Cutting edge
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Cutting edge : Endothelial-specific gene ablation of CD99L2 impairs leukocyte extravasation in vivo. / Seelige, Ruth; Natsch, Christiane; März, Sigrid; Jing, Ding; Frye, Maike; Butz, Stefan; Vestweber, Dietmar.
in: J IMMUNOL, Jahrgang 190, Nr. 3, 01.02.2013, S. 892-6.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Cutting edge
T2 - Endothelial-specific gene ablation of CD99L2 impairs leukocyte extravasation in vivo
AU - Seelige, Ruth
AU - Natsch, Christiane
AU - März, Sigrid
AU - Jing, Ding
AU - Frye, Maike
AU - Butz, Stefan
AU - Vestweber, Dietmar
PY - 2013/2/1
Y1 - 2013/2/1
N2 - CD99-like 2 (CD99L2) is a membrane protein with moderate sequence homology to CD99, which initiates cell aggregation of transfected cells and that is strongly expressed on endothelial cells, neutrophils, and lymphocytes. We showed recently that Abs against CD99L2 inhibit neutrophil, but not T lymphocyte, recruitment into inflamed tissues. In this study, we have generated conditional gene-deficient mice for CD99L2 and show by analyzing them in various inflammation models several results. First, gene ablation of CD99L2 impairs neutrophil recruitment into inflamed cremaster and peritoneum. Second, despite the strong expression of CD99L2 on peripheral neutrophils, only gene ablation on endothelial cells but not on myeloid cells affects neutrophil extravasation. Third, in contrast to our previous Ab-based results, recruitment of activated T cells into inflamed skin was impaired in mice lacking CD99L2 on endothelial cells. We conclude that CD99L2 is an essential endothelial Ag for leukocyte extravasation, which does not require homophilic interactions with CD99L2 on leukocytes.
AB - CD99-like 2 (CD99L2) is a membrane protein with moderate sequence homology to CD99, which initiates cell aggregation of transfected cells and that is strongly expressed on endothelial cells, neutrophils, and lymphocytes. We showed recently that Abs against CD99L2 inhibit neutrophil, but not T lymphocyte, recruitment into inflamed tissues. In this study, we have generated conditional gene-deficient mice for CD99L2 and show by analyzing them in various inflammation models several results. First, gene ablation of CD99L2 impairs neutrophil recruitment into inflamed cremaster and peritoneum. Second, despite the strong expression of CD99L2 on peripheral neutrophils, only gene ablation on endothelial cells but not on myeloid cells affects neutrophil extravasation. Third, in contrast to our previous Ab-based results, recruitment of activated T cells into inflamed skin was impaired in mice lacking CD99L2 on endothelial cells. We conclude that CD99L2 is an essential endothelial Ag for leukocyte extravasation, which does not require homophilic interactions with CD99L2 on leukocytes.
KW - 12E7 Antigen
KW - Animals
KW - Antibodies/pharmacology
KW - Antigens, CD/genetics
KW - Cells, Cultured
KW - Chemotaxis, Leukocyte/physiology
KW - Coculture Techniques
KW - Endothelial Cells/immunology
KW - Gene Knockdown Techniques
KW - Inflammation/immunology
KW - Lung/blood supply
KW - Male
KW - Mice
KW - Microcirculation
KW - Myeloid Cells/immunology
KW - Myositis/immunology
KW - Neutrophils/physiology
KW - Ovalbumin/immunology
KW - Peptide Fragments/immunology
KW - Peritonitis/chemically induced
KW - Radiation Chimera
KW - T-Lymphocytes/immunology
KW - Transendothelial and Transepithelial Migration/physiology
U2 - 10.4049/jimmunol.1202721
DO - 10.4049/jimmunol.1202721
M3 - SCORING: Journal article
C2 - 23293350
VL - 190
SP - 892
EP - 896
JO - J IMMUNOL
JF - J IMMUNOL
SN - 0022-1767
IS - 3
ER -