PuSH - Publikationsserver des Helmholtz Zentrums 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)
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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.
Weitere Metriken?
Zusatzinfos bearbeiten [➜Einloggen]
Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter 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
ISSN (print) / ISBN 0006-4971
e-ISSN 1528-0020
Zeitschrift Blood
Quellenangaben Band: 114, Heft: 8, Seiten: 1696-1706 Artikelnummer: , Supplement: ,
Verlag American Society of Hematology
Verlagsort Washington
Begutachtungsstatus Peer reviewed