Zamaneh Mikhak ◽  
James P. Strassner ◽  
Andrew D. Luster

T cell trafficking into the lung is critical for lung immunity, but the mechanisms that mediate T cell lung homing are not well understood. Here, we show that lung dendritic cells (DCs) imprint T cell lung homing, as lung DC–activated T cells traffic more efficiently into the lung in response to inhaled antigen and at homeostasis compared with T cells activated by DCs from other tissues. Consequently, lung DC–imprinted T cells protect against influenza more effectively than do gut and skin DC–imprinted T cells. Lung DCs imprint the expression of CCR4 on T cells, and CCR4 contributes to T cell lung imprinting. Lung DC–activated, CCR4-deficient T cells fail to traffic into the lung as efficiently and to protect against influenza as effectively as lung DC–activated, CCR4-sufficient T cells. Thus, lung DCs imprint T cell lung homing and promote lung immunity in part through CCR4.


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