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| 1 | Key residues of the receptor binding motif in the spike protein of SARS-CoV-2 that interact with ACE2 and neutralizing antibodies显示文摘Coronavirus disease 2019(COVID-19),caused by the novel human coronavirus SARS-CoV-2,is currently a major threat to public health worldwide.The viral spike protein binds the host receptor angiotensin-converting enzyme 2(ACE2)via the receptor-binding domain(RBD),and thus is believed to be a major target to block viral entry.Both SARS-CoV-2 and SARS-CoV share this mechanism.Here we functionally analyzed the key amino acid residues located within receptor binding motif of RBD that may interact with human ACE2 and available neutralizing antibodies.The in vivo experiments showed that immunization with either the SARS-CoV RBD or SARS-CoV-2 RBD was able to induce strong clade-specific neutralizing antibodies in mice;however,the cross-neutralizing activity was much weaker,indicating that there are distinct antigenic features in the RBDs of the two viruses.This finding was confirmed with the available neutralizing monoclonal antibodies against SARS-CoV or SARS-CoV-2.It is worth noting that a newly developed SARS-CoV-2 human antibody,HA001,was able to neutralize SARS-CoV-2,but failed to recognize SARS-CoV.Moreover,the potential epitope residues of HA001 were identified as A475 and F486 in the SARS-CoV-2 RBD,representing new binding sites for neutralizing antibodies.Overall,our study has revealed the presence of different key epitopes between SARS-CoV and SARSCoV-2,which indicates the necessity to develop new prophylactic vaccine and antibody drugs for specific control of the COVID-19 pandemic although the available agents obtained from the SARS-CoV study are unneglectable. | Chunyan Yi Xiaoyu Sun Jing Ye Longfei Ding Meiqin Liu Zhuo Yang Xiao Lu Yaguang Zhang Liyang Ma Wangpeng Gu Aidong Qu Jianqing Xu Zhengli Shi Zhiyang Ling Bing Sun | 2020 | Cellular & Molecular Immunology2020，17，6： | 13 |
| 2 | Protective humoral immunity in SARS-CoV-2 infected pediatric patients显示文摘After the rapid spread of SARS-CoV-2 in Wuhan,China,at the beginning of 2020,about 1.5 million confirmed cases and over 80,000 deaths have been reported around 200 countries and territories all over the world and the number continues to increase.However,we still have limited knowledge of this new coronavirus,especially the interaction between SARS-CoV-2 and our immune system. | Yaguang Zhang Jin Xu Ran Jia Chunyan Yi Wangpeng Gu Pengcheng Liu Xinran Dong Hao Zhou Bo Shang Shipeng Cheng Xiaoyu Sun Jing Ye Xuezhen Li Jia Zhang Zhiyang Ling Liyan Ma Bingbing Wu Mei Zeng Wenhao Zhou Bing Sun | 2020 | Cellular & Molecular Immunology2020，17，7： | 2 |
| 3 | HTR2A agonists play a therapeutic role by restricting ILC2 activation in papain-induced lung inflammation显示文摘Group 2 innate lymphoid cells(ILC2s)are a category of heterogeneous cells that produce the cytokines IL-5 and IL-13,which mediate the type 2 immune response.However,specific drug targets on lung ILC2s have rarely been reported.Previous studies have shown that type 2 cytokines,such as IL-5 and IL-13,are related to depression.Here,we demonstrated the negative correlation between the depression-associated monoamine neurotransmitter serotonin and secretion of the cytokines IL-5 and IL-13 by ILC2s in individuals with depression.Interestingly,serotonin ameliorates papain-induced lung inflammation by suppressing ILC2 activation.Our data showed that the serotonin receptor HTR2A was highly expressed on ILC2s from mouse lungs and human PBMCs.Furthermore,an HTR2A selective agonist(DOI)impaired ILC2 activation and alleviated the type 2 immune response in vivo and in vitro.Mice with ILC2-specific depletion of HTR2A(Il5^(cre/+)·Htr2a^(flox/flox)mice)abolished the DOI-mediated inhibition of ILC2s in a papain-induced mouse model of inflammation.In conclusion,serotonin and DOI could restrict the type 2 lung immune response,indicating a potential treatment strategy for type 2 lung inflammation by targeting HTR2A on ST2+ILC2s. | Zhishuo Wang Chenghua Yan Qizhen Du Yuying Huang Xuezhen Li Dan Zeng Ruizhi Mao Rama Krishna Gurram Shipeng Cheng Wangpeng Gu Lin Zhu Weiguo Fan Liyan Ma Zhiyang Ling Ju Qiu Dangsheng Li Enmei Liu Yaguang Zhang Yiru Fang Jinfang Zhu Bing Sun | 2023 | Cellular & Molecular Immunology2023，20，4： | 1 |
