IL-10 alters DC function via modulation of cell surface molecules resulting in impaired T-cell responses

2002 ◽  
Vol 215 (2) ◽  
pp. 162-172 ◽  
Author(s):  
Jacqueline M McBride ◽  
Thomas Jung ◽  
Jan E de Vries ◽  
Gregorio Aversa
Keyword(s):  
T Cell ◽  
Cell Surface ◽  
T Cell Responses ◽  
Cell Surface Molecules ◽  
Cell Responses ◽  
Surface Molecules ◽  
Dc Function

Cell-surface molecules involved in T-cell functions

1983 ◽  
Vol 4 (9) ◽  
pp. 256-259 ◽  
Author(s):  
Jeffrey A Bluestone ◽  
Richard J Hodes
Keyword(s):  
T Cell ◽  
Cell Surface ◽  
Cell Surface Molecules ◽  
Cell Functions ◽  
Surface Molecules

Specific T Cell Responses against Minor Histocompatibility Antigens Cannot Generally Be Explained by Absence of Their Allelic Counterparts on the Cell Surface

PROTEOMICS ◽  
2018 ◽  
Vol 18 (12) ◽  
pp. 1700250 ◽  
Author(s):  
Helena M. Bijen ◽  
Chopie Hassan ◽  
Michel G. D. Kester ◽  
George M. C. Janssen ◽  
Pleun Hombrink ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Surface ◽  
T Cell Responses ◽  
Histocompatibility Antigens ◽  
Minor Histocompatibility Antigens ◽  
Cell Responses

scholarly journals Specific interaction of lymphocyte function-associated antigen 3 with CD2 can inhibit T cell responses.

1993 ◽  
Vol 178 (1) ◽  
pp. 211-222 ◽  
Author(s):  
G T Miller ◽  
P S Hochman ◽  
W Meier ◽  
R Tizard ◽  
S A Bixler ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Surface ◽  
T Cell Activation ◽  
Cell Activation ◽  
Hepatitis B Surface Antigen ◽  
Specific Interaction ◽  
T Cell Responses ◽  
Accessory Cell ◽  
Lymphocyte Function ◽  
Cell Responses

Accessory cell surface molecules, such as T cell antigen CD2 and its ligand lymphocyte function-associated antigen 3 (LFA-3; CD58), are critical costimulatory pathways for optimal T cell activation in response to antigens. Interaction of CD2 with cell surface LFA-3 not only increases T cell/accessory cell adhesion, but also induces signal transduction events involved in the regulation of T cell responses. In this report, we show that specific interactions of LFA-3 with CD2 can result in T cell unresponsiveness to antigenic or mitogenic stimuli in vitro. By deletion of certain regions of the extracellular domain of LFA-3, we localized the CD2 binding site to the first domain of LFA-3. We then demonstrated that a soluble, purified first domain-LFA-3/IgG1 fusion protein (LFA3TIP) interacts with CD2 and binds to the same CD2 epitope as purified multimeric or cell surface-expressed LFA-3. LFA3TIP inhibits tetanus toxoid, hepatitis B surface antigen, anti-CD3 mAb, Con A, and phytohemagglutinin P-induced T cell proliferation, as well as xenogeneic and allogeneic mixed lymphocyte reactions (MLR). Unlike anti-LFA-3 or anti-CD2 monoclonal antibodies (mAbs) which inhibit T cell responses by blocking LFA-3/CD2 binding, LFA3TIP is capable of rendering T cells unresponsive to antigenic stimuli in situations where T cell activation is independent of CD2/LFA-3 interactions. Furthermore, LFA3TIP, but not blocking anti-CD2 mAbs, is capable of inducing T cell unresponsiveness to secondary stimulation in allogeneic MLR. This inhibition of T cell responses by LFA3TIP occurs through a different mechanism from that of mAbs to LFA-3 or CD2.

