Most MS folks know this. But here is the proof. I am sure someone has not
seen it spelled out like this.
1: Expert Opin Investig Drugs 2001 Mar;10(3):467-76
The immunotherapeutic potential of melatonin.
Center for Experimental Pathology, Istituto Cantonale di Patologia, PO Box,
The interaction between the brain and the immune system is essential for the
adaptive response of an organism against environmental challenges. In this
context, the pineal neurohormone melatonin (MEL) plays an important role.
T-helper cells express G-protein coupled cell membrane MEL receptors and,
perhaps, MEL nuclear receptors. Activation of MEL receptors enhances the
release of T-helper cell Type 1 (Th1) cytokines, such as gamma-interferon
(gamma-IFN) and IL-2, as well as of novel opioid cytokines. MEL has been
reported also to enhance the production of IL-1, IL-6 and IL-12 in human
monocytes. These mediators may counteract stress-induced immunodepression
and other secondary immunodeficiencies and protect mice against lethal viral
encephalitis, bacterial diseases and septic shock. Therefore, MEL has
interesting immunotherapeutic potential in both viral and bacterial
infections. MEL may also influence haemopoiesis either by stimulating
haemopoietic cytokines, including opioids, or by directly affecting specific
progenitor cells such as pre-B cells, monocytes and NK cells. MEL may thus
be used to stimulate the immune response during viral and bacterial
infections as well as to strengthen the immune reactivity as a prophylactic
procedure. In both mice and cancer patients, the haemopoietic effect of MEL
may diminish the toxicity associated with common chemotherapeutic protocols.
Through its pro-inflammatory action, MEL may play an adverse role in
autoimmune diseases. Rheumatoid arthritis patients have increased nocturnal
plasma levels of MEL and their synovial macrophages respond to MEL with an
increased production of IL-12 and nitric oxide (NO). In these patients,
inhibition of MEL synthesis or use of MEL antagonists might have a
therapeutic effect. In other diseases such as multiple sclerosis the role of
MEL is controversial. However, the correct therapeutic use of MEL or MEL
antagonists should be based on a complete understanding of their mechanism
of action. It is not yet clear whether MEL acts only on Th1 cells or also on
T-helper Type 2 cells (Th2). This is an important point as the Th1/Th2
balance is of crucial importance in the immune system homeostasis.
Furthermore, MEL being the endocrine messenger of darkness, its endogenous
synthesis depends on the photoperiod and shows seasonal variations.
Similarly, the pharmacological effects of MEL might also be
season-dependent. No information is available concerning this point.
Therefore, studies are needed to investigate whether the immunotherapeutic
effect of MEL changes with the alternating seasons.
PMID: 11227046 [PubMed - indexed for MEDLINE]