CD25 is a 55 kD glycoprotein, also known as the low affinity IL-2Rα, Ly-43, p55, or Tac. It is expressed on activated T and B cells, thymocyte subset, pre-B cells, and T regulatory cells. In association with CD122 (IL-2Rβ) and CD132(common γ chain), CD25 forms the high affinity signaling IL-2 receptor.
CD272, also known as B and T lymphocyte attenuator (BTLA), is an Ig superfamily co-inhitory receptor with structural similarity to programmed cell death 1 (PD-1) and CTLA-4. BTLA is expressed on B cells, T cells, macrophages, dendritic cells, NKT cells, and NK cells. Engagement of BTLA by its ligand herpes virus entry mediator (HVEM) is critical for negatively regulating immune response. The absence of BTLA with HVEM inhibitory interactions leads to increased experimental autoimmune encephalomyelitis severity, enhanced rejection of partially mismatched allografts, an increased CD8+ memory T cell population, increased severity of colitis, and reduced effectiveness of T regulatory cells. BTLA plays an important role in the induction of peripheral tolerance of both CD4+ and CD8+ T cells in vivo. Tolerant T cells have significantly higher expression of BTLA compared with effectors and naïve T cells. BTLA may cooperate with CTLA-4 and PD-1 to control T cell tolerance and autoimmunity. It was reported that BTLA may regulate T cell function by binding to B7-H4, but further studies are needed to confirm. The existence of three distinct BTLA alleles has been reported.
CD274, also known as B7-H1 or programmed death ligand 1 (PD-L1), is a 40 kD type I transmembrane protein and a member of the B7 family within the immunoglobulin receptor superfamily. It is expressed on T cells, B cells, NK cells, dendritic cells, IFN-γ activated endothelial cells, and monocytes. B7-H1 is one of the ligands of PD-1. The interaction of B7-H1 with PD-1 plays an important role in the inhibition of T cell responses. Other studies have shown that B7-H1 is able to costimulate T cell growth and cytokine production. CD274 is involved in costimulation essential for T cell proliferation and production of IL-10 and IFN-γ, in an IL-2-dependent and a PD-1-independent manner. Its interaction with PD-1 inhibits T cell proliferation and cytokine production.
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