Reactivity of lymphocytes to a progesterone receptor-specific monoclonal antibody

Szekeres-Barthó, Júlia; Szekeres, G; Debré, Patrice; Autran, Brigitte; Chaouat, G.

doi:10.1016/0008-8749(90)90083-4

Cited by 115 publications

(60 citation statements)

References 6 publications

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“…As previously mentioned, some data had suggested that the allogeneic stimulus of the fetal semi-allograft was important in upregulating P receptors in gamma/delta T cells [5,11,12]. The data presented in this report clearly show that an allogeneic stimulus is not a prerequisite for a significant rise in serum PIBF.…”

Section: Discussionsupporting

confidence: 73%

“…The use of the P receptor modulator mifepristone abrogated the immune suppression by a factor secreted by gamma/ delta TCR+ and/or CD8+ lymphocytes. This suggested that P was needed to interact with a P receptor on these lymphocytes to activate them which then secreted some immunosuppressive factor [5][6][7][8]. Thus, the term coined for this immunosuppressive factor was the progesterone induced blocking factor (PIBF), and it has now been purified and synthesized by recombinant DNA technology [2,9].…”

Section: Introductionmentioning

confidence: 99%

“…The suggestion that the allogeneic stimulus of the fetal-placental unit may be responsible for a hormone independent upregulation of P receptors on gamma/delta T cells was derived from both in vitro and in vivo studies [5,11]. This concept was further strengthened by the demonstration that lymphocyte immunotherapy can increase P receptors on lymphocytes [12] and can increase PIBF expression [13].…”

Section: Introductionmentioning

confidence: 99%

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Evidence that exposure to progesterone alone is a sufficient stimulus to cause a precipitous rise in the immunomodulatory protein the progesterone induced blocking factor (PIBF)

Cohen

Check

Dougherty

2015

J Assist Reprod Genet

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Purpose To determine if exposure to progesterone alone is sufficient to increase the production of the immunomodulatory protein known as the progesterone induced blocking factor (PIBF). Also to determine what method of progesterone delivery or form of P best stimulates PIBF secretion. Methods Serum samples from patients with infertility and paid volunteers were evaluated for both PIBF and progesterone at various times during the follicular phase and the luteal phase in both natural cycles and cycles involving embryo transfer after endogenous and exogenous progesterone exposure and after various synthetic progestins. PIBF was measured by a non-commercial research ELISA assay. Comparisons were made of serum PIBF before and after exposure to progesterone, 17-hydroxyprogesterone, and oral contraceptives. PIBF was also measured before and after transfer of embryos.Results Progesterone alone without exposure to the fetal allogeneic stimulus was able to produce a marked increase in s e r u m P I B F. N e i t h e r a s y n t h e t i c p r o g e s t i n (19-nortestosterone derivative) nor 17-hydroxyprogesterone caused an increase in PIBF. Some PIBF is generally detected even in the follicular phase. Conclusions A previous concept considered that an allogeneic stimulus, e.g., from the fetal semi-allograft, was necessary to induce de novo progesterone receptors in gamma delta T cells, which, in turn, when exposed to a high concentration of progesterone, would secrete high levels of PIBF. These data show that exposure to an allogeneic stimulus is not needed to cause a marked rise in PIBF, merely progesterone alone is sufficient.

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Section: Discussionsupporting

confidence: 73%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Evidence that exposure to progesterone alone is a sufficient stimulus to cause a precipitous rise in the immunomodulatory protein the progesterone induced blocking factor (PIBF)

Cohen

Check

Dougherty

2015

J Assist Reprod Genet

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“…It has been proposed that progesterone, via the progesterone receptor and glucocorticoid receptor-dependent pathways (70), modulates the immune response during pregnancy, including CD4 + and CD8 + T cell differentiation (25,46,71). Interestingly, compared with WT mice, CD4 + T cells from Pgr -/-mice express lower levels of TGF-β1 (35) and produce significantly more IFN-γ upon stimulation (36).…”

Section: Discussionmentioning

confidence: 99%

Progesterone and HMOX-1 promote fetal growth by CD8+ T cell modulation

Solano¹,

Kowal²,

O’Rourke³

et al. 2015

J. Clin. Invest.

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“…3 (1)(2)(3)(4)(5). In the presence of this hormone, PR-positive lymphocytes mainly ␥␦ TCR-positive cells (6) produce a mediator protein named the progesterone-induced blocking factor (PIBF) (7,8).…”

Section: P Eripheral Lymphocytes From Healthy Pregnant Women Express mentioning

confidence: 99%

Molecular Cloning and Immunologic Characterization of a Novel cDNA Coding for Progesterone-Induced Blocking Factor

Polgar

Kispál

Lachmann

et al. 2003

The Journal of Immunology

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Previous studies from our laboratory showed that the immunomodulatory effects of progesterone are mediated by a 34-kDa protein, named the progesterone-induced blocking factor (PIBF). Lymphocytes of women with threatened abortion fail to produce this factor. Via inducing a Th2 biased cytokine production and blocking of NK activity, PIBF prevents induced pregnancy loss in mice, suggesting that substitution therapy with PIBF could be useful as an alternative treatment of certain forms of recurrent spontaneous abortions. Our study was aimed at mapping the sequence and structure of PIBF coding cDNA and characterizing the encoded protein product. Screening of a human liver cDNA library revealed a 2765-bp clone with a 2271-bp open reading frame. The PIBF1 cDNA encodes a protein of 757 amino acid residues with an 89-kDa predicted molecular mass, which shows no significant amino acid sequence homology with any known protein. PIBF produced via recombinant technique is recognized by the Ab specific for the secreted lymphocyte PIBF Ab, and possesses the biological activities of the secreted lymphocyte PIBF. The full-length PIBF is associated with the nucleus, whereas secretion of shorter forms, such a 34-kDa protein is induced by activation of the cell. The 48-kDa N-terminal part of PIBF is biologically active, and the part of the molecule, responsible for modulating NK activity is encoded by exons 2–4. These data provide an initial step for exploiting the possible diagnostic and therapeutic potential of this immunomodulatory molecule.

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Reactivity of lymphocytes to a progesterone receptor-specific monoclonal antibody

Cited by 115 publications

References 6 publications

Evidence that exposure to progesterone alone is a sufficient stimulus to cause a precipitous rise in the immunomodulatory protein the progesterone induced blocking factor (PIBF)

Evidence that exposure to progesterone alone is a sufficient stimulus to cause a precipitous rise in the immunomodulatory protein the progesterone induced blocking factor (PIBF)

Progesterone and HMOX-1 promote fetal growth by CD8+ T cell modulation

Molecular Cloning and Immunologic Characterization of a Novel cDNA Coding for Progesterone-Induced Blocking Factor

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