Over-expression of integrin beta 3 can partially overcome the defect of integrin beta 3 signaling in transglutaminase 2 null macrophages

Beata Toth, Zsolt Sarang, Gyoergy Vereb, Ailiang Zhang, Sakae Tanaka, Gerry Melino, Laszlo Fesues, Zsuzsa Szondy

Research output: Contribution to journalArticlepeer-review

Abstract

Transglutaminase 2 (TG2) is a protein crosslinking enzyme with many additional biological functions. We have previously shown that in TG2(-/-) mice the in vivo clearance of apoptotic cells is defective leading to autoimmunity. TG2 contributes to the formation of phagocytic portals by binding to both integrin beta(3), a known phagocytic receptor, and its bridging molecule, MFG-E8. In TG2 null macrophages integrin beta(3) cannot accumulate around the apoptotic cells and its signaling is impaired. In the present study we describe a subline of TG2 null mice, in which a compensatory increase in integrin beta(3) expression, which resulted alone in a high receptor concentration around the apoptotic cells without the requirement for accumulation, partially corrected the defect in integrin beta(3) signaling. Our data provide a proof for the concept that the function of TG2 is to stabilize accumulated integrin beta(3) concentration in the phagocytic cup. (C) 2009 Elsevier B.V. All rights reserved.

Original languageEnglish
Pages (from-to)22-28
Number of pages7
JournalImmunology Letters
Volume126
Issue number1-2
DOIs
Publication statusPublished - 22 Sep 2009

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