Adhesion of human T cells to antigen-presenting cells through SIRP 2-CD47 interaction costimulates T-cell proliferation

نویسندگان

  • Laura Piccio
  • William Vermi
  • Kent S. Boles
  • Anja Fuchs
  • Carey A. Strader
  • Fabio Facchetti
  • Marina Cella
  • Marco Colonna
چکیده

Signal-regulatory proteins (SIRPs) are transmembrane glycoproteins belonging to the immunoglobulin (Ig) superfamily that are expressed in the immune and central nervous systems. SIRP binds CD47 and inhibits the function of macrophages, dendritic cells, and granulocytes, whereas SIRP 1 is an orphan receptor that activates the same cell types. A recently identified third member of the SIRP family, SIRP 2, is as yet uncharacterized in terms of expression, specificity, and function. Here, we show that SIRP 2 is expressed on T cells and activated natural killer (NK) cells and, like SIRP , binds CD47, mediating cell-cell adhesion. Consequently, engagement of SIRP 2 on T cells by CD47 on antigen-presenting cells results in enhanced antigen-specific T-cell proliferation. (Blood. 2005;105: 2421-2427)

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Adhesion of human T cells to antigen-presenting cells through SIRPbeta2-CD47 interaction costimulates T-cell proliferation.

Signal-regulatory proteins (SIRPs) are transmembrane glycoproteins belonging to the immunoglobulin (Ig) superfamily that are expressed in the immune and central nervous systems. SIRPalpha binds CD47 and inhibits the function of macrophages, dendritic cells, and granulocytes, whereas SIRPbeta1 is an orphan receptor that activates the same cell types. A recently identified third member of the SIR...

متن کامل

RED CELLS Species- and cell type–specific interactions between CD47 and human SIRP

CD47 on red blood cells (RBCs) reportedly signals “self” by binding SIRP on phagocytes, at least in mice. Such interactions across and within species, from mouse to human, are not yet clear and neither is the relation to cell adhesion. Using human SIRP 1 as a probe, antibody-inhibitable binding to CD47 was found only with human and pig RBCs (not mouse, rat, or cow). In addition, CD47mediated ad...

متن کامل

Costimulation of T Cell Activation by Integrin-associated Protein (CD47) Is an Adhesion-dependent, CD28-independent Signaling Pathway

The integrin-associated protein (IAP, CD47) is a 50-kD plasma membrane protein with a single extracellular immunoglobulin variable (IgV)-like domain, a multiply membrane-spanning segment, and alternatively spliced short cytoplasmic tails. On neutrophils, IAP has been shown to function in a signaling complex with beta 3 integrins. However, the function of IAP on T cells, which express little or ...

متن کامل

Human Leukocyte Antigen-G Expression on Dendritic Cells Induced by Transforming Growth Factor-β1 and CD4+ T Cells Proliferation

Background: During antigen capture and processing, mature dendritic cells (DC) express large amounts of peptide-MHC complexes and accessory molecules on their surface. DC are antigen-presenting cells that have an important role in tolerance and autoimmunity. The transforming growth factor-beta1 (TGF-β1) cytokine has a regulatory role on the immune and non-immune cells. The aim of this study is ...

متن کامل

CD47Low Status on CD4 Effectors Is Necessary for the Contraction/Resolution of the Immune Response in Humans and Mice

How do effector CD4 T cells escape cell death during the contraction of the immune response (IR) remain largely unknown. CD47, through interactions with thrombospondin-1 (TSP-1) and SIRP-α, is implicated in cell death and phagocytosis of malignant cells. Here, we reported a reduction in SIRP-α-Fc binding to effector memory T cells (T(EM)) and in vitro TCR-activated human CD4 T cells that was li...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2005