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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, Vol. 190, No. 3, 01.02.2013, p. 892-6.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Seelige, R, Natsch, C, März, S, Jing, D, Frye, M, Butz, S & Vestweber, D 2013, 'Cutting edge: Endothelial-specific gene ablation of CD99L2 impairs leukocyte extravasation in vivo', J IMMUNOL, vol. 190, no. 3, pp. 892-6. https://doi.org/10.4049/jimmunol.1202721

APA

Seelige, R., Natsch, C., März, S., Jing, D., Frye, M., Butz, S., & Vestweber, D. (2013). Cutting edge: Endothelial-specific gene ablation of CD99L2 impairs leukocyte extravasation in vivo. J IMMUNOL, 190(3), 892-6. https://doi.org/10.4049/jimmunol.1202721

Vancouver

Seelige R, Natsch C, März S, Jing D, Frye M, Butz S et al. Cutting edge: Endothelial-specific gene ablation of CD99L2 impairs leukocyte extravasation in vivo. J IMMUNOL. 2013 Feb 1;190(3):892-6. https://doi.org/10.4049/jimmunol.1202721

Bibtex

@article{d2a3eedfdc1245ce97442b6f16013e37,
title = "Cutting edge: Endothelial-specific gene ablation of CD99L2 impairs leukocyte extravasation in vivo",
abstract = "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.",
keywords = "12E7 Antigen, Animals, Antibodies/pharmacology, Antigens, CD/genetics, Cells, Cultured, Chemotaxis, Leukocyte/physiology, Coculture Techniques, Endothelial Cells/immunology, Gene Knockdown Techniques, Inflammation/immunology, Lung/blood supply, Male, Mice, Microcirculation, Myeloid Cells/immunology, Myositis/immunology, Neutrophils/physiology, Ovalbumin/immunology, Peptide Fragments/immunology, Peritonitis/chemically induced, Radiation Chimera, T-Lymphocytes/immunology, Transendothelial and Transepithelial Migration/physiology",
author = "Ruth Seelige and Christiane Natsch and Sigrid M{\"a}rz and Ding Jing and Maike Frye and Stefan Butz and Dietmar Vestweber",
year = "2013",
month = feb,
day = "1",
doi = "10.4049/jimmunol.1202721",
language = "English",
volume = "190",
pages = "892--6",
journal = "J IMMUNOL",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "3",

}

RIS

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 -