CD97 promotes spleen dendritic cell homeostasis through the mechanosensing of red blood cells-Reference-Cited by-同舟云学术

CD97 promotes spleen dendritic cell homeostasis through the mechanosensing of red blood cells

Published:2022-02-11 Issue:6581 Volume:375 Page:
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Liu Dan¹²^ORCID,Duan Lihui¹²,Rodda Lauren B.¹²^ORCID,Lu Erick¹²^ORCID,Xu Ying¹²,An Jinping¹²,Qiu Longhui³,Liu Fengchun³^ORCID,Looney Mark R.³^ORCID,Yang Zhiyong⁴⁵⁶^ORCID,Allen Christopher D. C.⁴⁵⁶^ORCID,Li Zhongmei⁷,Marson Alexander²³⁷^ORCID,Cyster Jason G.¹²^ORCID

Affiliation:

1. Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94143, USA.

2. Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143, USA.

3. Department of Medicine, University of California, San Francisco, San Francisco, CA 94143, USA.

4. Cardiovascular Research Institute, University of California San Francisco, San Francisco, CA 94143, USA.

5. Sandler Asthma Basic Research Center, University of California, San Francisco, San Francisco, CA 94143, USA.

6. Department of Anatomy, University of California, San Francisco, San Francisco, CA 94143, USA.

7. J. David Gladstone Institutes, San Francisco, CA 94158, USA.

Abstract

Dendritic cells (DCs) are crucial for initiating adaptive immune responses. However, the factors that control DC positioning and homeostasis are incompletely understood. We found that type-2 conventional DCs (cDC2s) in the spleen depend on Gα 13 and adhesion G protein–coupled receptor family member-E5 (Adgre5, or CD97) for positioning in blood-exposed locations. CD97 function required its autoproteolytic cleavage. CD55 is a CD97 ligand, and cDC2 interaction with CD55-expressing red blood cells (RBCs) under shear stress conditions caused extraction of the regulatory CD97 N-terminal fragment. Deficiency in CD55-CD97 signaling led to loss of splenic cDC2s into the circulation and defective lymphocyte responses to blood-borne antigens. Thus, CD97 mechanosensing of RBCs establishes a migration and gene expression program that optimizes the antigen capture and presentation functions of splenic cDC2s.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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