Ok, regarding the predominance of MS in women, here is something more recent which supports part of what I was saying in another thread.
Women produce and utilize progesterone at a much higher rate than men. But men need some progesterone, also. Since progesterone is increased in women during pregnancy, and women with MS seem to do better during pregnancy, I believe that benefit is linked to levels of progesterone. I'm not saying this is any SINGLE relative causal relationship in MS, but it may explain why MS is higher in women. It's the hormonal interplay that makes the difference between men and women, and may make the difference in predisposition to MS between men and women. Or at least be a large contributing factor. It's still complex overall, and this is oversimplification, but I thought it might be interesting.
Lupus. 2004;13(9):639-42. Links
Progesterone supplement in pregnancy: an immunologic therapy?
Ragusa A, de Carolis C, dal Lago A, Miriello D, Ruggiero G, Brucato A, Pisoni MP, Muscara M, Merati R, Maccario L, Nobili M.
Center for the Prevention, Diagnosis and Therapy of Immunological Diseases in Pregnancy, Niguarda Hospital, Milan, Italy. email@example.com
One of the most interesting functions of the placenta is the regulation of the maternal immune response such that the fetal semi-allograft is tolerated during pregnancy. Trophoblasts are presumed to be essential to this phenomenon because they lie at the maternal-fetal interface, where they are in direct contact with cells of the maternal immune system. Trophoblasts do not express classic major histocompatibility complex (MHC) class II molecules. Surprisingly, cytotrophoblasts express more HLA-G, a MHC class Ib molecule, as they invade the uterus. Progesterone plays an important role in postovulatory regulation of the menstrual cycle. If fertilization occurs, progesterone supports implantation of the ovum and maintains the pregnancy. Progesterone has been named the 'hormone of pregnancy', because in preparing the endometrium for embryo implantation and facilitating endometrial development, it is critical to the very survival of a pregnancy. In addition, this key hormone inhibits the rejection of T cell-mediated tissue and also decreases myometrial activity and sensitivity throughout pregnancy. The cellular actions of progesterone are mediated through intracellular progesterone receptors (PRs), which are well studied gene regulators, not express classic major histocompatibility complex. The more used paradigm is relative to the alteration of relationship TH1/TH2, but the complexity of the respective distributions of cytokines at the materno-fetal interface, strongly suggest that, as useful as it certainly was for a while, the Th1/Th2 paradigm must now be considered as an oversimplification. Rather, the existing data point to sequential windows and are suggestive of a system where an extreme complexity is allied to very precise timing and tuning. They also suggest that the materno-fetal relationship is not simply maternal tolerance of a foreign tissue, but a series of intricate mutual cytokine interactions governing selective immune regulation and also control of the adhesion and vascularization processes during this dialogue. However, as shifting the immune response toward the Th2 pattern (IL-4, IL-5, IL-6) may benefit the fetus, whereas development of proinflammatory Th1 cells (secreting IL-2, IFN g, TNF a) may be harmful. Now we are working to open comprise the precise behaviour of NK populations, with the hope of obtaining a diagnostic test of the condition of abortion from 'immunological causes'.
PMID: 15485093 [PubMed - in process]