Up‐modulation of interferon‐γ mediates the enhancement of spontanous cytotoxicity in prolactin‐activated natural killer cells

Matera, Lina; Contarini, M.; Bellone, Graziella; Forno, Brunella; Biglino, A

doi:10.1046/j.1365-2567.1999.00893.x

Cited by 48 publications

(29 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…NK cells also express IFN-␥ mRNA and release IFN-␥ in the presence of pituitary or recombinant PRL. 54 Cessario et al 55 reported enhanced yields of IFN-␥ in PRL-treated human peripheral blood mononuclear cells and correction of a defect in IFN-␥ production and altered lymphocyte proliferation in bromocriptine-treated mice with PRL supplementation. 1,10 Delayed or abrogated rejection of tumor in allogenic mice with anti-IFN-␥ antibody 56 and suppression of PRL-mediated augmentation of NK activity in the presence of anti-IFN-␥ MAb 54 further suggested that PRL may regulate antitumor immune responses through IFN-␥.…”

Section: Discussionmentioning

confidence: 99%

Prolactin regulates antitumor immune response through induction of tumoricidal macrophages and release of IL‐12

Majumder

Biswas

Chattopadhyay

2001

Intl Journal of Cancer

View full text Add to dashboard Cite

The involvement of PRL in regulating monocyte/macrophage functions is suggested by the presence of PRL-Rs in these cells. Here, we show that PRL, though it failed to activate mouse peritoneal resident macrophages (RMs), acted as a second signal and activated mouse peritoneal inflammatory macrophages (EMs) to a tumoricidal state. The cytotoxicity of mouse tumor-associated macrophages (TAMs) isolated at day 1 of tumor (Ehrlich ascites carcinoma, EAC) growth was enhanced by PRL. However, with progression of tumor growth, TAMs became nonresponsive to the hormone.

show abstract

Section: Discussionmentioning

confidence: 99%

Prolactin regulates antitumor immune response through induction of tumoricidal macrophages and release of IL‐12

Majumder

Biswas

Chattopadhyay

2001

Intl Journal of Cancer

View full text Add to dashboard Cite

show abstract

“…Recently, it was reported that PRL exhibited a dose-dependent enhancement upon both IgM and IgG secretion treated with anti-IgM and IL-2 or anti-IgM alone in vitro [15,16], indicating that PRL may affect peripheral B-cell function. PRL also increased the proliferating response and cytotoxicity of human, murine or rat NK cells to sensitive or insensitive tumor independently or synergistically with IL-2 in vitro [17][18][19][20]. We previously reported that PRL improved the hematopoiesis and lymphocyte development in syngeneic bone marrow transplantation [21][22][23][24], and exerted anti-tumor effects on tumor-bearing mice in vivo [25].…”

Section: Introductionmentioning

confidence: 99%

Expression of prolactin receptor and response to prolactin stimulation of human NK cell lines

Sun

Wei

et al. 2004

Cell Res

View full text Add to dashboard Cite

We have previously shown a critical role of prolactin (PRL) during maturation and anti-tumor effects of murine natural killer (NK) cells in vitro and in vivo. We extended that study by exploring the ability of human NK cell lines (NK-92 and YT cell) to express PRL receptor (PRL-R) and to respond to PRL stimulation in vitro. Both human NK cell lines constitutively expressed PRL-R on membrane and mRNA transcripts, NK-92 cells contained higher level of PRL-R than YT cells, which correlated to the enhanced capacity of the cells to proliferate and to lyse target cells in response to PRL stimulation in the presence of trace amount of IL-2 or IL-15 in vitro. Two differences between IL-2 and IL-15 in functioning on human NK cells were for the first time observed. PRL synergized with IL-15 to improve proliferation of NK cells in a dose-dependent manner without double peak manifesting like IL-2. Although PRL enhanced the cytotoxicity of IL-2 or IL-15 activated NK cells, it exerted the function through up-regulating gene expression of perforin without influence of FasL in IL-2-stimulated NK cells, while in IL-15-stimulated NK cells, PRL did the function through up-regulating gene expression of both perforin and FasL but not IFNγ. PRL increased expressions of IL-2Rα on membrane and of IL-2 mRNA in cells, indicating that PRL up-regulated NK cell function by improving positive feedback between IL-2 and IL-2R. The similar results were also observed in network between IL-15 and IL-15R. These data indicate a potential role of PRL in human NK cell modulation.

show abstract

“…For instance, PRL stimulates inducible NO synthase production, Ig release, and cytokine expression in human leukocytes (7)(8)(9)(10). Furthermore, PRL has anti-apoptotic properties that have been demonstrated in the Nb2 rat lymphoma (11) and in dexamethasone-treated thymocytes (12).…”

mentioning

confidence: 97%

Mechanism of Prostaglandin (PG)E2-Induced Prolactin Expression in Human T Cells: Cooperation of Two PGE2 Receptor Subtypes, E-Prostanoid (EP) 3 and EP4, Via Calcium- and Cyclic Adenosine 5′-Monophosphate-Mediated Signaling Pathways

Gerlo¹,

Verdood²,

Gellersen

et al. 2004

The Journal of Immunology

View full text Add to dashboard Cite

We previously reported that prolactin gene expression in the T-leukemic cell line Jurkat is stimulated by PGE2 and that cAMP acts synergistically with Ca2+ or protein kinase C on the activation of the upstream prolactin promoter. Using the transcription inhibitor actinomycin D, we now show that PGE2-induced prolactin expression requires de novo prolactin mRNA synthesis and that PGE2 does not influence prolactin mRNA stability. Furthermore, PGE2-induced prolactin expression was inhibited by protein kinase inhibitor fragment 14–22 and BAPTA-AM, which respectively, inhibit protein kinase A- and Ca2+-mediated signaling cascades. Using specific PGE2 receptor agonists and antagonists, we show that PGE2 induces prolactin expression through engagement of E-prostanoid (EP) 3 and EP4 receptors. We also found that PGE2 induces an increase in intracellular cAMP concentration as well as intracellular calcium concentration via EP4 and EP3 receptors, respectively. In transient transfections, 3000 bp flanking the leukocyte prolactin promoter conferred a weak induction of the luciferase reporter gene by PGE2 and cAMP, whereas cAMP in synergy with ionomycin strongly activated the promoter. Mutation of a C/EBP responsive element at −214 partially abolished the response of the leukocyte prolactin promoter to PGE2, cAMP, and ionomycin plus cAMP.

show abstract

Up‐modulation of interferon‐γ mediates the enhancement of spontanous cytotoxicity in prolactin‐activated natural killer cells

Cited by 48 publications

References 38 publications

Prolactin regulates antitumor immune response through induction of tumoricidal macrophages and release of IL‐12

Prolactin regulates antitumor immune response through induction of tumoricidal macrophages and release of IL‐12

Expression of prolactin receptor and response to prolactin stimulation of human NK cell lines

Mechanism of Prostaglandin (PG)E2-Induced Prolactin Expression in Human T Cells: Cooperation of Two PGE2 Receptor Subtypes, E-Prostanoid (EP) 3 and EP4, Via Calcium- and Cyclic Adenosine 5′-Monophosphate-Mediated Signaling Pathways

Contact Info

Product

Resources

About