Role of nerve growth factor in experimental autoimmune encephalomyelitis

The expression of neural regulatory molecules by immune cells that infiltra te the nervous system upon injury may be a mechanism for cross-regulation b etween the nervous system and the immune system. Several lines of evidence implicate nerve growth factor (NGF) signaling through its receptors (TrKA a nd p75(NGFR)) as a potential source of communication between the two system s. We observed changes in NGF mRNA expression and protein secretion by T ly mphocytes polarized toward the Th2 phenotype. The presence of NGF did not a ffect T cell proliferation or cytokine production in vitro. Mice treated wi th NGF by i.p. injection following induction of experimental autoimmune enc ephalomyelitis, an inflammatory, demyelinating disease of the central nervo us system, showed a delayed onset of disease and lower clinical scores duri ng the course of disease. These data suggest a role for NGF signaling in th e regulation of the immune response, possibly by enhancing sympathetic inne rvation of lymphoid tissues.