Journal
IMMUNOLOGY LETTERS
Volume 126, Issue 1-2, Pages 22-28Publisher
ELSEVIER
DOI: 10.1016/j.imlet.2009.07.009
Keywords
Macrophages; Apoptotic cells; Transglutaminase 2; Integrin signaling
Categories
Funding
- National Research Fund [OTKA T T049445, K 77587, F 67632, TS-44798]
- Ministry of Welfare [T (115/2006)]
- Hungarian Academy of Science
- MRC [MC_U132670600] Funding Source: UKRI
- Medical Research Council [MC_U132670600] Funding Source: researchfish
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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.
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