Polycystic ovaries require low Treg numbers

[Kofi]

This helps cement a theory I've been working on over the last year about
PCOS, androgens and viral infections.

Reprod Biol Endocrinol. 2009 May 18;7:47.
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The estrogen-injected female mouse: new insight into the etiology of
PCOS.
Chapman JC, Min SH, Freeh SM, Michael SD.
Department of Biological Sciences, Binghamton University, Binghamton,
New York 13902-6000, USA.

BACKGROUND: Female mice and rats injected with estrogen perinatally
become anovulatory and develop follicular cysts. The current consensus
is that this adverse response to estrogen involves the hypothalamus and
occurs because of an estrogen-induced alteration in the GnRH delivery
system. Whether or not this is true has yet to be firmly established.
The present study examined an alternate possibility in which anovulation
and cyst development occurs through an estrogen-induced disruption in
the immune system, achieved through the intermediation of the thymus
gland. METHODS, RESULTS AND CONCLUSION: A putative role for the thymus
in estrogen-induced anovulation and follicular cyst formation (a model
of PCOS) was examined in female mice by removing the gland prior to
estrogen injection. Whereas all intact, female mice injected with 20
microg estrogen at 5-7 days of age had ovaries with follicular cysts, no
cysts were observed in animals in which thymectomy at 3 days of age
preceded estrogen injection. In fact, after restoring immune function by
thymocyte replacement, the majority of thymectomized, estrogen-injected
mice had ovaries with corpora lutea. Thus, when estrogen is unable to
act on the thymus, ovulation occurs and follicular cysts do not develop.
This implicates the thymus in the cysts' genesis and discounts the role
of the hypothalamus. Subsequent research established that the disease is
transferable by lymphocyte infusion. Transfer took place between
100-day-old estrogen-injected and 15-day-old naive mice only when
recipients were thymectomized at 3 days of age. Thus, a prerequisite for
cyst formation is the absence of regulatory T cells. Their absence in
donor mice was judged to be the result of an estrogen-induced increase
in the thymus' vascular permeability, causing de facto circumvention of
the final stages of regulatory T cell development. The human thymus has
a similar vulnerability to steroid action during the fetal stage. We
propose that in utero exposure to excessive levels of steroids such as
estrogen has a long-term effect on the ability of the thymus to produce
regulatory T cells. In female offspring this can lead to PCOS [PMID
19450261]