Antigen-Specific Transfer of Functional Programmed Death Ligand 1 From Antigen Presenting Cells Onto Human CD8+ T Cells Via Trogocytosis

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 584-584
Author(s):  
Regina Gary ◽  
Simon Voelkl ◽  
Ralf Palmisano ◽  
Andreas Mackensen
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd8 T Cells ◽  
T Cell Responses ◽  
Antigen Presenting Cells ◽  
Programmed Death Ligand 1 ◽  
Cell Responses ◽  
Surface Molecules ◽  
Programmed Death ◽  
Antigen Presenting

Abstract Abstract 584 Specific T-cell responses are initiated by T-cell receptor (TCR) recognition of peptide-MHC-complexes on antigen presenting cells (APCs). Upon specific interaction of T cells with APCs T cells capture membrane fragments and surface molecules of APCs in a process termed trogocytosis. Exchange of membrane molecules/antigens between immune cells has been observed for a long time, but the mechanisms and functional consequences of these transfers remain unclear. Here, we demonstrate that human antigen-specific CD8+ T cells do acquire the co-inhibitory molecule programmed death ligand 1 (PD-L1) from mature monocyte-derived dendritic cells (mDC) and tumor cells in an antigen-specific manner. The kinetics of PD-L1 transfer revealed a maximal PD-L1 expression on antigen-specific T cells within 3–4 hours after co-incubation with antigen-pulsed APCs, being detectable up to 72 hours. Antigen-pulsed immature DCs were less effective in transfering surface molecules such as PD-L1 onto CD8+ T cells after antigen-specific recognition. Using a transwell system we could show that the acquisition of PD-L1 requires cell-cell contact. Furthermore, PD-L1 cannot be acquired by T cells from a lysate of mDCs. The transfer process is impaired after pretreatment of T cells with concanamycin A, a specific inhibitor of vacuolar ATPases, playing an important role in membrane trafficking. Moreover, fixation of DCs with glutaraldehyde completely abrogated the acquisition of PD-L1 on T cells suggesting that an active interaction between APCs and T cells is required for trogocytosis. Of importance, CD8+ T cells which acquired PD-L1 complexes, were able to induce apoptosis of neighbouring PD-1 expressing CD8+ T cells, that could be completely blocked by an anti-PD-L1 antibody. In summary our data demonstrate for the first time that human antigen-specific CD8+ T cells take up functionally active PD-L1 from APCs in an antigen-specific fashion, leading to apoptosis of PD-1 expressing T cells. The transfer of functionally active co-inhibitory molecules from APCs onto human CD8+ T cells may serve to limit clonal expansion of antigen-specific T-cell responses but may also play a major role for T-cell exhaustion in chronic infection and tumor immunosurveillance. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Nanoparticles Targeting Dendritic Cell Surface Molecules Effectively Block T Cell Conjugation and Shift Response

ACS Nano ◽  
2011 ◽  
Vol 5 (3) ◽  
pp. 1693-1702 ◽  
Author(s):  
Chuda Chittasupho ◽  
Laura Shannon ◽  
Teruna J. Siahaan ◽  
Charlotte M. Vines ◽  
Cory Berkland
Keyword(s):  
T Cell ◽  
Dendritic Cell ◽  
Cell Surface ◽  
Cell Surface Molecules ◽  
Surface Molecules ◽  
Shift Response

Identification of Cell Surface Molecules Characterizing Human Cutaneous T-cell Lymphomas

2002 ◽  
Vol 43 (4) ◽  
pp. 741-746 ◽  
Author(s):  
M. Nikolova ◽  
M. Bagot ◽  
L. Boumsell ◽  
A. Bensussan
Keyword(s):  
T Cell ◽  
Cell Surface ◽  
Cell Surface Molecules ◽  
Surface Molecules ◽  
T Cell Lymphomas

scholarly journals Targeting Antigens to Dendritic Cell Receptors for Vaccine Development

2013 ◽  
Vol 2013 ◽  
pp. 1-22 ◽  
Author(s):  
Vasso Apostolopoulos ◽  
Theresia Thalhammer ◽  
Andreas G. Tzakos ◽  
Lily Stojanovska
Keyword(s):  
T Cell ◽  
Cell Surface ◽  
Immune Responses ◽  
Vaccine Development ◽  
T Cell Responses ◽  
Dual Function ◽  
Antigen Delivery ◽  
Surface Receptors ◽  
Mhc Molecules ◽  
Cell Responses

Dendritic cells (DCs) are highly specialized antigen presenting cells of the immune system which play a key role in regulating immune responses. Depending on the method of antigen delivery, DCs stimulate immune responses or induce tolerance. As a consequence of the dual function of DCs, DCs are studied in the context of immunotherapy for both cancer and autoimmune diseases. In vaccine development, a major aim is to induce strong, specific T-cell responses. This is achieved by targeting antigen to cell surface molecules on DCs that efficiently channel the antigen into endocytic compartments for loading onto MHC molecules and stimulation of T-cell responses. The most attractive cell surface receptors, expressed on DCs used as targets for antigen delivery for cancer and other diseases, are discussed.

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