The gene for prolactin-inducible protein (PIP), uniquely expressed in exocrine organs, maps to chromosome 7

Myal, Yvonne; Gregory, Carolyn; Wang, Hui; Hamerton, J.L.; Shiu, Robert P. C.

doi:10.1007/bf01534877

Cited by 32 publications

(24 citation statements)

References 18 publications

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“…The gene coding for GCDFP-15 is localized in the long arm of chromosome 7 (24) and has recently been cloned (25). It is identical to the gene of the prolactin-inducible protein (PIP), independently described by Shiu and co-workers (23,32) in the T47D cell line.…”

Section: Introductionmentioning

confidence: 98%

PIP/GCDFP-15 gene expression and apocrine differentiation in carcinomas of the breast

Pagani

Sapino

Bergnolo

et al. 1994

Vichows Archiv A Pathol Anat

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The frequency and the significance of apocrine differentiation in carcinomas of the breast are uncertain, because of the lack of reliable and reproducible criteria for morphological diagnosis. The 15 kDa glycoprotein of cystic breast disease (GCDFP-15) is regarded as a specific functional marker of apocrine cells. Expression of the prolactin-inducible protein (PIP)/GCDFP-15 gene was investigated by Northern blot analysis and in situ hybridization in breast cancer cell lines and in an unselected series (33 cases) of primary carcinomas of the breast. On the same cases, histological assessment of apocrine differentiation and immunocytochemical detection of GCDFP-15 were also performed and correlated with follow-up data. The presence of PIP/GCDFP-15 mRNA was a feature of a relatively high number of cases, but was incompletely correlated with histological and immunocytochemical evidences of apocrine differentiation. Expression of the PIP/GCDFP-15 gene was significantly associated with relapse-free survival, and may represent a novel variable of functional and prognostic relevance.

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Section: Introductionmentioning

confidence: 98%

PIP/GCDFP-15 gene expression and apocrine differentiation in carcinomas of the breast

Pagani

Sapino

Bergnolo

et al. 1994

Vichows Archiv A Pathol Anat

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“…The function of PIP is not known, but it is suspected to play a role in host defense against pathogens [1][2][3][4][5][6] because it is expressed in tissues strategically located at several Correspondence: Dr. Jude E. Uzonna e-mail: jude.uzonna@med.umanitoba.ca ports of pathogen entry, including the skin, eyes, and mouth [7]. Although a definitive evidence showing a role for PIP in host immunity is lacking, its ability to potentially bind with several important host molecules including CD4 + T-cell receptor, IgG, actin, zinc α2-glycoprotein, fibronectin, and enamel pellicle suggests it may have important biological functions [8][9][10][11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Deficiency of prolactin‐inducible protein leads to impaired Th1 immune response and susceptibility to Leishmania major in mice

Liu

Mou

et al. 2015

Eur J Immunol

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Although the strategic production of prolactin-inducible protein (PIP) at several ports of pathogen entry into the body suggests it might play a role in host defense, no study has directly implicated it in immunity against any infectious agent. Here, we show for the first time that PIP deficiency is associated with reduced numbers of CD4 + T cells in peripheral lymphoid tissues and impaired CD4 + Th1-cell differentiation in vitro. In vivo, CD4+ T cells from OVA-immunized, PIP-deficient mice showed significantly impaired proliferation and IFN-γ production following in vitro restimulation. Furthermore, PIPdeficient mice were highly susceptible to Leishmani major infection and failed to control lesion progression and parasite proliferation. This susceptibility was associated with impaired NO production and leishmanicidal activity of PIP KO macrophages following IFN-γ and LPS stimulation. Collectively, our findings implicate PIP as an important regulator of CD4 + Th1-cell-mediated immunity. Keywords: IFN-γ r Leishmania r Macrophages r Protozoan r Th1 cellsAdditional supporting information may be found in the online version of this article at the publisher's web-site IntroductionThe mouse prolactin-inducible protein (PIP), also known as the mouse submaxillary gland protein, is a 14 kDa protein present in the saliva of mice. The function of PIP is not known, but it is suspected to play a role in host defense against pathogens [1][2][3][4][5][6] because it is expressed in tissues strategically located at several Correspondence: Dr. Jude E. Uzonna e-mail: jude.uzonna@med.umanitoba.ca ports of pathogen entry, including the skin, eyes, and mouth [7]. Although a definitive evidence showing a role for PIP in host immunity is lacking, its ability to potentially bind with several important host molecules including CD4 + T-cell receptor, IgG, actin, zinc α2-glycoprotein, fibronectin, and enamel pellicle suggests it may have important biological functions [8][9][10][11][12][13]. Indeed, it has been shown that PIP is a ligand of the CD4 molecule and a potent inhibitor of * These authors contributed equally to this manuscript.C 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim www.eji-journal.eu Eur. J. Immunol. 2015. 45: 1082-1091 Immunity to infection 1083 T-cell apoptosis induced by sequential CD4/T-cell receptor triggering, which in part modulates the immune response during viral infection by interfering with the functions mediated by the CD4 molecule [5,6,14]. Furthermore, PIP has been reported to exhibit a mitogenic effect for both normal and malignant breast epithelial cells [15], strongly suggesting that it might play a critical role in differentiation, proliferation, and function of immune cells.Our previous studies show that PIP KO mice have enlarged submandibular lymph nodes and thymic medulla [16]. However, to date, no studies have addressed the contributions of PIP in T-cell responses to either model Ags or infectious agents. Our major aim in the present study is to investigate whether PIP has immunoregulatory function...

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“…The amino acid sequence for GCDFP-15 has been determined [16] and the c-DNA has been cloned [24][25]. The genomic gene is located on chromosome 7 [25].…”

Section: Introductionmentioning

confidence: 99%

Secretion of breast gross cystic disease fluid proteins by T47D breast cancer cells in culture — modulation by steroid hormones

Haagensen

Stewart

Dilley

et al. 1992

Breast Cancer Res Tr

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The effect of steroid hormones on modulating the secretion rates of three human breast gross cystic disease fluid proteins (GCDFP-15, GCDFP-24, and GCDFP-44) by T47D breast carcinoma cells in tissue culture was evaluated. Androgens (dihydrotestosterone or fluoxymesterone) were capable of stimulating the secretion rates for all three GCDFP's while showing a minimal trend toward slowing the growth rate of T47D cells. This is the first study which shows that androgens can specifically stimulate all three of the major breast GCDFP's concomitantly. Progesterone, and three synthetic progestins, all showed inhibition of the growth rate of T47D cells while causing enhancement of the secretion of GCDFP-15 and GCDFP-44, and only minimal effect on the secretion rate of GCDFP-24. Estradiol was essentially neutral to the growth rate of the T47D cells in our test system. Estradiol did cause a mild enhancement of GCDFP-44 secretion rate, with no appreciable effect on GCDFP-15 or GCDFP-24 secretion rates. These findings suggest that an androgenic stimulus may be involved in the secretion of GCDFP's associated with breast gross cystic disease.

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The gene for prolactin-inducible protein (PIP), uniquely expressed in exocrine organs, maps to chromosome 7

Cited by 32 publications

References 18 publications

PIP/GCDFP-15 gene expression and apocrine differentiation in carcinomas of the breast

PIP/GCDFP-15 gene expression and apocrine differentiation in carcinomas of the breast

Deficiency of prolactin‐inducible protein leads to impaired Th1 immune response and susceptibility to Leishmania major in mice

Secretion of breast gross cystic disease fluid proteins by T47D breast cancer cells in culture — modulation by steroid hormones

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