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Siglec-G-CD24 axis controls the severity of graft-versus-host disease in mice.

Abstract：

:Activation of sialic-acid-binding immunoglobulin-like lectin-G (Siglec-G) by noninfectious damage-associated molecular patterns controls innate immune responses. However, whether it also regulates T-cell-mediated adaptive immune responses is not known. Graft-versus-host reaction is a robust adaptive immune response caused by allogeneic hematopoietic cell transplantation that have been activated by antigen-presenting cells (APCs) in the context of damaged host tissues following allogeneic hematopoietic cell transplantation. The role of infectious and noninfectious pattern recognition receptor-mediated activation in the induction and aggravation of graft-versus-host disease (GVHD) is being increasingly appreciated. But the role of pathways that control innate immune responses to noninfectious stimuli in modulating GVHD has heretofore not been recognized. We report that Siglec-G expression on host APCs, specifically on hematopoietic cells, negatively regulates GVHD in multiple clinically relevant murine models. Mechanistic studies with various relevant Siglec-G and CD24 knockout mice and chimeric animals, along with rescue experiments with novel CD24 fusion protein demonstrate that enhancing the interaction between Siglec-G on host APCs with CD24 on donor T cells attenuates GVHD. Taken together, our data demonstrate that Siglec-G-CD24 axis, controls the severity of GVHD and suggest that enhancing this interaction may represent a novel strategy for mitigating GVHD.

journal_name

Blood

journal_title

Blood

authors

Toubai T,Hou G,Mathewson N,Liu C,Wang Y,Oravecz-Wilson K,Cummings E,Rossi C,Evers R,Sun Y,Wu J,Choi SW,Fang D,Zheng P,Liu Y,Reddy P

doi

10.1182/blood-2013-12-545335

subject

Has Abstract

pub_date

2014-05-29 00:00:00

pages

3512-23

issue

22

eissn

0006-4971

issn

1528-0020

pii

blood-2013-12-545335

journal_volume

123

pub_type

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