Annual Review of Pathology-Mechanisms of Disease最新文献_第7页

Role of the Inflammasome in Liver Disease. 炎性体在肝脏疾病中的作用。

IF 36.2 1区医学

Annual Review of Pathology-Mechanisms of Disease Pub Date : 2022-01-24 DOI: 10.1146/annurev-pathmechdis-032521-102529

Marcelle de Carvalho Ribeiro, Gyongyi Szabo

{"title":"Role of the Inflammasome in Liver Disease.","authors":"Marcelle de Carvalho Ribeiro, Gyongyi Szabo","doi":"10.1146/annurev-pathmechdis-032521-102529","DOIUrl":"https://doi.org/10.1146/annurev-pathmechdis-032521-102529","url":null,"abstract":"The involvement of inflammasomes in the proinflammatory response observed in chronic liver diseases, such as alcohol-associated liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD), is widely recognized. Although there are different types of inflammasomes, most studies to date have given attention to NLRP3 (nucleotide-binding oligomerization domain-like receptor family, pyrin domain containing 3) in the pathogenesis of ALD, NAFLD/nonalcoholic steatohepatitis, and fibrosis. Canonical inflammasomes are intracellular multiprotein complexes that are assembled after the sensing of danger signals and activate caspase-1, which matures interleukin (IL)-1β, IL-18, and IL-37 and also induces a form of cell death called pyroptosis. Noncanonical inflammasomes activate caspase-11 to induce pyroptosis. We discuss the different types of inflammasomes involved in liver diseases with a focus on (a) signals and mechanisms of inflammasome activation, (b) the role of different types of inflammasomes and their products in the pathogenesis of liver diseases, and (c) potential therapeutic strategies targeting components of the inflammasomes or cytokines produced upon inflammasome activation.","PeriodicalId":50753,"journal":{"name":"Annual Review of Pathology-Mechanisms of Disease","volume":"17 ","pages":"345-365"},"PeriodicalIF":36.2,"publicationDate":"2022-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10501045/pdf/nihms-1905127.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10286464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 62

Pancreatic cancer. 癌症。

IF 36.2 1区医学

Annual Review of Pathology-Mechanisms of Disease Pub Date : 2021-08-31 DOI: 10.1146/annurev.pathol.3.121806.154305

A. Maitra, R. Hruban

引用次数: 45

Gut Microbiota in Intestinal and Liver Disease. 肠道和肝脏疾病中的肠道微生物群。

IF 36.2 1区医学

Annual Review of Pathology-Mechanisms of Disease Pub Date : 2021-01-24 Epub Date: 2020-11-24 DOI: 10.1146/annurev-pathol-030320-095722

Rheinallt M Jones, Andrew S Neish

{"title":"Gut Microbiota in Intestinal and Liver Disease.","authors":"Rheinallt M Jones, Andrew S Neish","doi":"10.1146/annurev-pathol-030320-095722","DOIUrl":"https://doi.org/10.1146/annurev-pathol-030320-095722","url":null,"abstract":"It is known that the gut microbiota, the numerically vast and taxonomically diverse microbial communities that thrive in a symbiotic fashion within our alimentary tract, can affect the normal physiology of the gastrointestinal tract and liver. Further, disturbances of the microbiota community structure from both endogenous and exogenous influences as well as the failure of host responsive mechanisms have been implicated in a variety of disease processes. Mechanistically, alterations in intestinal permeability and dysbiosis of the microbiota can result in inflammation, immune activation, and exposure to xenobiotic influences. Additionally, the gut and liver are continually exposed to small molecule products of the microbiota with proinflammatory, gene regulatory, and oxidative properties. Long-term coevolution has led to tolerance and incorporation of these influences into normal physiology and homeostasis; conversely, changes in this equilibrium from either the host or the microbial side can result in a wide variety of immune, inflammatory, metabolic, and neoplastic intestinal and hepatic disorders.","PeriodicalId":50753,"journal":{"name":"Annual Review of Pathology-Mechanisms of Disease","volume":"16 ","pages":"251-275"},"PeriodicalIF":36.2,"publicationDate":"2021-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1146/annurev-pathol-030320-095722","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38639867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 52

