Estrogen as an immunomodulator

Functional modification of CD11c+ liver dendritic cells during liver regeneration after partial hepatectomy in mice†

“…21 One interpretation of these results is that estrogen may drive Th2 and suppress Th1 responses, and that this is achieved by multiple interactions with cells of the immune system. 21,23,41 Our data demonstrate a significant increase in ER expression by DC isolated from livers 6 hours after PH (both in PBS-and Flt3L-treated animals), associated with concomitant increases in serum estrogen. These events occur together with the increased numbers of immature LDC, and with upregulation of IL-10 and downregulation of IFN-␥ gene expression by these cells.…”

“…9 In recent years, the role of dendritic cells ([DC] rare, bone marrow-derived, antigen-presenting cells) in the regulation of innate and adaptive immune responses has been well-documented. [15][16][17][18][19][20] Recently, several groups [21][22][23] have shown that estrogen administration leads to clinical improvement in experimental autoimmune encephalomyelitis, a model of multiple sclerosis, due to changes in DC function and the promotion of a Th2 immune response. In the current investigation, we have studied the role of murine DC in the early phase of liver regeneration after PH in normal animals, or those pretreated with the DC poietin Flt3L (fms-like tyrosine-3 ligand, a hematopoietic growth factor that expands dramatically the number of DC in lymphoid and non-lymphoid tissues, including the liver, 24 without changing their maturation state).…”

Zinc status and age-related changes in peripheral blood leukocyte subpopulations in healthy men and women aged 55–70 y: the ZENITH study

“…It is possible that the presence of oestrogen hormone in women delays ageing of the immune system, such that alterations occur in men at an earlier age than in women; thus resulting in our observation of different age-related associations in men and women. However, a clear understanding of the numerous effects that sex hormones have on immune function is lacking in current literature and, thus, such hypotheses cannot be confirmed (Verthelyi, 2001;Pietschmann et al, 2003;Lang, 2004). …”

Systemic reduction of functionally suppressive CD4dimCD25highFoxp3+ Tregs in human second trimester pregnancy is induced by progesterone and 17β-estradiol

“…Importantly, hormone concentrations corresponding to serum levels (33,34) caused slight but statistically not consistently significant changes that followed the very pronounced effects seen at higher concentrations. Expression of estrogen and progesterone receptors have been identified in various immune cells (35,36) but to our knowledge, only receptors for estrogen have been confirmed on Tregs (24).…”