
* Laboratory of Immunology, Istituto Dermopatico dellImmacolata, IRCCS, Rome, Italy; and
Department of Pharmacology and Therapeutics, McGill University, Montreal, Canada
Correspondence: Andrea la Sala, Laboratory of Immunology, Istituto Dermopatico dellImmacolata, IRCCS, Via dei Monti di Creta, 104, 00167 Rome, Italy. E-mail: lasala{at}idi.it
Nerve growth factor (NGF) receptors are expressed in different cell types outside the nervous system, and increasing evidence indicates that NGF can act as a regulatory molecule during inflammatory and immune responses. In this study, we show that triggering of the high-affinity NGF receptor TrkA with agonists protects monocytes from apoptosis induced by gliotoxin or UVB radiation. TrkA stimulation up-regulates the expression of the anti-apoptotic Bcl-2 family members, Bcl-2, Bcl-XL, and Bfl-1. On the other hand, TrkA stimulation does not change the expression of MHC, CD80, CD86, CD40, and CD54 molecules, nor the antigen-presenting function of monocytes. In addition, during in vitro monocyte to dendritic cell differentiation TrkA expression is progressively lost, suggesting that NGF selectively affects monocyte but not dendritic cell survival.
Key Words: neurotrophin ultraviolet B radiation dendritic cells Bcl-2
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