A progesterone-dependent immunomodulatory protein alters the Th1Th2 balance

Szekeres-Barthó, Júlia; Wegmann, T

doi:10.1016/0165-0378(96)00964-3

Cited by 312 publications

(158 citation statements)

References 40 publications

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“…Recently, a 34 kDa progesterone-induced blocking factor (PIBF) has been detected in sera from pregnant women [38]. PIBF seems to modulate the Th1/Th2 balance by inducing production of Th2-type cytokines [39], that are considered as essential in maintaining a successful pregnancy [40].…”

Section: Discussionmentioning

confidence: 99%

Suppression of Immunoglobulin Secretion by Soluble Annexin II

Aarli

Matre

1998

Scand J Immunol

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Aarli Å , Matre R. Suppression of Immunoglobulin Secretion by Soluble Annexin II. Scand J Immunol 1998;48:522-526 Annexin II (AII) belongs to a family of glycoproteins that bind negatively charged phospholipids in the presence of calcium. The annexins exert various biological functions. We have previously shown that soluble AII suppresses mitogen-induced lymphoproliferation in vitro. In this study we address the question of whether soluble AII may also affect immunoglobulin secretion. Mononuclear cells from peripheral blood were stimulated with pokeweed mitogen in vitro and immunoglobulin-secreting cells were quantified using an ELISPOT assay. Retroplacental serum and soluble AII significantly inhibited secretion of IgG and IgM when added at concentrations that did not affect lymphoproliferation or cell viability. The inhibitory effect was dose-and time dependent. Significant suppression was observed when soluble AII was added at concentrations of 0.1 and 0.01 mg/ml. The strongest inhibition was observed when soluble AII or retroplacental serum was added initially. The data demonstrate that soluble AII can suppress immunoglobulin secretion in vitro. AII seems to be a potent immunosuppressive substance. The presence of high levels of soluble AII in retroplacental serum may indicate a possible immunomodulatory role in normal pregnancy.

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Section: Discussionmentioning

confidence: 99%

Suppression of Immunoglobulin Secretion by Soluble Annexin II

Aarli

Matre

1998

Scand J Immunol

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“…Receptors for progesterone in lymphocytes appear to be selectively increased during pregnancy or mitogenic stimulation (50). Other studies have shown that lymphocytes cultured in the presence of progesterone produce an immunomodulatory protein that selectively induces IL-10, IL-4, and IL-3 production by ConA-stimulated lymphocytes (51 (Figure 2). We thus envisioned the possible appearance of autoreactive cells in the peripheral tissues (e.g., spleen) and expression of autoantibodies in the serum of estrogentreated mice.…”

Section: Animal Studesmentioning

confidence: 99%

Gender and risk of autoimmune diseases: possible role of estrogenic compounds.

Ahmed

Hissong

Verthelyi

et al. 1999

Environ Health Perspect

142

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A striking common feature of many autoimmune diseases in humans and experimental animals, despite differences in pathology, is that females are highly susceptible to autoimmune conditions compared to males. In several animal models, estrogens promote, whereas androgens abrogate, B-cell-mediated autoimmune diseases. To understand mechanisms by which estrogens regulate autoimmunity, it is first necessary to decipher estrogen effects on the normal immune system. Estrogen treatment of nonautoimmune mice diminished lymphocyte numbers in both developmental and mature lymphoid organs. Estrogen dysregulated T-and B-cell balance by inducing selective T-cell hypoactivity and B-cell hyperactivity. Even though estrogen did not alter the relative percentages of splenic T-cell subsets, splenic lymphocytes had a reduced proliferative response to T-cell stimulants and were refractory to rescue from activation-induced apoptosis compared to cells from placebo-treated mice. In contrast, estrogen induced B-cell hyperactivity (promoted autoantibodies to double-stranded DNA and phospholipids, increased numbers of plasma cells, and increased autoantibody yield per B cell). Note that treatment of normal mice with estrogen can alter T-and B-cell regulation and overcome B-cell tolerance to result in autoimmunity in normal individuals. Could environmental estrogens promote some human autoimmune disorders? Is there a link between environmental estrogens and autoimmune disorders, especially since these disorders are reported possibly more frequently? These provocative questions warrant investigation. Our findings on immunomodulatory effects may serve as a benchmark to examine whether endocrine-disrupting chemicals will have similar immunologic effects.

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“…Hormones like relaxin (produced by the corpus luteum) may also contribute to differentiation of Th cells or in favoring the shift of already differentiated Th cells to a type 1 profile [46]. On the other hand, progesterone has been shown to promote the development of a Th2 response, via an immunomodulatory protein known as progesteroneinduced blocking factor, which inhibits several Th1-type responses in vitro [47,48]. If there is a lack of suppression at the maternofetal interface, due to reduced levels of TGF-b2, a Th1 shift may be induced [49].…”

Section: T-helper 1 Versus T-helper 2 Responsementioning

confidence: 99%

Recurrent miscarriages: What is the role of cytokines?

Calleja‐Agius

Brincat

2008

Gynecological Endocrinology

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Recurrent miscarriage is defined as three or more consecutive miscarriages before 20 weeks of gestation. This condition is a frequent reproductive problem worldwide, affecting up to 1% of couples. Immune effector cell dysfunction has been implicated in the pathogenesis of early pregnancy loss. This dysfunction may involve defects in cytokines, growth factors and immunosuppressive factors at the maternofetal interface. This is a growing research field, especially the role of cytokines in recurrent miscarriage.

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A progesterone-dependent immunomodulatory protein alters the Th1Th2 balance

Cited by 312 publications

References 40 publications

Suppression of Immunoglobulin Secretion by Soluble Annexin II

Suppression of Immunoglobulin Secretion by Soluble Annexin II

Gender and risk of autoimmune diseases: possible role of estrogenic compounds.

Recurrent miscarriages: What is the role of cytokines?

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