Granzyme A from cytotoxic lymphocytes cleaves GSDMB to trigger pyroptosis in target cells

Author:

Zhou Zhiwei12ORCID,He Huabin32ORCID,Wang Kun2,Shi Xuyan2,Wang Yupeng12ORCID,Su Ya2ORCID,Wang Yao4,Li Da2ORCID,Liu Wang12ORCID,Zhang Yongliang5,Shen Lianjun5,Han Weidong4,Shen Lin6ORCID,Ding Jingjin27ORCID,Shao Feng1278ORCID

Affiliation:

1. Research Unit of Pyroptosis and Immunity, Chinese Academy of Medical Sciences and National Institute of Biological Sciences, Beijing, Beijing 102206, China.

2. National Institute of Biological Sciences, Beijing, Beijing 102206, China.

3. Peking University–Tsinghua University–National Institute of Biological Sciences Joint Graduate Program, School of Life Sciences, Tsinghua University, Beijing 100084, China.

4. Department of Molecular and Immunology and Department of Bio-therapeutics, Chinese PLA General Hospital, Beijing 100853, China.

5. Gracell Biotechnologies, Shanghai 200233, China.

6. Department of Gastrointestinal Oncology, Peking University Cancer Hospital and Institute, Beijing 100142, China.

7. National Laboratory of Biomacromolecules, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences (CAS), Beijing 100101, China.

8. Tsinghua Institute of Multidisciplinary Biomedical Research, Tsinghua University, Beijing 102206, China.

Abstract

Granzyme A lights a fire Cytotoxic T cells and natural killer cells use several strategies to kill infected or transformed cells. One such pathway entails the delivery of a family of serine proteases called granzymes to target cells through perforin-mediated pores to induce a form of programmed cell death called apoptosis. Zhou et al. show that granzyme A cleaves and activates gasdermin B (GSDMB), a central player in the highly inflammatory cell death process known as pyroptosis (see the Perspective by Nicolai and Raulet). GSDMB expression was highly expressed in some tissues and could be up-regulated by interferon-γ. Enforced expression of GSDMB in cancer cells enhanced tumor clearance in a mouse model, suggesting that this pathway may be a target for future cancer immunotherapies. Science , this issue p. eaaz7548 ; see also p. 943

Funder

National Natural Science Foundation of China

Chinese Academy of Sciences

Ministry of Science and Technology of the People's Republic of China

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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