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. Author manuscript; available in PMC: 2014 Oct 8.
Published in final edited form as: Immunol Lett. 2013 Oct 8;155(0):10.1016/j.imlet.2013.09.016. doi: 10.1016/j.imlet.2013.09.016

Figure 1. Overview of steady-state thymopoiesis in addition to therapeutic strategies currently in clinical trials to enhance thymic recovery after HSCT.

Figure 1

The increase in sex steroids during life is generally thought to progressively impair BM and thymic lymphopoiesis (1). SSA using a LHRH-Ag (2) (that blocks the upstream signals stimulating sex steroid production (3)) reverses the age-related decline in BM and thymic function and promotes their rejuvenation. Similarly, therapeutic administration with GH, KGF or IL-7 promotes the regeneration of T cell lymphopoiesis (4). The process of thymopoiesis begins when circulating BM-derived T-lineage progenitors (CTP) seeds the thymus in the cortico-medullary junction (CMJ) (5) and undergo a series of well-defined maturation steps. This all occurs under the guidance and close interaction with the thymic stromal microenvironment; which is comprised of cTEC, mTEC, fibroblasts, macrophages (Mθ) and DC, and which provide survival, differentiation and homing factors to the developing thymocytes. Approximately 95% of thymocytes produced daily die during the process of beta-selection (6), positive selection (7) and negative selection (8) by apoptosis, which results in the generation of self-restricted and self-tolerant naïve CD4+ and CD8+ T cells (SP4 and SP8) (8). Several intrathymic factors have been shown to be important for endogenous T cell regeneration and may have some therapeutic benefit including IL-7, KGF and IL-22. SCZ (Sub-capsular zone), ILC (Innate lymphoid cells)