Opposing Roles of Type I Interferons in Cancer Immunity. I型干扰素在肿瘤免疫中的对立作用。

IF 36.2 1区医学

Annual Review of Pathology-Mechanisms of Disease Pub Date : 2021-01-24 Epub Date: 2020-12-02 DOI: 10.1146/annurev-pathol-031920-093932

Giselle M Boukhaled, Shane Harding, David G Brooks

{"title":"Opposing Roles of Type I Interferons in Cancer Immunity.","authors":"Giselle M Boukhaled, Shane Harding, David G Brooks","doi":"10.1146/annurev-pathol-031920-093932","DOIUrl":"https://doi.org/10.1146/annurev-pathol-031920-093932","url":null,"abstract":"The immune system is tasked with identifying malignant cells to eliminate or prevent cancer spread. This involves a complex orchestration of many immune cell types that together recognize different aspects of tumor transformation and growth. In response, tumors have developed mechanisms to circumvent immune attack. Type I interferons (IFN-Is) are a class of proinflammatory cytokines produced in response to viruses and other environmental stressors. IFN-Is are also emerging as essential drivers of antitumor immunity, potently stimulating the ability of immune cells to eliminate tumor cells. However, a more complicated role for IFN-Is has arisen, as prolonged stimulation can promote feedback inhibitory mechanisms that contribute to immune exhaustion and other deleterious effects that directly or indirectly permit cancer cells to escape immune clearance. We review the fundamental and opposing functions of IFN-Is that modulate tumor growth and impact immune function and ultimately how these functions can be harnessed for the design of new cancer therapies.","PeriodicalId":50753,"journal":{"name":"Annual Review of Pathology-Mechanisms of Disease","volume":"16 ","pages":"167-198"},"PeriodicalIF":36.2,"publicationDate":"2021-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1146/annurev-pathol-031920-093932","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38667508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 64

Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance. 免疫检查点抑制剂治疗癌症:临床影响和反应和耐药机制。

IF 36.2 1区医学

Annual Review of Pathology-Mechanisms of Disease Pub Date : 2021-01-24 Epub Date: 2020-11-16 DOI: 10.1146/annurev-pathol-042020-042741

Sreya Bagchi, Robert Yuan, Edgar G Engleman

{"title":"Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance.","authors":"Sreya Bagchi, Robert Yuan, Edgar G Engleman","doi":"10.1146/annurev-pathol-042020-042741","DOIUrl":"https://doi.org/10.1146/annurev-pathol-042020-042741","url":null,"abstract":"Immune checkpoint inhibitors (ICIs) have made an indelible mark in the field of cancer immunotherapy. Starting with the approval of anti-cytotoxic T lymphocyte-associated protein 4 (anti-CTLA-4) for advanced-stage melanoma in 2011, ICIs-which now also include antibodies against programmed cell death 1 (PD-1) and its ligand (PD-L1)-quickly gained US Food and Drug Administration approval for the treatment of a wide array of cancer types, demonstrating unprecedented extension of patient survival. However, despite the success of ICIs, resistance to these agents restricts the number of patients able to achieve durable responses, and immune-related adverse events complicate treatment. Thus, a better understanding of the requirements for an effective and safe antitumor immune response following ICI therapy is needed. Studies of both tumoral and systemic changes in the immune system following ICI therapy have yielded insight into the basis for both efficacy and resistance. Ultimately, by building on these insights, researchers should be able to combine ICIs with other agents, or design new immunotherapies, to achieve broader and more durable efficacy as well as greater safety. Here, we review the history and clinical utility of ICIs, the mechanisms of resistance to therapy, and local and systemic immune cell changes associated with outcome.","PeriodicalId":50753,"journal":{"name":"Annual Review of Pathology-Mechanisms of Disease","volume":"16 ","pages":"223-249"},"PeriodicalIF":36.2,"publicationDate":"2021-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1146/annurev-pathol-042020-042741","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38714238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 763

