The thymus is a primary lymphoid organ with both endocrine and immune funct
ions. There is a large body of evidence indicating the existence of a compl
ex neuroendocrine control of the thymus physiology. This is supported by th
e historic observation that the thymus becomes involuted during the respons
e to stress. The thymus is dramatically affected by the acute phase respons
e (APR), a systemic reaction to tissue injury and/or infection accompanied
by profound neuroendocrine and metabolic changes. The APR comprises alterat
ions in behavior, body temperature, and production and release of cytokines
, particularly interleukin (IL)-1, IL-6 and TNF alpha, and glucocorticoids
(GCs) and is characterized by suddenly increased production of so-called ac
ute phase proteins (APPs). The stimulation of APR activates the hypothalami
c-pituitary-adrenal (HPA) axis, resulting in the suppression of specific im
munity, which might serve to protect the organism from adverse immune react
ions; the immunostimulatory hormones (e.g., PRL, GH, IGF-I) are suppressed,
whereas the production of APPs in the liver is stimulated by IL-6, catecho
lamines and GCs. The most striking effect of the latter on the immune syste
m is the induction of apoptosis in the thymus. In concert with GCs, elevate
d levels of catecholamines also selectively suppress immune response mechan
isms. APR may be regarded as an emergency response that represents a switch
of the host defense from the adaptive immune response which is slow to dev
elop and is commanded by the thymus and T-lymphocytes to a less specific, b
ut more rapid and intense reaction. Here we discuss the immunoregulatory ch
anges during the APR with a special emphasis on the role of thymus in this
process.