CD99-like 2 (CD99L2)-deficient mice are defective in the acute inflammatory response

Nakisha S. Rutledge, Evan W. Weber, Ryan Winger, Warren G. Tourtellotte, Seong Hoe Park, William A. Muller*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

6 Scopus citations


CD99-Like 2 (CD99L2) is a Type I glycoprotein expressed on leukocytes and endothelial cells as well as other cell types. It is related to CD99, although it shows only 38% sequence identity. CD99L2 has been shown to play a role in leukocyte extravasation in mice under various inflammatory conditions using anti-CD99L2 antibodies and, in one case by targeted deletion of CD99L2. We report here studies on an independently made CD99L2 "knockout mouse" that extend our knowledge of the role of CD99L2 in inflammation. CD99L2 deficiency did not affect the total or relative numbers of circulating leukocyte subsets, red blood cells, or platelets. Neither did CD99L2 deficiency affect the expression of ICAM-1, PECAM, or CD99 on endothelial cells. Mice lacking CD99L2 had a defective inflammatory response in the thioglycollate peritonitis model with a greater than 80% block in neutrophil infiltration and a nearly complete block in monocyte emigration into the peritoneal cavity measured 16 h after the inflammatory challenge. The mice will be a useful resource to study the role of CD99L2 in various acute and chronic inflammatory diseases.

Original languageEnglish (US)
Pages (from-to)455-459
Number of pages5
JournalExperimental and Molecular Pathology
Issue number3
StatePublished - Dec 1 2015


  • Adhesion molecule
  • CD99L2
  • Endothelium
  • Inflammation
  • Knockout mouse
  • Leukocyte

ASJC Scopus subject areas

  • Molecular Biology
  • Clinical Biochemistry
  • Pathology and Forensic Medicine


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