Over-expression of integrin β3 can partially overcome the defect of integrin β3 signaling in transglutaminase 2 null macrophages

Beáta Tóth, Zsolt Sarang, György Vereb, Ailiang Zhang, Sakae Tanaka, Gerry Melino, László Fésüs, Zsuzsa Szondy

Research output: Contribution to journal › Article

19 Citations (Scopus)

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 β3, a known phagocytic receptor, and its bridging molecule, MFG-E8. In TG2 null macrophages integrin β3 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 β3 expression, which resulted alone in a high receptor concentration around the apoptotic cells without the requirement for accumulation, partially corrected the defect in integrin β3 signaling. Our data provide a proof for the concept that the function of TG2 is to stabilize accumulated integrin β3 concentration in the phagocytic cup.

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

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Integrins
Macrophages
Autoimmunity
transglutaminase 2
Enzymes
Proteins

Keywords

  • Apoptotic cells
  • Integrin signaling
  • Macrophages
  • Transglutaminase 2

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

Over-expression of integrin β3 can partially overcome the defect of integrin β3 signaling in transglutaminase 2 null macrophages. / Tóth, Beáta; Sarang, Zsolt; Vereb, György; Zhang, Ailiang; Tanaka, Sakae; Melino, Gerry; Fésüs, László; Szondy, Zsuzsa.

In: Immunology Letters, Vol. 126, No. 1-2, 22.09.2009, p. 22-28.

Research output: Contribution to journal › Article

Tóth, B, Sarang, Z, Vereb, G, Zhang, A, Tanaka, S, Melino, G, Fésüs, L & Szondy, Z 2009, 'Over-expression of integrin β3 can partially overcome the defect of integrin β3 signaling in transglutaminase 2 null macrophages', Immunology Letters, vol. 126, no. 1-2, pp. 22-28. https://doi.org/10.1016/j.imlet.2009.07.009
Tóth B, Sarang Z, Vereb G, Zhang A, Tanaka S, Melino G et al. Over-expression of integrin β3 can partially overcome the defect of integrin β3 signaling in transglutaminase 2 null macrophages. Immunology Letters. 2009 Sep 22;126(1-2):22-28. https://doi.org/10.1016/j.imlet.2009.07.009
Tóth, Beáta ; Sarang, Zsolt ; Vereb, György ; Zhang, Ailiang ; Tanaka, Sakae ; Melino, Gerry ; Fésüs, László ; Szondy, Zsuzsa. / Over-expression of integrin β3 can partially overcome the defect of integrin β3 signaling in transglutaminase 2 null macrophages. In: Immunology Letters. 2009 ; Vol. 126, No. 1-2. pp. 22-28.
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