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. 2009 Feb 13;1(2):157–181. doi: 10.18632/aging.100024

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Copyright: ©2009 Bukovsky et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 10. — Immune adaptation and TCS "stop effect." (A) Immune adaptation (IA) and tissue longevity. The heart differentiates from early stages of ontogeny (LONG IA) and functions throughout life. The ovary differentiates later (MODERATE IA), and its normal function is limited by follicular renewal (until 35-40 years of age). Aging primordial follicles (apf) persist until exhausted (physiologic menopause). SHORTER period of ovarian development during IA causes earlier termination of follicular renewal during adulthood and results in POF. SHORT period of ovarian development during IA causes no follicular renewal and results in primary amenorrhea. Absence of corpora lutea (CL) during immune adaptation causes their cyclic degeneration, except during pregnancy, which is accompanied by immune suppression. fpf, fetal primordial follicles; fr, follicular renewal; POF, premature ovarian failure; CL, corpus luteum. Adapted from Ref. [31]. (B) Stages of cell differentiation during immune adaptation (left) sets TCS "stop effect" (StE) for tissue physiology and pathology during adulthood. Arrowheads indicate a tendency to StE "shifts" with age. Adapted from Ref. [3,30,33,108].