Acetylcholine (ACh) has been shown to modulate the function of mononuclear leukocytes, both by muscarinic and nicotinic ACh receptors. Acute stimulation of lymphocytes with ACh or muscarinic agonists enhances proinflammatory functions, whereas chronic application of the ACh agonist nicotine has an anti-inflammatory effect (Geng et al., 1996; Kawashima and Fujii, 2003). In macrophages, acute treatment with nicotine down-modulates effector functions (Wang et al., 2003, 2004). ACh regulating leukocytes might originate from the nervous system. However, once released, ACh is quickly degraded. Relevant concentrations occur only in the direct vicinity of nerve endings. Non-neuronal ACh acting in a paracrine or autocrine fashion is more likely to influence immune functions. Lymphocytes express all enzymes needed for ACh synthesis, including choline acetyltransferase (ChAT). In the rat, alternative splicing generates common ChAT and peripheral ChAT (pChAT). Up to now, ChAT expression by monocytes has not been demonstrated. We investigate pChAT in monocytes in an experimental model of acute renal allograft rejection. Inside the blood vessels of the transplant, huge numbers of activated, cytotoxic monocytes accumulate and probably contribute to graft destruction (Grau et al., 2001).