Molecules involved in the immunologic synapse between DCs and T cells. Molecules expressed on DCs are listed on the left, with their corresponding T-cell ligands listed on the right. In the right-hand column, stimulatory interactions are indicated in black text and inhibitory interactions are indicated in red. Signaling from T cells to DCs also occurs but is not shown here. Initial DC–T-cell interactions are mediated by adhesion molecules and semaphorins such as neuropilin-1.⁵⁰  Following engagement of the T-cell receptor by pMHC complexes (signal 1) and engagement of CD28 by B7-1 and B7-2 (signal 2), additional molecules are up-regulated on both cell types that determine the nature of the ensuing T-cell response. Up-regulated molecules include semaphorins such as SEM4-A and members of the B7, CD28, TNF, and TNFR families of costimulatory molecules. Bidirectional signaling between these molecules results in either further T-cell activation or in attenuation of the T-cell response, depending on the molecules involved. Both B7-H1 and B7-DC interact with PD-1 to inhibit activated T cells, but B7-DC can also work synergistically with B7-1 and B7-2 to enhance T-cell activation through an unknown receptor.^51,52  B7x transmits an inhibitory signal by way of BTLA (B and T lymphocyte attenuator),⁵³  and B7-H3 can also transmit an inhibitory signal but through an unknown receptor.⁵⁴  Thromboxane A₂ (TXA₂) secreted by the DCs also attenuates the DC–T-cell interaction by way of the thromboxane receptor (TP) on the T cell.⁵⁵  Inhibitory molecules are thought to prevent excessive inflammation and autoimmunity. Alternative names for B7 family members are CD80 (B7-1), CD86 (B7-2), PD-L1 (B7-H1), PD-L2 (B7-DC), B7-H2 or ICOSL (B7RP-1), and B7-H4 (B7x).