Antibodies against type I interferon: detection and association with severe clinical outcome in COVID-19 patients.
Antibodies against type I interferon: detection and association with severe clinical outcome in COVID-19 patients.
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对I型干扰素的抗体：Covid-19患者的检测和与严重临床结果相关性。
DOI：
10.1002/cti2.1327
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发表时间：
2021
影响因子：
5.8
通讯作者：
Trouillet-Assant S
中科院分区：
文献类型：
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作者：
Goncalves D;Mezidi M;Bastard P;Perret M;Saker K;Fabien N;Pescarmona R;Lombard C;Walzer T;Casanova JL;Belot A;Richard JC;Trouillet-Assant S
据报道，重症 COVID-19 患者 I 型干扰素 (IFN-I) 免疫力受损。部分患者中存在针对 IFN-I 的循环自身抗体（auto-Abs）可以解释这种缺陷。我们着手改进一组危重 COVID-19 患者中 IFN-I 自身抗体的检测和定量，以便更好地评估这些抗体随着大流行的进展的流行情况，以及它们与疾病临床病程的相关性。使用市售试剂盒（Thermo Fisher，目录#BMS217）测定了入住法国里昂临终关怀医院 ICU 的 84 名重症 COVID-19 患者血清中抗 IFN-α2 抗体的浓度。 84 名重症 COVID-19 患者中，共有 21 名 (25%) 的循环抗 IFN-α2 抗体高于临界值 (> 34 ng mL−1)。其中，21 名患者中有 15 名具有抗 IFN-α2 中和活性的抗体，即 84 名危重患者中的 15 名（18%）。此外，我们注意到大多数使用中和抗 IFN-α2 抗体的患者的 IFN-I 反应受损。使用或不使用中和抗 IFN-α2 自身抗体的临床特征或结果没有显着差异。我们在 COVID-19 患者入住 ICU 期间的血清中检测到了抗 IFN-α2 自身抗体。最后，我们还发现了针对多种 IFN-I 亚型（包括 IFN-ω）的自身抗体。我们报道，18% 的重症 COVID-19 患者的 IFN-I 自身抗体呈阳性，而所有轻度 COVID-19 患者均为阴性，这证实了这些抗体的存在与发展为重症 COVID-19 形式的较高风险相关。我们在此报告，18% 的重症 COVID-19 患者的能够中和 I 型干扰素 (IFN) 的自身抗体呈阳性。这一发现进一步证实了 IFN-I 自身抗体在抗病毒免疫反应中的有害作用，支持在 IFN-I 反应受损的 COVID-19 患者中使用非自身抗体靶向的重组 I 型干扰素（例如 IFN-β）。
Impairment of type I interferon (IFN‐I) immunity has been reported in critically ill COVID‐19 patients. This defect can be explained in a subset of patients by the presence of circulating autoantibodies (auto‐Abs) against IFN‐I. We set out to improve the detection and the quantification of IFN‐I auto‐Abs in a cohort of critically ill COVID‐19 patients, in order to better evaluate the prevalence of these Abs as the pandemic progresses, and how they correlate with the clinical course of the disease. The concentration of anti‐IFN‐α2 Abs was determined in the serum of 84 critically ill COVID‐19 patients who were admitted to ICU in Hospices Civils de Lyon, France, using a commercially available kit (Thermo Fisher, Catalog #BMS217). A total of 21 of 84 (25%) critically ill COVID‐19 patients had circulating anti‐IFN‐α2 Abs above cut‐off (> 34 ng mL−1). Among them, 15 of 21 had Abs with neutralising activity against IFN‐α2, that is 15 of 84 (18%) critically ill patients. In addition, we noticed an impairment of the IFN‐I response in the majority of patients with neutralising anti‐IFN‐α2 Abs. There was no significant difference in the clinical characteristics or outcome of with or without neutralising anti‐IFN‐α2 auto‐Abs. We detected anti‐IFN‐α2 auto‐Abs in COVID‐19 patients' sera throughout their ICU stay. Finally, we also found auto‐Abs against multiple subtypes of IFN‐I including IFN‐ω. We reported that 18% of critically ill COVID‐19 patients were positive for IFN‐I auto‐Abs, whereas all mild COVID‐19 patients were negative, confirming that the presence of these antibodies is associated with a higher risk of developing a critical COVID‐19 form. We report here that 18% of severe COVID‐19 patients were positive for autoantibodies able to neutralize type I interferon (IFN). This finding further confirms the deleterious role of IFN‐I auto‐Abs in the antiviral immune response supporting the use of recombinant type I IFNs not targeted by the auto‐Abs (e.g. IFN‐β) in COVID‐19 patients with an impairment of the IFN‐I response.
