ABSTRACT
I. INTRODUCTION The T-helper (Th)1/Th2 balance is critically skewed, one way or the other, in several common human diseases, such as acute and chronic infections, autoimmunity, atopy/ allergy, and tumor growth [1,2]. These diseases frequently develop and progress in settings of hyperactivity or hypoactivity of specific neuroendocrine pathways [3-8]. Evidence accumulated over the last decade also suggests that various neuroendocrine mediators are involved in the control of the Th1/Th2 balance. Thus, the question arises: Are the changes in the Th1/Th2 balance and the activity of neuroendocrine pathways seen in the course of some common human diseases causally linked, or are these associations an epiphenomenon?