| 4 | Vitamin B6 regulates IL-33 homeostasis to alleviate type 2 inflammation显示文摘Interleukin-33(IL-33)is a crucial nuclear cytokine that induces the type 2 immune response and maintains immune homeostasis.The fine-tuned regulation of IL-33 in tissue cells is critical to control of the type 2 immune response in airway inflammation,but the mechanism is still unclear.Here,we found that healthy individuals had higher phosphate-pyridoxal(PLP,an active form of vitamin B6)concentrations in the serum than asthma patients.Lower serum PLP concentrations in asthma patients were strongly associated with worse lung function and inflammation.In a mouse model of lung inflammation,we revealed that PLP alleviated the type 2 immune response and that this inhibitory effect relied on the activity of IL-33.A mechanistic study showed that in vivo,pyridoxal(PL)needed to be converted into PLP,which inhibited the type 2 response by regulating IL-33 stability.In mice heterozygous for pyridoxal kinase(PDXK),the conversion of PL to PLP was limited,and IL-33 levels were increased in the lungs,aggravating type 2 inflammation.Furthermore,we found that the mouse double minute 2 homolog(MDM2)protein,an E3 ubiquitin-protein ligase,could ubiquitinate the N-terminus of IL-33 and sustain IL-33 stability in epithelial cells.PLP reduced MDM2-mediated IL-33 polyubiquitination and decreased the level of IL-33 through the proteasome pathway.In addition,inhalation of PLP alleviated asthma-related effects in mouse models.In summary,our data indicate that vitamin B6 regulates MDM2-mediated IL-33 stability to constrain the type 2 response,which might help develop a potential preventive and therapeutic agent for allergy-related diseases. | Songling Zhu Shufen Zhong Kebin Cheng Li-Sha Zhang Jiu-wu Bai Zu Cao Su Wang Wen Chen Shipeng Cheng Liyan Ma Zhiyang Ling Yuying Huang Wangpeng Gu Xiaoyu Sun Chunyan Yi Meng Zhao Shuo Liang Jin-Fu Xu Bing Sun Yaguang Zhang | 2023 | Cellular & Molecular Immunology2023，20，7： | 1 |
| 5 | A SARS-CoV-2 antibody retains potent neutralization against Omicron by targeting conserved RBM residues显示文摘The newly emerged Omicron(B.1.1.529)variant of SARS-CoV-2 is quickly overtaking the Delta variant and becoming the dominant strain around the world due to its enhanced transmissibility and high immune escape potential[1,2].Compared to the Wuhan strain,the Omicron variant carries 37 spike mutations,of which 15 are within the receptor-binding domain(RBD)(Fig.1A).A high mutation rate is associated with remarkable resistance to current vaccines and RBD-specific antibody therapeutics[2,3,4]. | Chunyan Yi Zhiyang Ling Xiao Lu Yadong Fu Zhuo Yang Sonam Wangmo Shuangfeng Chen Yaguang Zhang Liyan Ma Wangpeng Gu Hongzhou Lu Xiaoyu Sun Bing Sun | 2022 | Cellular & Molecular Immunology2022，19，5： | 1 |
| 6 | TRIM34 attenuates colon inflammation and tumorigenesis by sustaining barrier integrity显示文摘Loss of the colonic inner mucus layer leads to spontaneously severe colitis and colorectal cancer.However,key host factors that may control the generation of the inner mucus layer are rarely reported.Here,we identify a novel function of TRIM34 in goblet cells(GCs)in controlling inner mucus layer generation.Upon DSS treatment,TRIM34 deficiency led to a reduction in Muc2 secretion by GCs and subsequent defects in the inner mucus layer.This outcome rendered TRIM34-deficient mice more susceptible to DSS-induced colitis and colitis-associated colorectal cancer.Mechanistic experiments demonstrated that TRIM34 controlled TLR signaling-induced Nox/Duox-dependent ROS synthesis,thereby promoting the compound exocytosis of Muc2 by colonic GCs that were exposed to bacterial TLR ligands.Clinical analysis revealed that TRIM34 levels in patient samples were correlated with the outcome of ulcerative colitis(UC)and the prognosis of rectal adenocarcinoma.This study indicates that TRIM34 expression in GCs plays an essential role in generating the inner mucus layer and preventing excessive colon inflammation and tumorigenesis. | Qiaoshi Lian Shanshan Yan Qi Yin Chenghua Yan Wanwei Zheng Wangpeng Gu Xinhao Zhao Weiguo Fan Xuezhen Li Liyan Ma Zhiyang Ling Yaguang Zhang Jie Liu Jinsong Li Bing Sun | 2021 | Cellular & Molecular Immunology2021，18，2： | 0 |
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