ICAMs Are Not Obligatory for Functional Immune Synapses between Naive CD4 T Cells and Lymph Node DCs

• DOI: 10.1016/j.celrep.2017.12.103
• Publication Date: 2018-01-28T14:22:33Z
• Authors: Sara W. Feigelson; Adam Solomon; Adi Biram; Miki Hatzav; Moria Lichtenstein; Ofer Regev; Stav Kozlovski; Diana Varol; Caterina Curato; Dena Leshkowitz; Steffen Jung; Ziv Shulman; Ronen Alon
• Keywords: CD4-Positive T-Lymphocytes; 0301 basic medicine; T cell activation; QH301-705.5; adaptive immunity; differentiation; Dendritic Cells; vaccination; Intercellular Adhesion Molecule-1; 3. Good health; 03 medical and health sciences; antigens; inflammation; Humans; Lymph Nodes; Biology (General)

Protective immune responses depend on the formation of immune synapses between T cells and antigen-presenting cells (APCs). The two main LFA-1 ligands, ICAM-1 and ICAM-2, are co-expressed on many cell types, including APCs and blood vessels. Although these molecules were suggested to be key players in immune synapses studied in vitro, their contribution to helper T cell priming in vivo is unclear. Here, we used transgenic mice and intravital imaging to examine the role of dendritic cell (DC) ICAM-1 and ICAM-2 in naive CD4 T cell priming and differentiation in skin-draining lymph nodes. Surprisingly, ICAM deficiency on endogenous CD40-stimulated lymph node DCs did not impair their ability to arrest and prime CD4 lymphocyte activation and differentiation into Th1 and Tfh effectors. Thus, functional T cell receptor (TCR)-specific helper T cell synapses with antigen-presenting DCs and subsequent proliferation and early differentiation into T effectors do not require LFA-1-mediated T cell adhesiveness to DC ICAMs.