Immunometabolism (Cobham (Surrey, England))最新文献

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MicroRNA-regulated B cells in obesity. 微rna调控的B细胞与肥胖有关。
Immunometabolism (Cobham (Surrey, England)) Pub Date : 2022-08-05 eCollection Date: 2022-07-01 DOI: 10.1097/IN9.0000000000000005
Alyssa J Matz, Lili Qu, Keaton Karlinsey, Beiyan Zhou
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引用次数: 0
Sex bias in systemic lupus erythematosus: a molecular insight. 系统性红斑狼疮的性别偏见:分子洞察力。
Immunometabolism (Cobham (Surrey, England)) Pub Date : 2022-07-29 eCollection Date: 2022-07-01 DOI: 10.1097/IN9.0000000000000004
Moumita Bose, Caroline Jefferies
{"title":"Sex bias in systemic lupus erythematosus: a molecular insight.","authors":"Moumita Bose, Caroline Jefferies","doi":"10.1097/IN9.0000000000000004","DOIUrl":"10.1097/IN9.0000000000000004","url":null,"abstract":"<p><p>Acknowledging sex differences in immune response is particularly important when we consider the differences between men and women in the incidence of disease. For example, over 80% of autoimmune disease occurs in women, whereas men have a higher incidence of solid tumors compared to women. In general women have stronger innate and adaptive immune responses than men, explaining their ability to clear viral and bacterial infections faster, but also contributing to their increased susceptibility to autoimmune disease. The autoimmune disease systemic lupus erythematosus (SLE) is the archetypical sexually dimorphic disease, with 90% of patients being women. Various mechanisms have been suggested to account for the female prevalence of SLE, including sex hormones, X-linked genes, and epigenetic regulation of gene expression. Here, we will discuss how these mechanisms contribute to pathobiology of SLE and how type I interferons work with them to augment sex specific disease pathogenesis in SLE.</p>","PeriodicalId":73349,"journal":{"name":"Immunometabolism (Cobham (Surrey, England))","volume":" ","pages":"e00004"},"PeriodicalIF":0.0,"publicationDate":"2022-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9358995/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40696932","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
PERK promotes immunosuppressive M2 macrophage phenotype by metabolic reprogramming and epigenetic modifications through the PERK-ATF4-PSAT1 axis. PERK通过代谢重编程和表观遗传修饰通过PERK- atf4 - psat1轴促进免疫抑制M2巨噬细胞表型。
Immunometabolism (Cobham (Surrey, England)) Pub Date : 2022-07-01 DOI: 10.1097/IN9.0000000000000007
Uday P Pratap, Ratna K Vadlamudi
{"title":"PERK promotes immunosuppressive M2 macrophage phenotype by metabolic reprogramming and epigenetic modifications through the PERK-ATF4-PSAT1 axis.","authors":"Uday P Pratap,&nbsp;Ratna K Vadlamudi","doi":"10.1097/IN9.0000000000000007","DOIUrl":"https://doi.org/10.1097/IN9.0000000000000007","url":null,"abstract":"<p><p>The endoplasmic reticulum (ER) is a specialized organelle that participates in multiple cellular functions including protein folding, maturation, trafficking, and degradation to maintain homeostasis. However, hostile conditions in the tumor microenvironment (TME) disturb ER homeostasis. To overcome these conditions, cells activate ER stress response pathways, which are shown to augment the suppressive phenotypes of immune cells; however, the molecular mechanisms underpinning this process remain elusive. Here, we discuss a recent study by Raines et al, that suggests the role of the helper T-cell 2 (TH2) cytokine interleukin-4 (IL-4), and the TME in facilitating a protein kinase RNA-like ER kinase (PERK)-signaling cascade in macrophages, which promotes immunosuppressive M2 macrophage activation and proliferation. Further, the authors showed that PERK signaling promotes both mitochondrial respirations to fulfill cellular energy requirements and signaling through ATF4, which regulate phosphoserine aminotransferase 1 (PSAT1) activity to mediate the serine biosynthesis pathway. These results highlight a previously uncharacterized role for PERK in cellular metabolism and epigenetic modification in M2 macrophages, and thus offers a new therapeutic strategy for overcoming the immunosuppressive effects in the TME.</p>","PeriodicalId":73349,"journal":{"name":"Immunometabolism (Cobham (Surrey, England))","volume":"4 3","pages":"e00007"},"PeriodicalIF":0.0,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9359065/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9178090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 3
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