•  

Interleukin-33-induced expression of PIBF1 by decidual B cells protects against preterm labor (Dec 2016)

nature
Title:
Interleukin-33-induced expression of PIBF1 by decidual B cells protects against preterm labor
Journal:
Nat Med. 2017 Jan;23(1):128-135.
Author(s):
Huang B1, Faucette AN1, Pawlitz MD1, Pei B1, Goyert JW1, Zhou JZ1, El-Hage NG1, Deng J2, Lin J1, Yao F1, Dewar RS 3rd1, Jassal JS1, Sandberg ML3, Dai J1, Cols M4, Shen C4, Polin LA5, Nichols RA1,6, Jones TB1,6, Bluth MH7, Puder KS1, Gonik B1, Nayak NR1, Puscheck E1, Wei WZ5, Cerutti A8,9,10,11, Colonna M11,12, Chen K1,5,11.
Author(s) affiliation:
1 Department of Obstetrics and Gynecology, Wayne State University, Detroit, Michigan, USA.
2 Department of Obstetrics, Gynecology and Reproductive Sciences, Yale School of Medicine, New Haven, Connecticut, USA.
3 Leadership in Medicine Program, Union College, Schenectady, New York, USA.
4 Immunology Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
5 Department of Oncology, Wayne State University, Detroit, Michigan, USA.
6Department of Obstetrics and Gynecology-Med Ed, Beaumont Dearborn Hospital, Dearborn, Michigan, USA.
7Department of Pathology, Wayne State University, Detroit, Michigan, USA.
8Catalan Institute for Research and Advanced Studies, Barcelona Biomedical Research Park, Barcelona, Spain.
9 Program for Inflammatory and Cardiovascular Disorders, Institut Hospital del Mar d'Investigacions Mèdiques, Barcelona, Spain.
10 Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
11Mucosal Immunology Studies Team, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
12 Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri, USA.
 

 

Short description:
Preterm birth (PTB) is a leading cause of neonatal death worldwide1. Intrauterine and systemic infection and inflammation cause 30–40% of spontaneous preterm labor (PTL)2, which precedes PTB. Although antibody production is a major immune defense mechanism against infection, and B cell dysfunction has been implicated in pregnancy complications associated with PTL3, 4, the functions of B cells in pregnancy are not well known5, 6, 7, 8. We found that choriodecidua of women undergoing spontaneous PTL harbored functionally altered B cell populations. B cell–deficient mice were markedly more susceptible than wild-type (WT) mice to PTL after inflammation, but B cells conferred interleukin (IL)-10-independent protection against PTL. B cell deficiency in mice resulted in a lower uterine level of active progesterone-induced blocking factor 1 (PIBF1), and therapeutic administration of PIBF1 mitigated PTL and uterine inflammation in B cell–deficient mice. B cells are a significant producer of PIBF1 in human choriodecidua and mouse uterus in late gestation. PIBF1 expression by B cells is induced by the mucosal alarmin IL-33 (ref. 9). Human PTL was associated with diminished expression of the α-chain of IL-33 receptor on choriodecidual B cells and a lower level of active PIBF1 in late gestation choriodecidua. These results define a vital regulatory cascade involving IL-33, decidual B cells and PIBF1 in safeguarding term pregnancy and suggest new therapeutic approaches based on IL-33 and PIBF1 to prevent human PTL.
Link to the journal
 

 

Abstract taken from PubMed

Abstract:
Preterm birth (PTB) is a leading cause of neonatal death worldwide. Intrauterine and systemic infection and inflammation cause 30-40% of spontaneous preterm labor (PTL), which precedes PTB. Although antibody production is a major immune defense mechanism against infection, and B cell dysfunction has been implicated in pregnancy complications associated with PTL, the functions of B cells in pregnancy are not well known. We found that choriodecidua of women undergoing spontaneous PTL harbored functionally altered B cell populations. B cell-deficient mice were markedly more susceptible than wild-type (WT) mice to PTL after inflammation, but B cells conferred interleukin (IL)-10-independent protection against PTL. B cell deficiency in mice resulted in a lower uterine level of active progesterone-induced blocking factor 1 (PIBF1), and therapeutic administration of PIBF1 mitigated PTL and uterine inflammation in B cell-deficient mice. B cells are a significant producer of PIBF1 in human choriodecidua and mouse uterus in late gestation. PIBF1 expression by B cells is induced by the mucosal alarmin IL-33 (ref. 9). Human PTL was associated with diminished expression of the α-chain of IL-33 receptor on choriodecidual B cells and a lower level of active PIBF1 in late gestation choriodecidua. These results define a vital regulatory cascade involving IL-33, decidual B cells and PIBF1 in safeguarding term pregnancy and suggest new therapeutic approaches based on IL-33 and PIBF1 to prevent human PTL.
Link to the paper on PubMed
 




 

IVF-Worldwide.com endeavors to ensure that the information in this article is accurate,reliable and up to date. However, the information is provided "as is" without warranty of any kind. IVF-Worldwide does not accept any responsibility or liability for the accuracy,content, completeness, legality, or reliability of the information contained in this article.
IVF-Worldwide.com is not responsible for the content of other websites linked to or referenced from this website. The website does not endorse the information, content,presentation or accuracy of such other websites and does not make any warranty,express or implied, regarding them.