Blocking leukocyte emigration and inflammation by interfering with CD99l2

一种CD99L2、-CD99L2的技术，应用在抗炎症领域，能够解决不是等问题
CN101437539BInactive Publication Date: 2013-10-02CORNELL RES FOUNDATION INC
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Patent Information

Authority / Receiving Office
CN · China
Patent Type
Patents(China)
Current Assignee / Owner
CORNELL RES FOUNDATION INC
Publication Date
2013-10-02
Estimated Expiration
Not applicable · inactive patent

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Abstract

The present invention provides methods and compositions for modulating transendothelial migration (TEM) of leukocytes. In particular, inhibition of TEM can provide a potent therapeutic approach to treating inflammatory conditions. The invention specifically relates to the discovery that the adhesion molecule CD99L2 mediates TEM of leukocytes. CD99L2 is present on endothelial cells and leukocytes and mediates leukocyte-endothelial cell adhesion. Blockade of CD99L2 by use of a specific antibody blocks migration of leukocytes into a site of inflammation. CD99L2 shows functional analogy to the structurally-related molecule, CD99, inhibition of which, in conjunction with inhibition of PECAM, causes near total blockade of TEM. Thus, blocking CD99L2 on either endothelial cells or monocytes can block migration 80-90%. In conjunction with PECAM inhibitors, TEM blockade can approach 100%. Therapeutic treatments involving inhibition of CD99L2 show significant promise in remediation of inflammatory conditions.
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Description

[0001] Research leading to the present invention was supported in part by Grant No. HL64774 from the National Institutes of Health. Accordingly, the US Government may have certain rights in this invention. technical field

[0002] The present invention relates to anti-inflammatory methods, in particular to modulating transendothelial migration of leukocytes, and compositions for blocking transendothelial migration of leukocytes. Background technique

[0003] References cited by numbers throughout this specification are listed in the "References" section following the examples.

[0004] Previous studies (1-12) have demonstrated the transendothelial migration of platelet / endothelial cell adhesion molecule-1 (PECAM) in neutrophils (PMN), monocytes (Mo) and natural killer cells (NK) (TEM) in the key role. However, even under optimal circumstances, anti-PECAM agents block only 80-90% of leukocyte influx. While this is as good or better than the block of inflammation obtained b...

Claims

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