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The morphology of a CD4+ T cell changes from round to round-flattened during the IS formation. TCR is shown red, ICAM-1 is green, and scale bar is 2 Οm. Before IS formation, TCR was uniformed on the surface of T cell. After IS formation, TCR and ICAM-1 was accumulated at the interface of T-DC

Additional file 8: Figure S6. of Morphological change of CD4+ T cell during contact with DC modulates T-cell activation by accumulation of F-actin in the immunology synapse

The relationship between morphological changes and T-cell activation before and after IS formation. (A) Shape index changes and Ca2+ signals in a CD4+ T cell whose morphology changed to elongated-flattened (left panel). At 1,080 s, IS between CD4+ T cell and DC was formed. Before IS formation, the morphology of CD4+ T cell changed from round to elongated-flattened. At 1,680 s, the morphology of CD4+ T cell changed from elongated-flattened to round-flattened. The peak of Ca2+ signal was occurred before IS formation (at 800 s) and Ca2+ signal sustained at a low level. Images of the morphology and Ca2+ signals of the elongated-flattened T cell before and after IS formations are shown in the right panel. (B) Shape index changes and Ca2+ signals in a CD4+ T cell whose morphology changed to flattened (left panel). Images of the morphology and Ca2+ signals of the round-flattened T cell are shown in the right panel. IS between T cell and DC was formed at 560 s, when Ca2+ signal was at the highest level. The dotted white line depicts the contact boundary between the OT-II CD4+ T cells and the DCs. The calcium intensity was pseudo-colored with hues ranging from blue (low) to red (high). Ca2+ signalling was obtained every 40 s. ICAM-1 was labelled to be green. TCR was labelled to be red. After IS formation, TCR and ICAM-1 were accumulated into the IS of DC-T. Scale bar = 2 μm. (C-E) The distribution of ZAP-70, PLC-γ, PKC-θ (blue) and TCR (red) in the resting CD4+ T cell are shown in panel C to E, reseparately. Scale bar = 2 μm

Additional file 6: Figure S4. of Morphological change of CD4+ T cell during contact with DC modulates T-cell activation by accumulation of F-actin in the immunology synapse

Ca2+ responses in CD4+ T cells were measured and presented by △F/F. (A) The shape index change and Ca2+ signal in a CD4+ T cell whose morphology changed to elongated-flattened (top panel). (B) The shape index change and Ca2+ signal of a CD4+ T cell whose morphology changed to flattened (top panel). (C) The shape index change and Ca2+ signal in a resting T cell. (A-C) Ca2+ signalling was obtained every 10-s or 40-s. (D) Average Ca2+ responses of CD4+ T cells whose morphology changed to round-flattened or to elongated-flattened. (Data are shown as mean ± s.e.m., two-tailed Student’s t-test, ***p < 0.001). (E) Ca2+ response of a CD4+ T cell after it contacted DC pulsed OVA(323–339) in the presence of the cytochalasin D or not. (F) Average Ca2+ responses were measured in CD4+ T cells during the IS formation in the presence of cytochalasin D, nocodazole, TG or cytochalasin D and TG. (mean ± s.e.m, n = 25, three independent experiments), ***P < 0.001 (two-tailed Student’s t-test). (G) Average Ca2+ responses were measured in elongated and/ or CD4+ T cells during contact with DC in the presence of the cytochalasin D or TG treatment. (mean ± s.e.m, n = 25, three independent experiments), ** P < 0.01, ***P < 0.001 (two-tailed Student’s t-test). (H) Ca2+ response in a CD4+ T cell with TG stimulation and in a CD4+ T cell forming IS with TG pretreatment. (I) Ca2+ response of a CD4+ T cell with the cytochalasin D and TG treatment and a CD4+ T cells that formed IS with the cytochalasin D and TG pretreatment

Additional file 7: Figure S5. of Morphological change of CD4+ T cell during contact with DC modulates T-cell activation by accumulation of F-actin in the immunology synapse

The distribution of microtubules in CD4+ T cells which made contact with DCs. The distribution of microtubules was measured in an elongated-flattened CD4+ T cell (top line) or a round-flattened CD4+ T cell (middle line). In the presence of the nocodazole, the distribution of microtubules was measured in a CD4+ T cell (bottom line). TCR (red) and ICAM-1 (green) are used to mark the structure of IS, respectively. Dotted white line depicts the contact boundary of CD4+ T cells and DCs. Scale bar is 2 Οm

data_sheet_1_Soluble CD83 Alleviates Experimental Autoimmune Uveitis by Inhibiting Filamentous Actin-Dependent Calcium Release in Dendritic Cells.PDF

<p>Soluble CD83 (sCD83) is the extracellular domain of the membrane-bound CD83 molecule, and known for its immunoregulatory functions. Whether and how sCD83 participates in the pathogenesis of uveitis, a serious inflammatory disease of the eye that can cause visual disability and blindness, is unknown. By flow cytometry and imaging studies, we show that sCD83 alleviates experimental autoimmune uveitis (EAU) through a novel mechanism. During onset and recovery of EAU, the level of sCD83 rises in the serum and aqueous humor, and CD83⁺ leukocytes infiltrate the inflamed eye. Systemic or topical application of sCD83 exerts a protective effect by decreasing inflammatory cytokine expression, reducing ocular and splenic leukocyte including CD4⁺ T cells and dendritic cells (DCs). Mechanistically, sCD83 induces tolerogenic DCs by decreasing the synaptic expression of co-stimulatory molecules and hampering the calcium response in DCs. These changes are caused by a disruption of the cytoskeletal rearrangements at the DC–T cell contact zone, leading to altered localization of calcium microdomains and suppressed T-cell activation. Thus, the ability of sCD83 to modulate DC-mediated inflammation in the eye could be harnessed to develop new immunosuppressive therapeutics for autoimmune uveitis.</p