Cd27, a member of the tumour necrosis factor receptor superfamily (TNFRSF7), plays a key role in T-cell activation by providing a costimulatory signal. Its ligation with CD70 enhances T-cell proliferation and differentiation to effector and memory T cells. It is also constitutively expressed on a broad range of T-cells (αβ and γδ), NK-cells and B-cells, and involved in regulating lymphocyte function [2,3]. The CD27-CD70 pathway is associated with multiple biological processes and disease conditions, including anti-viral immunity, cancer, and autoimmune diseases [2,3,4]. Genetic models, such as KO/CKO mouse models, can be valuable for studying its functions.

In naive CD8+ T cells, CD27 ligation by trimeric CD70 ligand triggers internalization and degradation, recruiting TRAF2 and SHP-1, and modulating TCR and CD28 signals to promote memory-associated gene regulatory networks, which is relevant to T-cell immunotherapy [1]. In mice, co-stimulation of CD8+ T-cells through CD27 promotes immune activation and enhances primary, secondary, memory and recall responses towards viral infections [3]. Blockade of the CD27-CD70 pathway has been shown to ameliorate disease manifestations in animal models of autoimmune diseases, like murine collagen-induced arthritis and experimental colitis [4].

In conclusion, Cd27 is crucial for T-cell activation, differentiation, and immune responses. Studies using KO/CKO mouse models have revealed its role in anti-viral immunity and autoimmune diseases, suggesting that targeting the CD27-CD70 pathway could be a potential therapeutic strategy for these disease areas.