Autoimmunity and premature ovarian failure.

Abstract:

PURPOSE OF REVIEW:The different patterns of autoreactivity that may account for the premature infertility observed in patients with premature ovarian failure are described. RECENT FINDINGS:Animal model studies have detailed fundamental immune dysregulatory patterns that induce ovarian failure in the context of global polyglandular involvement, as well as autoimmune mechanisms that induce ovarian failure in the context of targeted ovarian pathology. Recent studies on premature ovarian failure patients implicate the ubiquitously expressed glycolytic enzyme, alpha-enolase, as a potential antigenic target, particularly in those patients with polyglandular involvement; and the ovarian-specific maternal-effect protein, Mater, whose expression is essential for fertility. SUMMARY:Several fundamentally distinct mechanisms may account for premature ovarian failure, including global immune dysregulation, particularly in patients with polyglandular autoimmunity. Premature ovarian failure may also be due to inflammatory autoimmunity targeted to ovarian-specific germline antigens (e.g., zona pellucida proteins or Mater) or differentiation/regulatory factors (e.g., inhibin-alpha). Moreover, the ovarian autoimmunity may be mediated by T cells (e.g., those targeting zona pellucida proteins) or B cells/antibodies (e.g., those targeting inhibin-alpha). Thus premature ovarian failure appears to be a complex disease entity with multiple underlying etiopathogenic contributions including the possibility of several distinctly different autoimmune mechanisms.

authors

Tuohy VK,Altuntas CZ

doi

10.1097/GCO.0b013e328220e90c

subject

Has Abstract

pub_date

2007-08-01 00:00:00

pages

366-9

issue

4

eissn

1040-872X

issn

1473-656X

pii

00001703-200708000-00014

journal_volume

19

pub_type

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