Journal
JOURNAL OF IMMUNOLOGY
Volume 175, Issue 8, Pages 5146-5151Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.175.8.5146
Keywords
-
Categories
Funding
- NCI NIH HHS [CA33572] Funding Source: Medline
- NIAID NIH HHS [AI44922] Funding Source: Medline
Ask authors/readers for more resources
The steroid hormone estrogen regulates the differentiation, survival or function of diverse immune cells. Previously, we found that physiological amounts of 17 beta-estradiol act via estrogen receptors (ER) to promote the GM-CSF-mediated differentiation of dendritic cells (DC),from murine bone marrow progenitors in ex vivo cultures. Of the two major subsets of CD11c(+) DC that develop in these cultures, estrogen is preferentially required for the differentiation of a CD11b(int)Ly6C(-) population, although it also promotes increased numbers of a CD11b(high) Ly6C(+) population. Although both DC subsets express ER alpha, only the CD11b(high) Ly6C(+) DC express ER beta, perhaps providing a foundation for the differential regulation of these two DC types by estrogen. The two DC populations exhibit distinct phenotypes in terms of capacity for costimulatory molecule and MHC expression, and Ag internalization, which predict functional differences. The CD11b(int)Ly6C(-) population shows the greatest increase in MHC and CD86 expression after LPS activation. Most notably, the estrogen-dependent CD11b(int)Ly6C(-) DC express langerin (CD207) and contain Birbeck granules characteristic of Langerhans cells. These data show that estrogen promotes a DC population with the unique features of epidermal Langerhans cells and suggest that differentiation of Langerhans cells in vivo will be dependent upon local estrogen levels and ER-mediated signaling events in skin.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available