Background and Objective
The function of immune cells is dependent upon a constant and adequate supply of energy (ATP), which is mainly formed by oxidative phosphorylation (OXPHOS). In arthritis, microenvironmental conditions are characterized by low levels of oxygen and glucose. Thus, effector cells of the innate immune system are recruited to sites where they face an acute need to respond to these demanding conditions. We investigated how immune cells maintain viability and function under these circumstances, and which immune processes are limited to what extent by energy deficiency.