The Role of the Immune Checkpoint Molecules PD-1/PD-L1 and TIM-3/Gal-9 in the Pathogenesis of Preeclampsia-A Narrative Review

被引:20
作者
Mittelberger, Johanna [1 ]
Seefried, Marina [1 ]
Franitza, Manuela [1 ]
Garrido, Fabian [1 ]
Ditsch, Nina [1 ]
Jeschke, Udo [1 ]
Dannecker, Christian [1 ]
机构
[1] Univ Hosp Augsburg, Dept Obstet & Gynecol, Stenglinstr 2, D-86156 Augsburg, Germany
来源
MEDICINA-LITHUANIA | 2022年 / 58卷 / 02期
关键词
preeclampsia; immune checkpoint molecules; PD-1; PD-L1; TIM-3; Gal-9; CELL IMMUNOGLOBULIN MUCIN-3; T-CELLS; PD-1; PATHWAY; EXPRESSION; TOLERANCE; PREGNANCY; TIM-3; PDL1; LINK;
D O I
10.3390/medicina58020157
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Preeclampsia is a pregnancy-specific disease which is characterized by abnormal placentation, endothelial dysfunction, and systemic inflammation. Several studies have shown that the maternal immune system, which is crucial for maintaining the pregnancy by ensuring maternal-fetal-tolerance, is disrupted in preeclamptic patients. Besides different immune cells, immune checkpoint molecules such as the programmed cell death protein 1/programmed death-ligand 1 (PD-1/PD-L1 system) and the T-cell immunoglobulin and mucin domain-containing protein 3/Galectin-9 (TIM-3/Gal-9 system) are key players in upholding the balance between pro-inflammatory and anti-inflammatory signals. Therefore, a clear understanding about the role of these immune checkpoint molecules in preeclampsia is essential. This review discusses the role of these two immune checkpoint systems in pregnancy and their alterations in preeclampsia.
引用
收藏
页数:12
相关论文
共 55 条
[1]   TIM-3 Regulates Innate Immune Cells To Induce Fetomaternal Tolerance [J].
Chabtini, Lola ;
Mfarrej, Bechara ;
Mounayar, Marwan ;
Zhu, Bing ;
Batal, Ibrahim ;
Dakle, Pranal J. ;
Smith, Brian D. ;
Boenisch, Olaf ;
Najafian, Nader ;
Akiba, Hisaya ;
Yagita, Hideo ;
Guleria, Indira .
JOURNAL OF IMMUNOLOGY, 2013, 190 (01) :88-96
[2]   Basics of PD-1 in self-tolerance, infection, and cancer immunity [J].
Chikuma, Shunsuke .
INTERNATIONAL JOURNAL OF CLINICAL ONCOLOGY, 2016, 21 (03) :448-455
[3]   The Link between the PDL1 Costimulatory Pathway and Th17 in Fetomaternal Tolerance [J].
D'Addio, Francesca ;
Riella, Leonardo V. ;
Mfarrej, Bechara G. ;
Chabtini, Lola ;
Adams, La Tonya ;
Yeung, Melissa ;
Yagita, Hideo ;
Azuma, Miyuki ;
Sayegh, Mohamed H. ;
Guleria, Indira .
JOURNAL OF IMMUNOLOGY, 2011, 187 (09) :4530-4541
[4]  
Daraei N, 2019, IRAN J IMMUNOL, V16, P163, DOI [10.22034/IJI.2019.80259, 10.22034/iji.2019.80259]
[5]   The abnormal expression of Tim-3 is involved in the regulation of myeloid-derived suppressor cells and its correlation with preeclampsia [J].
Dong, Shuai ;
Shah, Neelam Kumari ;
He, Jin ;
Han, Shumei ;
Xie, Min ;
Wang, Ying ;
Cheng, Tingting ;
Liu, Zitao ;
Shu, Chang .
PLACENTA, 2021, 114 :108-114
[6]   Immune checkpoint molecules soluble program death ligand 1 and galectin-9 are increased in pregnancy [J].
Enninga, Elizabeth Ann L. ;
Harrington, Susan M. ;
Creedon, Douglas J. ;
Ruano, Rodrigo ;
Markovic, Svetomir N. ;
Dong, Haidong ;
Dronca, Roxana S. .
AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, 2018, 79 (02)
[7]   The PD-1 pathway in tolerance and autoimmunity [J].
Francisco, Loise M. ;
Sage, Peter T. ;
Sharpe, Arlene H. .
IMMUNOLOGICAL REVIEWS, 2010, 236 :219-242
[8]   Maternal soluble PD-1 levels are significantly increased in women with preeclampsia [J].
Gu, Yang ;
Morgan, John ;
Lewis, David F. ;
Cooper, Danielle B. ;
McCathran, Charles E. ;
Wang, Yuping .
AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, 2020, 83 (01)
[9]   A critical role for the programmed death ligand 1 in fetomaternal tolerance [J].
Guleria, I ;
Khosroshahi, A ;
Ansari, MJ ;
Habicht, A ;
Azuma, M ;
Yagita, H ;
Noelle, RJ ;
Sayegh, MH .
JOURNAL OF EXPERIMENTAL MEDICINE, 2005, 202 (02) :231-237
[10]   A link between PDL1 and T regulatory cells in fetomaternal tolerance [J].
Habicht, Antje ;
Dada, Shirine ;
Jurewicz, Mollie ;
Fife, Brian T. ;
Yagita, Hideo ;
Azuma, Miyuki ;
Sayegh, Mohamed H. ;
Guleria, Indira .
JOURNAL OF IMMUNOLOGY, 2007, 179 (08) :5211-5219