Impaired T cell activation and increased Th2 lineage commitment in Annexin-1-deficient T cells

Fulvio D'Acquisto, Nikolaos Paschalidis, Andre' L F Sampaio, Ahmed Merghani, Roderick J Flower, Mauro Perretti

Research output: Contribution to journalArticlepeer-review


Annexin-1 is a well-known endogenous anti-inflammatory protein that modulates the activation of cells of the innate immune system such as neutrophils and macrophages. We have recently reported a positive role for the exogenous protein on T cell differentiation, however, whether such a role holds true for the endogenous protein has yet to be determined. This aspect has been investigated here finding that Annexin-1-deficient T cells display an impaired activation and proliferation in response to anti-CD3 plus anti-CD28 stimulation. Furthermore, differentiation of T cells from Annexin-1-deficient mice in Th0/Th1/Th2 or Th17 skewing conditions demonstrated an increased Th2 phenotype compared to cells from control littermates. Similar results were obtained when we analyzed the Th1/Th2 profile of lymph node cells obtained from mice immunized with keyhole limpet hemocyanin or the inflammatory infiltrate in mouse model of allergic inflammation. These results demonstrate a novel modulatory role of endogenous Annexin-1 in TCR signaling and T cell differentiation and suggest this protein might play a dual and complementary role in the innate and adaptive immune response.

Original languageEnglish
Pages (from-to)3131-3142
Number of pages12
JournalCurrent opinion in immunology
Issue number11
Publication statusPublished - Nov 2007


  • Animals
  • Annexin A1
  • Cell Differentiation
  • Cell Proliferation
  • Cells, Cultured
  • Electrophoretic Mobility Shift Assay
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • Flow Cytometry
  • Lymphocyte Activation
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Reverse Transcriptase Polymerase Chain Reaction
  • T-Lymphocyte Subsets
  • T-Lymphocytes
  • Journal Article
  • Research Support, Non-U.S. Gov't

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