TAFA2, also known as FAM19A2, is a cytokine specifically expressed in the central nervous system. It belongs to the chemokine CC family and plays vital roles in multiple biological processes. TAFA2 is involved in neuronal cell survival, migration, and neurite outgrowth. It functions through activation of pathways like Rac1-p38, cAMP/PKA/CREB/BCL2, and may interact with receptors such as ADGRL1, CCR2 [1,2,3]. Genetic models, especially knockout mouse models, are valuable for studying its functions.

Tafa-2 knockout mice showed impairments in spatial learning, memory, and anxiety-like behaviors. Tafa-2 deficiency led to severe neuronal reduction and increased apoptosis in the brain via down-regulation of PI3K/Akt and MAPK/Erk pathways [4]. In addition, TAFA2 was transiently up-regulated during the inflammatory phase of fracture healing in mice, enhancing human skeletal (stromal) stem cell (hMSC) migration through activation of the Rac1-p38 pathway, without altering hMSC differentiation [1]. Also, in liver injury models, TAFA2 ablation and specific knockdown in neurons reduced liver injury as TAFA2 interacted with CCR2 and promoted macrophage activation [3].

In conclusion, TAFA2 is essential for neuronal survival, neurobiological functions, and plays a role in processes like stem cell migration and liver injury. The use of Tafa-2 knockout mouse models has revealed its significance in neurological disorders, bone fracture healing, and liver injury, providing insights into potential therapeutic targets for these disease areas.