Lethal Infectious Diseases as Inborn Errors of Immunity: Toward a Synthesis of the Germ and Genetic Theories. 致命的传染病是先天的免疫错误:迈向细菌和遗传理论的综合。

IF 28.4 1区医学

Annual Review of Pathology-Mechanisms of Disease Pub Date : 2021-01-24 Epub Date: 2020-04-14 DOI: 10.1146/annurev-pathol-031920-101429

Jean-Laurent Casanova, Laurent Abel

{"title":"Lethal Infectious Diseases as Inborn Errors of Immunity: Toward a Synthesis of the Germ and Genetic Theories.","authors":"Jean-Laurent Casanova, Laurent Abel","doi":"10.1146/annurev-pathol-031920-101429","DOIUrl":"10.1146/annurev-pathol-031920-101429","url":null,"abstract":"It was first demonstrated in the late nineteenth century that human deaths from fever were typically due to infections. As the germ theory gained ground, it replaced the old, unproven theory that deaths from fever reflected a weak personal or even familial constitution. A new enigma emerged at the turn of the twentieth century, when it became apparent that only a small proportion of infected individuals die from primary infections with almost any given microbe. Classical genetics studies gradually revealed that severe infectious diseases could be driven by human genetic predisposition. This idea gained ground with the support of molecular genetics, in three successive, overlapping steps. First, many rare inborn errors of immunity were shown, from 1985 onward, to underlie multiple, recurrent infections with Mendelian inheritance. Second, a handful of rare and familial infections, also segregating as Mendelian traits but striking humans resistant to other infections, were deciphered molecularly beginning in 1996. Third, from 2007 onward, a growing number of rare or common sporadicinfections were shown to result from monogenic, but not Mendelian, inborn errors. A synthesis of the hitherto mutually exclusive germ and genetic theories is now in view.","PeriodicalId":50753,"journal":{"name":"Annual Review of Pathology-Mechanisms of Disease","volume":"16 ","pages":"23-50"},"PeriodicalIF":28.4,"publicationDate":"2021-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7923385/pdf/nihms-1673949.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37834358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Spectrum of Helicobacter-Mediated Diseases. 幽门螺杆菌介导疾病的光谱。

IF 36.2 1区医学

Annual Review of Pathology-Mechanisms of Disease Pub Date : 2021-01-24 Epub Date: 2020-11-16 DOI: 10.1146/annurev-pathol-032520-024949

Karen Robinson, John C Atherton

{"title":"The Spectrum of Helicobacter-Mediated Diseases.","authors":"Karen Robinson, John C Atherton","doi":"10.1146/annurev-pathol-032520-024949","DOIUrl":"https://doi.org/10.1146/annurev-pathol-032520-024949","url":null,"abstract":"Helicobacter pylori is the leading cause of peptic ulcer disease. The infection has been implicated in more than 75% of duodenal ulcer cases and 17% of gastric ulcer cases. H. pylori has been classified as a human carcinogen, since it is the main cause of distal gastric adenocarcinoma and B cell mucosa-associated lymphoid tissue lymphoma. Evidence also links H. pylori with extragastric conditions including iron deficiency anemia, idiopathic thrombocytopenic purpura, and vitamin B12 deficiency. Studies indicate that H. pylori may be protective against other conditions of the gastrointestinal tract (e.g., reflux esophagitis and related pathologies) and elsewhere in the body (e.g., asthma). The infection is asymptomatic in the vast majority of cases; more serious outcomes occur in only 10-15% of infected individuals. Despite extensive research over the past 3 decades, there is no effective vaccine, and the circumstances leading to disease development remain unclear. In addition, there is now a growing prevalence of antimicrobial resistance in H. pylori. This review discusses these important issues.","PeriodicalId":50753,"journal":{"name":"Annual Review of Pathology-Mechanisms of Disease","volume":"16 ","pages":"123-144"},"PeriodicalIF":36.2,"publicationDate":"2021-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1146/annurev-pathol-032520-024949","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38714237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 60

Perspectives and Advances in the Understanding of Tuberculosis. 理解结核病的前景和进展。

IF 36.2 1区医学

Annual Review of Pathology-Mechanisms of Disease Pub Date : 2021-01-24 DOI: 10.1146/annurev-pathol-042120-032916

