Optimal　T-cell　activation　requires　both　an　antigen-specific　and　a　costimulatory　signal.　CD167　is　a　tyrosine　kinase　receptor　for　native　type　I　collagen,　its　physiologic　functions　include　matrix　homeostasis　and　cell　growth,　adhesion,　branching,　and　migration,　but　the　specific　role　of　CD　167　in　T　cells　has　not　yet　been　characterized.　In　this　study,　we　found　that　CD167　expression　oil　T　cells　was　up-regulated　after　activation.　Cooperation　of　CD167　engagement　with　suboptimal　TCR/CD3　signals　induced　T-cell　proliferation,　enhanced　expression　of　activation　markers　such　as　CD25　and　CD69,　elevated　intracellular　calcium　mobilization　and　tyrosine　phosphorylation,　and　introduced　a　bias　toward　a　T(H)l/Tc1　immune　response.　Cooperation　of　CD167　engagement　also　enhanced　mixed　lymphocyte　responses　to　alloantigens.　Moreover,　CD167　rapidly　localized　to　the　aggregated　lipid　rafts　upon　T-cell　activation,　this　provided　a　molecular　base　for　the　Signaling　machinery　of　CD167.　Together　these　findings,　we　demonstrate　For　the　first　time　that　CD167　Could　serve　as　a　novel　costimulatory　receptor　for　T-cell　activation.