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The lung vascular filter as a site of immune induction for T cell responses to large embolic antigen

Monique Willart UGent, Hendrik Jan de Heer, Hamida Hammad UGent, Thomas Soullié, Kim Deswarte UGent, Björn E Clausen, Louis Boon, Henk C Hoogsteden and Bart Lambrecht UGent (2009) JOURNAL OF EXPERIMENTAL MEDICINE. 206(12). p.2823-2835
abstract
The bloodstream is an important route of dissemination of invading pathogens. Most of the small bloodborne pathogens, like bacteria or viruses, are filtered by the spleen or liver sinusoids and presented to the immune system by dendritic cells (DCs) that probe these filters for the presence of foreign antigen (Ag). However, larger pathogens, like helminths or infectious emboli, that exceed 20 mu m are mostly trapped in the vasculature of the lung. To determine if Ag trapped here can be presented to cells of the immune system, we used a model of venous embolism of large particulate Ag (in the form of ovalbumin [OVA]-coated Sepharose beads) in the lung vascular bed. We found that large Ags were presented and cross-presented to CD4 and CD8 T cells in the mediastinal lymph nodes (LNs) but not in the spleen or liver-draining LNs. Dividing T cells returned to the lungs, and a short-lived infiltrate consisting of T cells and DCs formed around trapped Ag. This infiltrate was increased when the Toll-like receptor 4 was stimulated and full DC maturation was induced by CD40 triggering. Under these conditions, OVA-specific cytotoxic T lymphocyte responses, as well as humoral immunity, were induced. The T cell response to embolic Ag was severely reduced in mice depleted of CD11c(hi) cells or Ly6C/G(+) cells but restored upon adoptive transfer of Ly6C(hi) monocytes. We conclude that the lung vascular filter represents a largely unexplored site of immune induction that traps large bloodborne Ags for presentation by monocyte-derived DCs.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
adaptive immunity, pulmonary granuloma-formation, steady-state, distinct, macrophage populations, in-vivo depletion, Plasmacytoid dendritic cells, blood monocyte subsets, CD8(+), tissues
journal title
JOURNAL OF EXPERIMENTAL MEDICINE
J. Exp. Med.
volume
206
issue
12
pages
2823 - 2835
Web of Science type
Article
Web of Science id
000272079300019
JCR category
MEDICINE, RESEARCH & EXPERIMENTAL
JCR impact factor
14.505 (2009)
JCR rank
3/90 (2009)
JCR quartile
1 (2009)
ISSN
0022-1007
DOI
10.1084/jem.20082401
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
805249
handle
http://hdl.handle.net/1854/LU-805249
date created
2009-12-09 12:42:07
date last changed
2012-11-06 11:16:56
@article{805249,
  abstract     = {The bloodstream is an important route of dissemination of invading pathogens. Most of the small bloodborne pathogens, like bacteria or viruses, are filtered by the spleen or liver sinusoids and presented to the immune system by dendritic cells (DCs) that probe these filters for the presence of foreign antigen (Ag). However, larger pathogens, like helminths or infectious emboli, that exceed 20 mu m are mostly trapped in the vasculature of the lung. To determine if Ag trapped here can be presented to cells of the immune system, we used a model of venous embolism of large particulate Ag (in the form of ovalbumin [OVA]-coated Sepharose beads) in the lung vascular bed. We found that large Ags were presented and cross-presented to CD4 and CD8 T cells in the mediastinal lymph nodes (LNs) but not in the spleen or liver-draining LNs. Dividing T cells returned to the lungs, and a short-lived infiltrate consisting of T cells and DCs formed around trapped Ag. This infiltrate was increased when the Toll-like receptor 4 was stimulated and full DC maturation was induced by CD40 triggering. Under these conditions, OVA-specific cytotoxic T lymphocyte responses, as well as humoral immunity, were induced. The T cell response to embolic Ag was severely reduced in mice depleted of CD11c(hi) cells or Ly6C/G(+) cells but restored upon adoptive transfer of Ly6C(hi) monocytes. We conclude that the lung vascular filter represents a largely unexplored site of immune induction that traps large bloodborne Ags for presentation by monocyte-derived DCs.},
  author       = {Willart, Monique and de Heer, Hendrik Jan and Hammad, Hamida and Soulli{\'e}, Thomas and Deswarte, Kim and Clausen, Bj{\"o}rn E and Boon, Louis and Hoogsteden, Henk C and Lambrecht, Bart},
  issn         = {0022-1007},
  journal      = {JOURNAL OF EXPERIMENTAL MEDICINE},
  keyword      = {adaptive immunity,pulmonary granuloma-formation,steady-state,distinct,macrophage populations,in-vivo depletion,Plasmacytoid dendritic cells,blood monocyte subsets,CD8(+),tissues},
  language     = {eng},
  number       = {12},
  pages        = {2823--2835},
  title        = {The lung vascular filter as a site of immune induction for T cell responses to large embolic antigen},
  url          = {http://dx.doi.org/10.1084/jem.20082401},
  volume       = {206},
  year         = {2009},
}

Chicago
Willart, Monique, Hendrik Jan de Heer, Hamida Hammad, Thomas Soullié, Kim Deswarte, Björn E Clausen, Louis Boon, Henk C Hoogsteden, and Bart Lambrecht. 2009. “The Lung Vascular Filter as a Site of Immune Induction for T Cell Responses to Large Embolic Antigen.” Journal of Experimental Medicine 206 (12): 2823–2835.
APA
Willart, M., de Heer, H. J., Hammad, H., Soullié, T., Deswarte, K., Clausen, B. E., Boon, L., et al. (2009). The lung vascular filter as a site of immune induction for T cell responses to large embolic antigen. JOURNAL OF EXPERIMENTAL MEDICINE, 206(12), 2823–2835.
Vancouver
1.
Willart M, de Heer HJ, Hammad H, Soullié T, Deswarte K, Clausen BE, et al. The lung vascular filter as a site of immune induction for T cell responses to large embolic antigen. JOURNAL OF EXPERIMENTAL MEDICINE. 2009;206(12):2823–35.
MLA
Willart, Monique, Hendrik Jan de Heer, Hamida Hammad, et al. “The Lung Vascular Filter as a Site of Immune Induction for T Cell Responses to Large Embolic Antigen.” JOURNAL OF EXPERIMENTAL MEDICINE 206.12 (2009): 2823–2835. Print.