Role of CMV chemokine receptor M33 in airway graft rejection in a mouse transplant model

2021 ◽  
pp. 101415
Author(s):  
Isabella Hanka ◽  
Thomas Stamminger ◽  
Martina Ramsperger-Gleixner ◽  
V. Annika Kuckhahn ◽  
Regina Müller ◽  
...  
2019 ◽  
Vol 39 (6) ◽  
Author(s):  
Tao Qiu ◽  
Jiangqiao Zhou ◽  
Tianyu Wang ◽  
Zhongbao Chen ◽  
Xiaoxiong Ma ◽  
...  

AbstractAcute lung injury (ALI) is an acute inflammatory disease. Leukocyte immunoglobulin-like receptor B4 (LILRB4) is an immunoreceptor tyrosine-based inhibitory motif (ITIM)-bearing inhibitory receptor that is implicated in various pathological processes. However, the function of LILRB4 in ALI remains largely unknown. The aim of the present study was to explore the role of LILRB4 in ALI. LILRB4 knockout mice (LILRB4 KO) were used to construct a model of ALI. Bone marrow cell transplantation was used to identify the cell source of the LILRB4 deficiency-aggravated inflammatory response in ALI. The effect on ALI was analyzed by pathological and molecular analyses. Our results indicated that LILRB4 KO exacerbated ALI triggered by LPS. Additionally, LILRB4 deficiency can enhance lung inflammation. According to the results of our bone marrow transplant model, LILRB4 regulates the occurrence and development of ALI by bone marrow-derived macrophages (BMDMs) rather than by stromal cells in the lung. The observed inflammation was mainly due to BMDM-induced NF-κB signaling. In conclusion, our study demonstrates that LILRB4 deficiency plays a detrimental role in ALI-associated BMDM activation by prompting the NF-κB signal pathway.


BMC Cancer ◽  
2014 ◽  
Vol 14 (1) ◽  
Author(s):  
Anastasios Stofas ◽  
Georgia Levidou ◽  
Christina Piperi ◽  
Christos Adamopoulos ◽  
Georgia Dalagiorgou ◽  
...  

2020 ◽  
Vol 22 (4) ◽  
Author(s):  
Gaetano Alfano ◽  
Giovanni Guaraldi ◽  
Francesco Fontana ◽  
Erica Franceschini ◽  
Giovanni Dolci ◽  
...  

1984 ◽  
Vol 159 (1) ◽  
pp. 57-67 ◽  
Author(s):  
L LeFrancois ◽  
M J Bevan

We have investigated which T cell subclass defined by cytolysis with monoclonal anti-Lyt-1.2 and anti-Lyt-2.2 antibodies is required to adoptively transfer the ability to reject skin grafts. B6.Thy-1.1 spleen cells immune to graft antigens were fractionated with antibody plus C' and transferred to adult thymectomized, irradiated, bone marrow-reconstituted (ATXBM) B6.Thy-1.2 hosts that were simultaneously grafted with BALB.B skin. We found that when the ATXBM hosts were used 6 wk after irradiation and marrow reconstitution, both Lyt-1-depleted and Lyt-2-depleted immune spleen cells could transfer the ability to promptly reject skin grafts. However, such ATXBM recipients of Lyt-2-depleted cells that had rejected skin grafts were found to contain graft-specific CTL that were largely of host (B6.Thy-1.2) origin. When ATXBM hosts were used for the experiment 1 wk after irradiation and marrow reconstitution, no host-derived graft-specific CTL could be detected. However, graft rejection occurred in recipients of anti-Lyt-1- or anti-Lyt-2 plus C'-treated immune cells and specific CTL were generated from spleen cells of both groups. Thus, in the absence of a host-derived response, adoptively transferred immune Lyt-2+ cells, either resistant to, or that escaped from, antibody plus C' treatment, are able to expand in response to the antigenic stimulus provided by the graft. A more complete elimination of specific T cell subclasses is therefore needed to assess the relative contribution of a particular subset to the graft rejection process.


2010 ◽  
Vol 19 (5) ◽  
pp. 597-612 ◽  
Author(s):  
Preeti Chhabra ◽  
Kunjie Wang ◽  
Qiang Zeng ◽  
Mladen Jecmenica ◽  
Linda Langman ◽  
...  

2020 ◽  
Vol 39 (4) ◽  
pp. S472
Author(s):  
D. Zotos ◽  
L. Goldring ◽  
R. Farighi ◽  
L. Sullivan ◽  
Y. Cristiano ◽  
...  

2008 ◽  
Vol 134 (7) ◽  
pp. 2025-2035 ◽  
Author(s):  
Maria Apostolaki ◽  
Menelaos Manoloukos ◽  
Manolis Roulis ◽  
Marc–André Wurbel ◽  
Werner Müller ◽  
...  

Author(s):  
M. Hohmann ◽  
D.M. Habiel ◽  
M.S. Espindola ◽  
G. Huang ◽  
Y.A.P.J. Sa ◽  
...  

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