Rachel L Kinsella, Dennis X Zhu, Gregory A Harrison, Anne E Mayer Bridwell, Jerome Prusa, Sthefany M Chavez, Christina L Stallings

{"title":"Perspectives and Advances in the Understanding of Tuberculosis.","authors":"Rachel L Kinsella, Dennis X Zhu, Gregory A Harrison, Anne E Mayer Bridwell, Jerome Prusa, Sthefany M Chavez, Christina L Stallings","doi":"10.1146/annurev-pathol-042120-032916","DOIUrl":"10.1146/annurev-pathol-042120-032916","url":null,"abstract":"Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis (TB), remains a leading cause of death due to infection in humans. To more effectively combat this pandemic, many aspects of TB control must be developed, including better point of care diagnostics, shorter and safer drug regimens, and a protective vaccine. To address all these areas of need, better understanding of the pathogen, host responses, and clinical manifestations of the disease is required. Recently, the application of cutting-edge technologies to the study of Mtb pathogenesis has resulted in significant advances in basic biology, vaccine development, and antibiotic discovery. This leaves us in an exciting era of Mtb research in which our understanding of this deadly infection is improving at a faster rate than ever, and renews hope in our fight to end TB. In this review, we reflect on what is known regarding Mtb pathogenesis, highlighting recent breakthroughs that will provide leverage for the next leaps forward in the field.","PeriodicalId":50753,"journal":{"name":"Annual Review of Pathology-Mechanisms of Disease","volume":"16 ","pages":"377-408"},"PeriodicalIF":36.2,"publicationDate":"2021-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38861088","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 22

Metabolic Gatekeepers of Pathological B Cell Activation. 病理性B细胞活化的代谢守门人。

IF 36.2 1区医学

Annual Review of Pathology-Mechanisms of Disease Pub Date : 2021-01-24 Epub Date: 2020-12-15 DOI: 10.1146/annurev-pathol-061020-050135

Teresa Sadras, Lai N Chan, Gang Xiao, Markus Müschen

{"title":"Metabolic Gatekeepers of Pathological B Cell Activation.","authors":"Teresa Sadras, Lai N Chan, Gang Xiao, Markus Müschen","doi":"10.1146/annurev-pathol-061020-050135","DOIUrl":"https://doi.org/10.1146/annurev-pathol-061020-050135","url":null,"abstract":"Unlike other cell types, B cells undergo multiple rounds of V(D)J recombination and hypermutation to evolve high-affinity antibodies. Reflecting high frequencies of DNA double-strand breaks, adaptive immune protection by B cells comes with an increased risk of malignant transformation. In addition, the vast majority of newly generated B cells express an autoreactive B cell receptor (BCR). Thus, B cells are under intense selective pressure to remove autoreactive and premalignant clones. Despite stringent negative selection, B cells frequently give rise to autoimmune disease and B cell malignancies. In this review, we discuss mechanisms that we term metabolic gatekeepers to eliminate pathogenic B cell clones on the basis of energy depletion. Chronic activation signals from autoreactive BCRs or transforming oncogenes increase energy demands in autoreactive and premalignant B cells. Thus, metabolic gatekeepers limit energy supply to levels that are insufficient to fuel either a transforming oncogene or hyperactive signaling from an autoreactive BCR.","PeriodicalId":50753,"journal":{"name":"Annual Review of Pathology-Mechanisms of Disease","volume":"16 ","pages":"323-349"},"PeriodicalIF":36.2,"publicationDate":"2021-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1146/annurev-pathol-061020-050135","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38713563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 8

The Hippo Pathway in Liver Homeostasis and Pathophysiology. Hippo通路在肝脏稳态和病理生理中的作用。

IF 36.2 1区医学

Annual Review of Pathology-Mechanisms of Disease Pub Date : 2021-01-24 Epub Date: 2020-11-24 DOI: 10.1146/annurev-pathol-030420-105050

Jordan H Driskill, Duojia Pan

引用次数: 52