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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：
2.9
作者：
Trouillet-Assant S;Albert Vega C;Bal A;Nazare JA;Fascia P;Paul A;Massardier-Pilonchery A;D Aubarede C;Guibert N;Pitiot V;Lahousse M;Boibieux A;Makhloufi D;Simon C;Rabilloud M;Trabaud MA;Gueyffier F;Fassier JB;COVID-SER study group
通讯作者：
COVID-SER study group
影响因子：
14.2
作者：
Trouillet-Assant, Sophie;Viel, Sebastien;Belot, Alexandre
通讯作者：
Belot, Alexandre
IFN型IFN免疫的先天误差在危及生命的Covid-19。
DOI：
10.1126/science.abd4570
发表时间：
2020-10-23
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Zhang Q;Bastard P;Liu Z;Le Pen J;Moncada-Velez M;Chen J;Ogishi M;Sabli IKD;Hodeib S;Korol C;Rosain J;Bilguvar K;Ye J;Bolze A;Bigio B;Yang R;Arias AA;Zhou Q;Zhang Y;Onodi F;Korniotis S;Karpf L;Philippot Q;Chbihi M;Bonnet-Madin L;Dorgham K;Smith N;Schneider WM;Razooky BS;Hoffmann HH;Michailidis E;Moens L;Han JE;Lorenzo L;Bizien L;Meade P;Neehus AL;Ugurbil AC;Corneau A;Kerner G;Zhang P;Rapaport F;Seeleuthner Y;Manry J;Masson C;Schmitt Y;Schlüter A;Le Voyer T;Khan T;Li J;Fellay J;Roussel L;Shahrooei M;Alosaimi MF;Mansouri D;Al-Saud H;Al-Mulla F;Almourfi F;Al-Muhsen SZ;Alsohime F;Al Turki S;Hasanato R;van de Beek D;Biondi A;Bettini LR;D'Angio' M;Bonfanti P;Imberti L;Sottini A;Paghera S;Quiros-Roldan E;Rossi C;Oler AJ;Tompkins MF;Alba C;Vandernoot I;Goffard JC;Smits G;Migeotte I;Haerynck F;Soler-Palacin P;Martin-Nalda A;Colobran R;Morange PE;Keles S;Çölkesen F;Ozcelik T;Yasar KK;Senoglu S;Karabela ŞN;Rodríguez-Gallego C;Novelli G;Hraiech S;Tandjaoui-Lambiotte Y;Duval X;Laouénan C;COVID-STORM Clinicians;COVID Clinicians;Imagine COVID Group;French COVID Cohort Study Group;CoV-Contact Cohort;Amsterdam UMC Covid-19 Biobank;COVID Human Genetic Effort;NIAID-USUHS/TAGC COVID Immunity Group;Snow AL;Dalgard CL;Milner JD;Vinh DC;Mogensen TH;Marr N;Spaan AN;Boisson B;Boisson-Dupuis S;Bustamante J;Puel A;Ciancanelli MJ;Meyts I;Maniatis T;Soumelis V;Amara A;Nussenzweig M;García-Sastre A;Krammer F;Pujol A;Duffy D;Lifton RP;Zhang SY;Gorochov G;Béziat V;Jouanguy E;Sancho-Shimizu V;Rice CM;Abel L;Notarangelo LD;Cobat A;Su HC;Casanova JL
通讯作者：
Casanova JL
影响因子：
3.8
作者：
Pescarmona, Remi;Belot, Alexandre;Viel, Sebastien
通讯作者：
Viel, Sebastien