Article

CD147 (Basigin/Emmprin) identifies FoxP3+CD45RO+CTLA4+-activated human regulatory T cells.

Centre for Molecular Medicine Norway, Nordic European Molecular Biology Laboratory Partnership, Oslo, Norway.
Blood (Impact Factor: 9.78). 09/2011; 118(19):5141-51. DOI: 10.1182/blood-2011-02-339242
Source: PubMed

ABSTRACT Human CD4(+)FoxP3(+) T cells are functionally and phenotypically heterogeneous providing plasticity to immune activation and regulation. To better understand the functional dynamics within this subset, we first used a combined strategy of subcellular fractionation and proteomics to describe differences at the protein level between highly purified human CD4(+)CD25(+) and CD4(+)CD25(-) T-cell populations. This identified a set of membrane proteins highly expressed on the cell surface of human regulatory T cells (Tregs), including CD71, CD95, CD147, and CD148. CD147 (Basigin or Emmprin) divided CD4(+)CD25(+) cells into distinct subsets. Furthermore, CD147, CD25, FoxP3, and in particular CTLA-4 expression correlated. Phenotypical and functional analyses suggested that CD147 marks the switch between resting (CD45RA(+)) and activated (CD45RO(+)) subsets within the FoxP3(+) T-cell population. Sorting of regulatory T cells into CD147(-) and CD147(+) populations demonstrated that CD147 identifies an activated and highly suppressive CD45RO(+) Treg subset. When analyzing CD4(+) T cells for their cytokine producing potential, CD147 levels grouped the FoxP3(+) subset into 3 categories with different ability to produce IL-2, TNF-α, IFN-γ, and IL-17. Together, this suggests that CD147 is a direct marker for activated Tregs within the CD4(+)FoxP3(+) subset and may provide means to manipulate cells important for immune homeostasis.

0 Followers
 · 
121 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: CD147, a member of the immunoglobulin super family, is a well-known potent inducer of extracellular matrix metalloproteinases. Studies show that CD147 is upregulated in inflammatory diseases. Atherosclerosis is a chronic inflammatory disease of the artery wall. Further understanding of the functions of CD147 in atherosclerosis and atherothrombosis may provide a new strategy for preventing and treating cardiovascular disease. In this review, we discuss how CD147 contributes to atherosclerosis and atherothrombosis.
    Journal of Cardiovascular Translational Research 01/2015; DOI:10.1007/s12265-015-9608-6 · 2.69 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: CD147 is a widely expressed integral plasma membrane glycoprotein and has been involved in a variety of physiological and pathological activities in combination with different partners, including cyclophilins, caveolin-1, monocarboxylate transporters, and integrins. Recent data demonstrate that both CyPA and CD147 significantly contribute to renal inflammation, acute kidney injury, renal fibrosis, and renal cell carcinoma. Here we review the current understanding of cyclophilin A and CD147 expression and functions in kidney diseases and potential implications for treatment of kidney diseases.
    Mediators of Inflammation 01/2014; 2014:728673. DOI:10.1155/2014/728673 · 2.42 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The addition of extracorporeal photopheresis (ECP) to a standard immunosuppressive drug therapy after heart transplantation in clinical studies has shown to be beneficial, for example, by reducing acute rejection, allograft vasculopathy or CMV infection. However, the protocols varied considerably, have a predetermined finite number of ECP treatments and adjuvant immunosuppressive regimens used in combination with ECP have differed significantly. Furthermore, there are scarce data to guide which patients should be treated with ECP and when or who would benefit further if ECP were to be continued long term to increase the safety by reducing immunosuppressive drug toxicities without losing efficacy. The knowledge of the tolerance-inducing effects of ECP-like upregulation of regulatory T cells and of dendritic cells may allow to develop a strategy to monitor immunomodulation effects of ECP to further identify ECP responders, the optimal individual ECP schedule and whether ECP therapy can replace or reduce immunosuppressive drug therapy.
    Immunotherapy 08/2014; 6(8):927-944. DOI:10.2217/imt.14.69 · 2.44 Impact Factor