Ligand activation of nerve growth factor receptor TrkA protects monocytes from apoptosis

Nerve growth factor (NGF) receptors are expressed in different cell types o utside the nervous system, and increasing evidence indicates that NGF can a ct as a regulatory molecule during inflammatory and immune responses. In th is study, we show that triggering of the high-affinity NGF receptor TrkA wi th agonists protects monocytes from apoptosis induced by gliotoxin ol UVB r adiation. TrkA stimulation up-regulates the expression of the anti-apoptoti c Bcl-2 family members, Bcl-2, Bcl-X-I, and Bfl-1. On the other hand, TrkA stimulation does not change. the expression of MHC, CD80, CD86, CD40, and C D54 molecules, nor the antigen-presenting function of monocytes, in additio n, during in vitro monocyte to dendritic cell differentiation TrkA expressi on is progressively lost, suggesting that NGF selectively affects monocyte but not dendritic cell survival.