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J Transl Med. 2014 May 6;12:113. doi: 10.1186/1479-5876-12-113.

Interleukin-2 alters distribution of CD144 (VE-cadherin) in endothelial cells.

Author information

1
Rutgers Cancer Institute of New Jersey, Rutgers University, 195 Little Albany Street, Room 2007, New Brunswick, NJ 08901, USA. howard.kaufman@rutgers.edu.

Abstract

BACKGROUND:

High-dose IL-2 (HDIL2) is approved for the treatment of metastatic melanoma and renal cell carcinoma, but its use is limited in part by toxicity related to the development of vascular leak syndrome (VLS). Therefore, an understanding of the mechanisms that underlie the initiation and progression of HDIL2-induced increases in endothelial cell (EC) permeability leading to VLS are of clinical importance.

METHODS:

We established a novel ex vivo approach utilizing primary human pulmonary microvascular ECs to evaluate EC barrier dysfunction in response to IL-2.

RESULTS:

Complementary in vitro studies using exogenous IL-2 and ex vivo studies using serum from patients treated with IL-2 demonstrate that HDIL2 induces VLS through CD144 (vascular endothelial (VE)-cadherin) redistribution.

CONCLUSIONS:

These findings provide new insight into how IL-2 induces VLS and identifies VE-cadherin as a potential target for preventing IL-2-related VLS.

PMID:
24885155
PMCID:
PMC4062649
DOI:
10.1186/1479-5876-12-113
[Indexed for MEDLINE]
Free PMC Article
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