PuSH - Publication Server of Helmholtz Zentrum München

Kneilling, M.* ; Mailhammer, R. ; Hültner, L. ; Schönberger, T.* ; Fuchs, K.* ; Schaller, M.* ; Bukala, D.* ; Massberg, S.* ; Sander, C.A.* ; Braumüller, H.* ; Eichner, M.* ; Maier, K.L. ; Hallmann, R.* ; Pichler, B.J.* ; Haubner, R.* ; Gawaz, M. ; Pfeffer, K.* ; Biedermann, T.* ; Röcken, M.*

Direct crosstalk between mast cell-TNF and TNFR1-expressing endothelia mediates local tissue inflammation.

Blood 114, 1696-1706 (2009)
DOI PMC
Open Access Green as soon as Postprint is submitted to ZB.
Signaling through tumor necrosis factor receptor 1 (TNFR1) controls bacterial infections and the induction of inflammatory Th1 cell-mediated autoimmune diseases. By dissecting Th1 cell-mediated delayed-type hypersensitivity responses (DTHRs) into single steps, we localized a central defect to the missing TNFR1 expression by endothelial cells (Ecs). Adoptive transfer and mast cell knockin experiments into Kit(W)/Kit(W-v), TNF-/-, and TNFR1(-/-) mice showed that the signaling defect exclusively affects mast cell-EC interactions but not T cells or antigen-presenting cells. As a consequence, TNFR1(-/-) mice had strongly reduced mRNA and protein expression of P-selectin, E-selectin, ICAM-1, and VCAM-1 during DTHR elicitation. In consequence, intravital fluorescence microscopy revealed up to 80% reduction of leukocyte rolling and firm adhesion in TNFR1(-/-) mice. As substitution of TNF-/- mice with TNF-producing mast cells fully restored DTHR in these mice, signaling of mast cell-derived TNF through TNFR1-expressing Ecs is essential for the recruitment of leukocytes into sites of inflammation.
Impact Factor
Scopus SNIP
Web of Science
Times Cited
Scopus
Cited By
Altmetric
10.432
3.040
28
37
Tags
Annotations
Special Publikation
Hide on homepage

Edit extra information
Edit own tags
Private
Edit own annotation
Private
Hide on publication lists
on hompage
Mark as special
publikation
Publication type Article: Journal article
Document type Scientific Article
Keywords tumor-necrosis-factor; contact hypersensitivity response; intercellular-adhesion molecule-1; versus-host-disease; factor-receptor; t-cells; p-selectin; mice deficient; ultraviolet-b; factor-alpha
Language english
Publication Year 2009
HGF-reported in Year 0
ISSN (print) / ISBN 0006-4971
e-ISSN 1528-0020
Journal Blood
Quellenangaben Volume: 114, Issue: 8, Pages: 1696-1706 Article Number: , Supplement: ,
Publisher American Society of Hematology
Publishing Place Washington
Reviewing status Peer reviewed
POF-Topic(s) 30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
30202 - Environmental Health
Research field(s) Immune Response and Infection
Lung Research
PSP Element(s) G-501400-005
G-505000-001
PubMed ID 19546478
Scopus ID 70349566472
Erfassungsdatum 2009-12-31