CD80 and CD86 differentially regulate mechanical interactions of T-cells with antigen-presenting dendritic cells and B-cells

PLoS One. 2012;7(9):e45185. doi: 10.1371/journal.pone.0045185. Epub 2012 Sep 14.

Abstract

Functional T-cell responses are initiated by physical interactions between T-cells and antigen-presenting cells (APCs), including dendritic cells (DCs) and B-cells. T-cells are activated more effectively by DCs than by B-cells, but little is known about the key molecular mechanisms that underpin the particular potency of DC in triggering T-cell responses. To better understand the influence of physical intercellular interactions on APC efficacy in activating T-cells, we used single cell force spectroscopy to characterize and compare the mechanical forces of interactions between DC:T-cells and B:T-cells. Following antigen stimulation, intercellular interactions of DC:T-cell conjugates were stronger than B:T-cell interactions. DCs induced higher levels of T-cell calcium mobilization and production of IL-2 and IFNγ than were elicited by B-cells, thus suggesting that tight intercellular contacts are important in providing mechanically stable environment to initiate T-cell activation. Blocking antibodies targeting surface co-stimulatory molecules CD80 or CD86 weakened intercellular interactions and dampen T-cell activation, highlighting the amplificatory roles of CD80/86 in regulating APC:T-cell interactions and T-cell functional activation. The variable strength of mechanical forces between DC:T-cells and B:T-cell interactions were not solely dependent on differential APC expression of CD80/86, since DCs were superior to B-cells in promoting strong interactions with T-cells even when CD80 and CD86 were inhibited. These data provide mechanical insights into the effects of co-stimulatory molecules in regulating APC:T-cell interactions.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antigen Presentation / immunology
  • B-Lymphocytes / immunology
  • B-Lymphocytes / metabolism*
  • B7-1 Antigen / metabolism*
  • B7-2 Antigen / metabolism*
  • Calcium / metabolism
  • Cell Communication* / immunology
  • Cell Lineage
  • Dendritic Cells / immunology
  • Dendritic Cells / metabolism*
  • Histocompatibility Antigens Class I / metabolism
  • Immunophenotyping
  • Lymphocyte Activation / immunology
  • Mice
  • Mice, Knockout
  • T-Lymphocytes / immunology
  • T-Lymphocytes / metabolism*

Substances

  • B7-1 Antigen
  • B7-2 Antigen
  • Histocompatibility Antigens Class I
  • Calcium

Grants and funding

Biomedical Research Council (BMRC) and Joint Council Office Grant (JCO Grant No: 10/03/FG/05/03) from the Agency for Science, Technology and Research (A*STAR) are acknowledged for funding this study. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.