Introduction

The early hypothesis that the brain and immune system communicated with each other was first proposed from the results of a study on the effect of taste aversion conditioning of humoral immune responsiveness (Ader and Cohen, 1975). Many studies have since confirmed the existence of such a bidirectional regulation [reviewed in (Besedovsky and Del Rey, 1996;Ader, 2000; Kohm and Sanders, 2001)] and provide plausible mechanisms by which the immune system alerts the brain that it is responding to an antigen, as well as mechanisms by which the brain regulates the level of immune cell activity that develops (Figure 5.1). Four key discoveries indicate that mechanisms exist by which the brain is able to communicate with cells of the peripheral immune system. First, primary and secondary lymphoid organs are innervated with sympathetic nerve fibers, and mechanisms exist by which signals are sent from the activated immune system to the brain. Second, the sympathetic neurotransmitter norepinephrine (NE) is released from nerve terminals residing within the parenchyma of lymphoid tissues after antigen or cytokine administration. Third, lymphoid cells, except for Th2 cells, express the p2-adrenergic receptor (p2AR) that binds NE to transduce extracellular signals to the cell interior. And finally, NE regulates lymphocyte activity at the level of gene expression. Although NE appears to regulate immune system activity overall, we will focus this chapter to a discussion of the role NE plays in regulating CD4+ T-cell and B-cell activity, with special emphasis placed on the role it plays in regulating the level of cytokine and antibody produced.

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