Modulatory Effects of Oestrogen on Immunologic Responsiveness

Rj, Ablin; Gr, Bruns; Pd, Guinan; H, Al Sheik; Im, Bush

doi:10.1159/000473154

Cited by 6 publications

(3 citation statements)

References 21 publications

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“…Rheumatoid arthritis is also more prevalent in women than in men (37). Another example is the longer period required for the tissue rejection response in females (38). Castration shortens skin graft rejection time, suggesting that a deficiency of sex steroids activates the cellmediated immune response (39).…”

Section: Resultsmentioning

confidence: 99%

Estrogen deficiency stimulates B lymphopoiesis in mouse bone marrow.

Masuzawa

Miyaura²,

Onoe³

et al. 1994

J. Clin. Invest.

213

141

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We have found that an estrogen deficiency causes a marked increase in bone marrow cells. To examine the effect of estrogen on hemopoiesis, we characterized the increased population of bone marrow cells after ovariectomy (OVX). In OVX mice, the percentage of myeloid cells and granulocytes was decreased, whereas that of B220-positive B lymphocytes was selectively increased 2-4 wk after surgery. The total number of myeloid cells and granulocytes did not change appreciably, but that of B220-positive cells was greatly increased by OVX. When OVX mice were treated with estrogen, the increased B lymphopoiesis returned to normal. B220-positive cells were classified into two subpopulations, B220I0W and B220i9'h. The majority of the B220'W cells were negative for the IgM ,u chain, whereas most of the B220"'4" cells were ,i-positive. OVX selectively increased the precursors of B lymphocytes identified by B2201w. ,unegative phenotype, suggesting that an estrogen deficiency stimulates accumulation of B lymphocyte precursors. When bone marrow-derived stromal cells (ST2) were pretreated with estrogen then co-cultured with bone marrow cells in the presence of estrogen, the stromal cell-dependent B lymphopoiesis was greatly inhibited. The present study suggests that estrogen plays an important role in the regulation of B lymphocyte development in mouse bone marrow. (J. Clin.

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Section: Resultsmentioning

confidence: 99%

Estrogen deficiency stimulates B lymphopoiesis in mouse bone marrow.

Masuzawa

Miyaura²,

Onoe³

et al. 1994

J. Clin. Invest.

213

141

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“…In experimental animals, estrogen administration was also reported to accelerate autoimmune diseases (5,6). In parallel with these observations, intensive studies on the immuno-logical effects of estrogen have been reported (7)(8)(9)(10). It was, however, noticed that the effects of estrogen on the immune system so far described did not sufficiently elucidate possible mechanisms of sex hormones involved in the occurrence of autoimmune diseases.…”

mentioning

confidence: 92%

Estrogen administration activates extrathymic T cell differentiation in the liver.

Okuyama

Abo

Seki

et al. 1992

The Journal of Experimental Medicine

139

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Slln'lmaryIn addition to T cell differentiation in the thymus, we have recently reported that extrathymic T cell differentiation occurs preferentially in the sinusoids of the liver. Although this extrathymic pathway is relatively minor in normal mice, it becomes predominant in mice with autoimmune diseases, athymic mice, and aged mice. In the present study, injection of normal male C3H/He mice, 6-8 wk of age, with 1 mg of estrogen resulted in an increase in mononuclear cells (MNC) yielded from the liver and a drastic decrease in thymocytes approximately 10 d after such injection. This unique modulation was not observed with hydrocortisone injection (5 rag/mouse, i.p.) nor with irradiation (5 Gy/mouse). Rather, these immunosuppressive treatments induced a simultaneous decrease in cell number in both the liver and thymus. A time-kinetics study on the cell number and spontaneous cell proliferation revealed that an increase in spontaneous cell proliferation in the liver preceded the increase in the number of liver MNC, and a decrease in spontaneous cell proliferation in the thymus preceded the decrease in the number of thymocytes. At this time, an enrichment ofc~/3 T cells with intermediate T cell receptors (TCRs), including forbidden T cell oligoclones and V38 + cells, which are characterized as extrathymic o#3 T cells with unique properties, took place in the liver. On the other hand, the thymic atrophy induced by estrogen resulted in a prominent decrease in immature double-positive (CD4+8 +) 0#3 T cells with dull TCRs. These results indicate that estrogen administration activates an extrathymic pathway of T cell differentiation in the liver and reciprocally inactivates the intrathymic pathway. As extrathymic T cells have unique characteristics such as autoreactivity, the present findings might be intimately related to a female predominance of autoimmune diseases and suggest a possible role of estrogen in this phenomenon.

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“…Depressed cellular immunity has been reported in women taking oral contraceptives (Barnes et al, 1974). Studies by Ablin et al (1979) have also demonstrated depressed cellular immunity in prostate cancer patients receiving estrogen therapy.…”

Section: Pharmacological Levelsmentioning

confidence: 99%