Interferon lambda in inflammation and autoimmune rheumatic diseases.
Interferon lambda in inflammation and autoimmune rheumatic diseases.
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炎症和自身免疫性风湿病中的干扰素。
DOI：
10.1038/s41584-021-00606-1
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发表时间：
2021-06
期刊：
影响因子：
--
通讯作者：
Kaplan MJ
中科院分区：
文献类型：
--
作者：
Goel RR;Kotenko SV;Kaplan MJ
干扰素是一种有效的抗病毒细胞因子，可以调节免疫力以应对感染或其他危险信号。除了抗病毒功能外，I型干扰素（IFNα和IFNβ）在自身免疫性疾病的发病机制中也很重要。III型干扰素（IFNλs）最初被描述为抑制病毒在上皮屏障表面复制同时限制炎性损伤的专门系统。然而，现在的证据表明，III型干扰素对先天性和适应性免疫应答具有复杂的影响，并且在系统性自身免疫性疾病中也可能是致病的。在许多自身免疫性风湿性疾病（包括系统性红斑狼疮）中，IFNλs的浓度在血液和组织中增加，并进一步与特定的临床和实验室参数相关。本综述旨在对目前有关IFNλ生物学的文献以及III型干扰素如何导致自身免疫性免疫失调和组织损伤进行批判性评价。III型干扰素对自身免疫性风湿性疾病治疗策略的潜在影响，如干扰素阻断，也被认为是。III型干扰素（IFNλs）影响先天性和适应性免疫应答，并与自身免疫性风湿性疾病的发病机制有关。在这篇综述中，作者概述了IFNλs在风湿性疾病中的作用，并讨论了针对它们的治疗策略。III型干扰素（IFNλs）对于上皮屏障表面针对病原体的免疫防御至关重要，并且最初被描述为I型干扰素系统的抗炎对应物。IFNλs对先天免疫和适应性免疫都有复杂的影响，并在某些情况下可以促进炎症。与I型干扰素类似，III型干扰素浓度在患有自身免疫性风湿性疾病如系统性红斑狼疮（SLE）的患者的血液和受影响的组织中增加。IFNλs的浓度与临床和免疫学参数相关，并且似乎对SLE的细胞特异性和组织特异性疾病过程具有非冗余的影响。目前靶向IFNα或其受体的生物疗法不能阻断IFNλs的作用。需要进一步的研究来充分描述IFNλs的环境依赖性作用，并优化自身免疫性风湿病患者的治疗。
Interferons are potent antiviral cytokines that modulate immunity in response to infection or other danger signals. In addition to their antiviral functions, type I interferons (IFNα and IFNβ) are important in the pathogenesis of autoimmune diseases. Type III interferons (IFNλs) were initially described as a specialized system that inhibits viral replication at epithelial barrier surfaces while limiting inflammatory damage. However, evidence now suggests that type III interferons have complex effects on both innate and adaptive immune responses and might also be pathogenic in systemic autoimmune diseases. Concentrations of IFNλs are increased in blood and tissues in a number of autoimmune rheumatic diseases, including systemic lupus erythematosus, and are further associated with specific clinical and laboratory parameters. This Review is aimed at providing a critical evaluation of the current literature on IFNλ biology and how type III interferons might contribute to immune dysregulation and tissue damage in autoimmunity. The potential effects of type III interferons on treatment strategies for autoimmune rheumatic diseases, such as interferon blockade, are also considered. Type III interferons (IFNλs) affect innate and adaptive immune responses and are associated with the pathogenesis of autoimmune rheumatic diseases. In this Review, the authors provide an overview of IFNλs in rheumatic diseases and discuss therapeutic strategies to target them. Type III interferons (IFNλs) are critical for immune defence against pathogens at epithelial barrier surfaces and were initially described as an anti-inflammatory counterpart to the type I interferon system. IFNλs have complex effects on both innate and adaptive immunity and can promote inflammation in certain contexts. Similar to type I interferons, type III interferon concentrations are increased in the blood and affected tissues of patients with autoimmune rheumatic diseases such as systemic lupus erythematosus (SLE). Concentrations of IFNλs correlate with clinical and immunological parameters and seem to have non-redundant effects on cell-specific and tissue-specific disease processes in SLE. Current biologic therapies that target IFNα or its receptor do not block the effects of IFNλs. Additional research is needed to fully characterize the context-dependent effects of IFNλs and to optimize treatment for patients with autoimmune rheumatic diseases.
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影响因子：
4.4
作者：
Benhammadi, Mohamed;Mathe, Justine;Perreault, Claude
通讯作者：
Perreault, Claude
影响因子：
3.4
作者：
Amezcua-Guerra, Luis M.;Marquez-Velasco, Ricardo;Bojalil, Rafael
通讯作者：
Bojalil, Rafael
影响因子：
13.3
作者：
Casey, Kerry A.;Smith, Michael A.;White, Wendy, I
通讯作者：
White, Wendy, I
危及生命的Covid-19患者中针对I型IFN的自身抗体。
DOI：
10.1126/science.abd4585
发表时间：
2020-10-23
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Bastard P;Rosen LB;Zhang Q;Michailidis E;Hoffmann HH;Zhang Y;Dorgham K;Philippot Q;Rosain J;Béziat V;Manry J;Shaw E;Haljasmägi L;Peterson P;Lorenzo L;Bizien L;Trouillet-Assant S;Dobbs K;de Jesus AA;Belot A;Kallaste A;Catherinot E;Tandjaoui-Lambiotte Y;Le Pen J;Kerner G;Bigio B;Seeleuthner Y;Yang R;Bolze A;Spaan AN;Delmonte OM;Abers MS;Aiuti A;Casari G;Lampasona V;Piemonti L;Ciceri F;Bilguvar K;Lifton RP;Vasse M;Smadja DM;Migaud M;Hadjadj J;Terrier B;Duffy D;Quintana-Murci L;van de Beek D;Roussel L;Vinh DC;Tangye SG;Haerynck F;Dalmau D;Martinez-Picado J;Brodin P;Nussenzweig MC;Boisson-Dupuis S;Rodríguez-Gallego C;Vogt G;Mogensen TH;Oler AJ;Gu J;Burbelo PD;Cohen JI;Biondi A;Bettini LR;D'Angio M;Bonfanti P;Rossignol P;Mayaux J;Rieux-Laucat F;Husebye ES;Fusco F;Ursini MV;Imberti L;Sottini A;Paghera S;Quiros-Roldan E;Rossi C;Castagnoli R;Montagna D;Licari A;Marseglia GL;Duval X;Ghosn J;HGID Lab;NIAID-USUHS Immune Response to COVID Group;COVID Clinicians;COVID-STORM Clinicians;Imagine COVID Group;French COVID Cohort Study Group;Milieu Intérieur Consortium;CoV-Contact Cohort;Amsterdam UMC Covid-19 Biobank;COVID Human Genetic Effort;Tsang JS;Goldbach-Mansky R;Kisand K;Lionakis MS;Puel A;Zhang SY;Holland SM;Gorochov G;Jouanguy E;Rice CM;Cobat A;Notarangelo LD;Abel L;Su HC;Casanova JL
通讯作者：
Casanova JL
影响因子：
56.9
作者：
Broggi, Achille;Ghosh, Sreya;Zanoni, Ivan
通讯作者：
Zanoni, Ivan