Tetraspanin CD53: an overlooked regulator of immune cell function

Dunlock, Vera-Marie E.

doi:10.1007/s00430-020-00677-z

Cited by 42 publications

(42 citation statements)

References 55 publications

(66 reference statements)

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“…CD53 is the most connected protein in the PPI network. It is mainly expressed on the membranes of immune cells, where it helps regulate many of their functions, including adhesion, migration, and cell fusion ( Dunlock, 2020 ), and plays an important role in antigen presentation. Many studies have shown that CD53 is increased in obese and inflammatory tissues, and regulating its expression may be an effective treatment for obesity with complications ( Nair et al, 2005 ; Zhao et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Differentially Expressed Genes and Enriched Signaling Pathways in the Adipose Tissue of Obese People

Meng

Sun

et al. 2021

Front. Genet.

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As the prevalence of obesity increases, so does the occurrence of obesity-related complications, such as cardiovascular and cerebrovascular diseases, diabetes, and some cancers. Increased adipose tissue is the main cause of harm in obesity. To better understand obesity and its related complications, we analyzed the mRNA expression profiles of adipose tissues from 126 patients with obesity and 275 non-obese controls. Using an integrated bioinformatics method, we explored the functions of 113 differentially expressed genes (DEGs) between them. Gene ontology (GO) and kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment analyses revealed that upregulated DEGs were enriched in immune cell chemotaxis, complement-related cascade activation, and various inflammatory signaling pathways, while downregulated DEGs enriched in nutrient metabolism. The CIBERSORT algorithm indicated that an increase in macrophages may be the main cause of adipose tissue inflammation, while decreased γδ T cells reduce sympathetic action, leading to dysregulation of adipocyte thermogenesis. A protein-protein interaction network was constructed using the STRING database, and the top 10 hub genes were identified using the cytoHubba plug-in in Cytoscape. All were confirmed to be obesity-related using a separate dataset. In addition, we identified chemicals related to these hub genes that may contribute to obesity. In conclusion, we have successfully identified several hub genes in the development of obesity, which provide insights into the possible mechanisms controlling obesity and its related complications, as well as potential biomarkers and therapeutic targets for further research.

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Section: Discussionmentioning

confidence: 99%

Differentially Expressed Genes and Enriched Signaling Pathways in the Adipose Tissue of Obese People

Meng

Sun

et al. 2021

Front. Genet.

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“…This causes firm adhesion and arrest of the cells, and finally, exit from the blood vessels via diapedesis [32]. Five tetraspanin family members, CD9, CD37, CD53, CD81, CD82, and CD151, are involved in the regulation of α4β1 and/or β2 integrins on several leukocyte types [40][41][42][43][44][45][46][47][48][49], but their role on rolling and transmigration of DC precursor cells into peripheral tissues is not explored. Cd37 and Cd81 knockout mice have a normal immune system development [50,51], and it is therefore not expected that these tetraspanins are required for homing of DC precursor cells to peripheral tissues.…”

Section: Seeding Of Peripheral Tissuesmentioning

confidence: 99%

Molecular mechanisms of dendritic cell migration in immunity and cancer

Winde

Munday

Acton

2020

Med Microbiol Immunol

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Dendritic cells (DCs) are a heterogeneous population of antigen-presenting cells that act to bridge innate and adaptive immunity. DCs are critical in mounting effective immune responses to tissue damage, pathogens and cancer. Immature DCs continuously sample tissues and engulf antigens via endocytic pathways such as phagocytosis or macropinocytosis, which result in DC activation. Activated DCs undergo a maturation process by downregulating endocytosis and upregulating surface proteins controlling migration to lymphoid tissues where DC-mediated antigen presentation initiates adaptive immune responses. To traffic to lymphoid tissues, DCs must adapt their motility mechanisms to migrate within a wide variety of tissue types and cross barriers to enter lymphatics. All steps of DC migration involve cell-cell or cell-substrate interactions. This review discusses DC migration mechanisms in immunity and cancer with a focus on the role of cytoskeletal processes and cell surface proteins, including integrins, lectins and tetraspanins. Understanding the adapting molecular mechanisms controlling DC migration in immunity provides the basis for therapeutic interventions to dampen immune activation in autoimmunity, or to improve anti-tumour immune responses.

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“…In our cerebral malaria signature, we see that the immune-cell specific tetraspanin CD53, which is downregulated in cerebral patients, can be a better marker for cerebral disease status, as it also belongs to one of the gene pairs in the K-TSPs analysis, and was shown to be down-regulated during neutrophil activation with TNF (Mollinedo et al, 1998). Furthermore, CD53 plays an important role in the adaptive immune response, especially in B cell activation and differentiation (Dunlock, 2020), and its deficiency is associated with recurrent infections (Mollinedo et al, 1997). Moreover, its expression is preserved between blood and brain tissue highlighting its importance as a diagnostic biomarker for cerebral malaria (Cai et al, 2010).…”

Section: Discussionmentioning

confidence: 87%

Host Blood Gene Signatures Can Detect the Progression to Severe and Cerebral Malaria

Omar

Marchionni

Häcker

et al. 2021

Front. Cell. Infect. Microbiol.

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Malaria is a major international public health problem that affects millions of patients worldwide especially in sub-Saharan Africa. Although many tests have been developed to diagnose malaria infections, we still lack reliable diagnostic biomarkers for the identification of disease severity, especially in endemic areas where the diagnosis of cerebral malaria is very difficult and requires the exclusion of all other possible causes. Previous host and pathogen transcriptomic studies have not yielded homogenous results that can be harnessed into a reliable diagnostic tool. Here we utilized a multi-cohort analysis approach using machine-learning algorithms to identify blood gene signatures that can distinguish severe and cerebral malaria from moderate and non-cerebral cases. Using a Regularized Random Forest model, we identified 28-gene and 32-gene signatures that can reliably distinguish severe and cerebral malaria, respectively. We tested the specificity of both signatures against other common infectious diseases to ensure the signatures reliability and suitability as diagnostic markers. The severe and cerebral malaria gene-signatures were further integrated through k-top scoring pairs classifiers into ten and nine gene pairs that could distinguish severe and cerebral malaria, respectively. These signatures have various implications that can be utilized as blood diagnostic tools for malaria severity in endemic countries.

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Tetraspanin CD53: an overlooked regulator of immune cell function

Cited by 42 publications

References 55 publications

Differentially Expressed Genes and Enriched Signaling Pathways in the Adipose Tissue of Obese People

Differentially Expressed Genes and Enriched Signaling Pathways in the Adipose Tissue of Obese People

Molecular mechanisms of dendritic cell migration in immunity and cancer

Host Blood Gene Signatures Can Detect the Progression to Severe and Cerebral Malaria

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