Literature DB >> 19640696

Monocytes/macrophages in renal allograft rejection.

Alex B Magil1.   

Abstract

Monocytes/macrophages (MO) have long been recognized to be involved in renal allograft rejection. Monocytes/macrophages have been detected in the glomerular, vascular, and tubulointerstitial compartments during rejection. The recent demonstration that peritubular capillary deposition of complement split factor C4d, a marker for antibody-mediated rejection, is associated with relatively marked MO infiltration of the allograft during acute rejection is a significant development in our understanding of the role of the MO in rejection. High levels of MO in rejecting allografts have been associated with severe rejection, and glomerular MO infiltration in particular has been shown to be an indicator of poor graft outcome.

Mesh:

Substances:

Year:  2009        PMID: 19640696     DOI: 10.1016/j.trre.2009.06.005

Source DB:  PubMed          Journal:  Transplant Rev (Orlando)        ISSN: 0955-470X            Impact factor:   3.943


  29 in total

Review 1.  An overview on non-T cell pathways in transplant rejection and tolerance.

Authors:  Wentao Liu; Xian C Li
Journal:  Curr Opin Organ Transplant       Date:  2010-08       Impact factor: 2.640

2.  Graft-derived CCL2 increases graft injury during antibody-mediated rejection of cardiac allografts.

Authors:  T Abe; C A Su; S Iida; W M Baldwin; N Nonomura; S Takahara; R L Fairchild
Journal:  Am J Transplant       Date:  2014-08       Impact factor: 8.086

Review 3.  Macrophages: contributors to allograft dysfunction, repair, or innocent bystanders?

Authors:  Roslyn B Mannon
Journal:  Curr Opin Organ Transplant       Date:  2012-02       Impact factor: 2.640

4.  Increased expression of peripheral blood leukocyte genes implicate CD14+ tissue macrophages in cellular intestine allograft rejection.

Authors:  Chethan Ashokkumar; Mylarappa Ningappa; Sarangarajan Ranganathan; Brandon W Higgs; Qing Sun; Lori Schmitt; Sara Snyder; Jennifer Dobberstein; Maria Branca; Ronald Jaffe; Adriana Zeevi; Robert Squires; Feras Alissa; Benjamin Shneider; Kyle Soltys; Geoffrey Bond; Kareem Abu-Elmagd; Abhinav Humar; George Mazariegos; Hakon Hakonarson; Rakesh Sindhi
Journal:  Am J Pathol       Date:  2011-08-18       Impact factor: 4.307

5.  Deficiency of C5aR prolongs renal allograft survival.

Authors:  Qijun Li; Qi Peng; Guolan Xing; Ke Li; Naiyin Wang; Conrad A Farrar; Lucy Meader; Steven H Sacks; Wuding Zhou
Journal:  J Am Soc Nephrol       Date:  2010-07-22       Impact factor: 10.121

6.  Macrophages as Effectors of Acute and Chronic Allograft Injury.

Authors:  Yianzhu Liu; Malgorzata Kloc; Xian C Li
Journal:  Curr Transplant Rep       Date:  2016-10-25

7.  Netrin-1 attenuates cardiac ischemia reperfusion injury and generates alternatively activated macrophages.

Authors:  Xiaogang Mao; Hui Xing; Aihua Mao; Hong Jiang; Li Cheng; Yun Liu; Xiaozhen Quan; Lin Li
Journal:  Inflammation       Date:  2014-04       Impact factor: 4.092

8.  NK cells are required for costimulatory blockade induced tolerance to vascularized allografts.

Authors:  William van der Touw; Bryna Burrell; Girdhari Lal; Jonathan S Bromberg
Journal:  Transplantation       Date:  2012-09-27       Impact factor: 4.939

9.  HLA class I antibodies trigger increased adherence of monocytes to endothelial cells by eliciting an increase in endothelial P-selectin and, depending on subclass, by engaging FcγRs.

Authors:  Nicole M Valenzuela; Arend Mulder; Elaine F Reed
Journal:  J Immunol       Date:  2013-05-20       Impact factor: 5.422

10.  Nuclear factor-κB activation inhibitor attenuates ischemia reperfusion injury and inhibits Hmgb1 expression.

Authors:  Zhiyong Shi; Aimin Lian; Fuquan Zhang
Journal:  Inflamm Res       Date:  2014-09-11       Impact factor: 4.575

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.