Neutrophils, Monocytes, and Dendritic Cells Express the Same Specialized Form of PSGL-1 as Do Skin-Homing Memory T Cells: Cutaneous Lymphocyte Antigen

2001 ◽  
Vol 285 (3) ◽  
pp. 577-587 ◽  
Author(s):  
J.David Kieffer ◽  
Robert C. Fuhlbrigge ◽  
Dieter Armerding ◽  
Caroline Robert ◽  
Katalin Ferenczi ◽  
...  
Nature ◽  
10.1038/40166 ◽  
1997 ◽  
Vol 389 (6654) ◽  
pp. 978-981 ◽  
Author(s):  
Robert C. Fuhlbrigge ◽  
J. David Kieffer ◽  
Dieter Armerding ◽  
Thomas S. Kupper

2006 ◽  
Vol 117 (2) ◽  
pp. 418-425 ◽  
Author(s):  
Janine Bilsborough ◽  
Donald Y.M. Leung ◽  
Mark Maurer ◽  
Michael Howell ◽  
Mark Boguniewcz ◽  
...  

Blood ◽  
2008 ◽  
Vol 111 (5) ◽  
pp. 2497-2498
Author(s):  
Susumu Nakae ◽  
Keisuke Oboki ◽  
Hirohisa Saito

IgE/antigen-FcϵRI crosslinking promotes antigen internalization and apoptosis in mouse mast cells. Dendritic cells uptake the apoptotic mast cells carrying internalized antigens, and thus can efficiently present the antigens to memory T cells.


2019 ◽  
Vol 116 (20) ◽  
pp. 9969-9978 ◽  
Author(s):  
Andreia S. Da Costa ◽  
Jessica B. Graham ◽  
Jessica L. Swarts ◽  
Jennifer M. Lund

Immunological memory exists so that following infection an expanded population of pathogen-specific lymphocytes can rapidly and efficiently control infection in the case of reexposure. However, in the case of CD8+ T lymphocytes, a population of unconventional CD44+CD122+ virtual memory T cells (TVM) has been described that possesses many, though not all, features of “true memory” T cells, without the requirement of first encountering cognate antigen. Here, we demonstrate a role for regulatory T cell-mediated restraint of TVM at least in part through limiting IL-15 trans-presentation by CD11b+ dendritic cells. Further, we show that keeping TVM in check ensures development of functional, antigen-specific “true” memory phenotype CD8+ T cells that can assist in pathogen control upon reexposure.


2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Jean-François Daudelin ◽  
Mélissa Mathieu ◽  
Salix Boulet ◽  
Nathalie Labrecque

Following activation, naïve CD8+T cells will differentiate into effectors that differ in their ability to survive: some will persist as memory cells while the majority will die by apoptosis. Signals given by antigen-presenting cells (APCs) at the time of priming modulate this differential outcome. We have recently shown that, in opposition to dendritic cell (DC), CD40-activated B-(CD40-B) cell vaccination fails to efficiently produce CD8+memory T cells. Understanding why CD40-B-cell vaccination does not lead to the generation of functional long-lived memory cells is essential to define the signals that should be provided to naïve T cells by APCs. Here we show that CD40-B cells produce very low amount of IL-6 when compared to DCs. However, supplementation with IL-6 during CD40-B-cell vaccination did not improve memory generation. Furthermore, IL-6-deficient DCs maintained the capacity to promote the formation of functional CD8+effectors and memory cells. Our results suggest that in APC vaccination models, IL-6 provided by the APCs is dispensable for proper CD8+T-cell memory generation.


2006 ◽  
Vol 80 (6) ◽  
pp. 2863-2872 ◽  
Author(s):  
David M. Koelle ◽  
Jay Huang ◽  
Michael T. Hensel ◽  
Christopher L. McClurkan

ABSTRACT Herpes simplex virus (HSV) infections of humans are characterized by intermittent, lytic replication in epithelia. Circulating HSV-specific CD4 T cells express lower levels of preformed cutaneous lymphocyte-associated antigen (CLA), a skin-homing receptor, than do circulating HSV-specific CD8 T cells but, paradoxically, move into infected skin earlier than CD8 cells. Memory CD4 T cells develop strong and selective expression of CLA and E-selectin ligand while responding to HSV antigen in vitro. We now show that interleukin-12, type I interferon, and transforming growth factor beta are each involved in CLA expression by memory HSV type 2 (HSV-2)-specific CD4 T cells in peripheral blood mononuclear cells (PBMC). A reduction of the number of monocytes and dendritic cells from PBMC reduces CLA expression by HSV-2-responsive CD4 lymphoblasts, while their reintroduction restores this phenotype, identifying these cells as possible sources of CLA-promoting cytokines. Plasmacytoid dendritic cells are particularly potent inducers of CLA on HSV-reactive CD4 T cells. These observations are consistent with cooperation between innate and acquired immunity to promote a pattern of homing receptor expression that is physiologically appropriate for trafficking to infected tissues.


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