The Immune Response and Effectiveness of COVID-19 Therapies.

[1]  Aaron J. Wilk,et al.  A single-cell atlas of the peripheral immune response in patients with severe COVID-19 , 2020, Nature Medicine.

[2]  Akiko Iwasaki,et al.  Type I and Type III Interferons – Induction, Signaling, Evasion, and Application to Combat COVID-19 , 2020, Cell Host & Microbe.

[3]  D. Acharya,et al.  Dysregulation of type I interferon responses in COVID-19 , 2020, Nature Reviews Immunology.

[4]  M. Rotondi,et al.  The cytokine storm in COVID-19: An overview of the involvement of the chemokine/chemokine-receptor system , 2020, Cytokine & Growth Factor Reviews.

[5]  M. Merad,et al.  Pathological inflammation in patients with COVID-19: a key role for monocytes and macrophages , 2020, Nature Reviews Immunology.

[6]  Y. Shoenfeld,et al.  Convalescent plasma in Covid-19: Possible mechanisms of action , 2020, Autoimmunity Reviews.

[7]  Jie Dong,et al.  Heightened Innate Immune Responses in the Respiratory Tract of COVID-19 Patients , 2020, Cell Host & Microbe.

[8]  Yi Wang,et al.  Remdesivir in adults with severe COVID-19: a randomised, double-blind, placebo-controlled, multicentre trial , 2020, The Lancet.

[9]  K. Brengel-Pesce,et al.  Type I IFN immunoprofiling in COVID-19 patients , 2020, Journal of Allergy and Clinical Immunology.

[10]  M. Tay,et al.  The trinity of COVID-19: immunity, inflammation and intervention , 2020, Nature Reviews Immunology.

[11]  John D Lambris,et al.  Complement as a target in COVID-19? , 2020, Nature Reviews Immunology.

[12]  H. Ulrich,et al.  CD147 as a Target for COVID-19 Treatment: Suggested Effects of Azithromycin and Stem Cell Engagement , 2020, Stem Cell Reviews and Reports.

[13]  M. Matucci-Cerinic,et al.  COVID-19, immune system response, hyperinflammation and repurposing antirheumatic drugs , 2020, Turkish journal of medical sciences.

[14]  Abhinav Nellore,et al.  Human Leukocyte Antigen Susceptibility Map for Severe Acute Respiratory Syndrome Coronavirus 2 , 2020, Journal of Virology.

[15]  M. Netea,et al.  Complex Immune Dysregulation in COVID-19 Patients with Severe Respiratory Failure , 2020, Cell Host & Microbe.

[16]  David Berlin,et al.  Complement associated microvascular injury and thrombosis in the pathogenesis of severe COVID-19 infection: A report of five cases , 2020, Translational Research.

[17]  Stefano Volpi,et al.  On the Alert for Cytokine Storm: Immunopathology in COVID‐19 , 2020, Arthritis & rheumatology.

[18]  Erwan L'Her,et al.  Compassionate Use of Remdesivir for Patients with Severe Covid-19 , 2020, The New England journal of medicine.

[19]  Q. Ye,et al.  The pathogenesis and treatment of the `Cytokine Storm' in COVID-19 , 2020, Journal of Infection.

[20]  Zhiguang Zhou,et al.  Can we use interleukin-6 (IL-6) blockade for coronavirus disease 2019 (COVID-19)-induced cytokine release syndrome (CRS)? , 2020, Journal of Autoimmunity.

[21]  R. Kahwash,et al.  Will Complement Inhibition be the New Target in Treating COVID-19 Related Systemic Thrombosis? , 2020, Circulation.

[22]  Xuetao Cao.  COVID-19: immunopathology and its implications for therapy , 2020, Nature Reviews Immunology.

[23]  Matthew Rowland,et al.  Trials of anti-tumour necrosis factor therapy for COVID-19 are urgently needed , 2020, The Lancet.

[24]  Yan Peng,et al.  Effectiveness of convalescent plasma therapy in severe COVID-19 patients , 2020, Proceedings of the National Academy of Sciences.

[25]  Y. Shoenfeld.  Corona (COVID-19) time musings: Our involvement in COVID-19 pathogenesis, diagnosis, treatment and vaccine planning , 2020, Autoimmunity Reviews.

[26]  D. McGonagle,et al.  The Role of Cytokines including Interleukin-6 in COVID-19 induced Pneumonia and Macrophage Activation Syndrome-Like Disease , 2020, Autoimmunity Reviews.

[27]  Guiqiang Wang,et al.  Cytokine release syndrome in severe COVID-19: interleukin-6 receptor antagonist tocilizumab may be the key to reduce mortality , 2020, International Journal of Antimicrobial Agents.

[28]  Taojiao Wang,et al.  Clinical and immunologic features in severe and moderate Coronavirus Disease 2019. , 2020, The Journal of clinical investigation.

[29]  S. Jawhara.  Could Intravenous Immunoglobulin Collected from Recovered Coronavirus Patients Protect against COVID-19 and Strengthen the Immune System of New Patients? , 2020, International journal of molecular sciences.

[30]  A. Singanayagam,et al.  Immunosuppression for hyperinflammation in COVID-19: a double-edged sword? , 2020, The Lancet.

[31]  Ying Wang,et al.  COVID-19 infection: the perspectives on immune responses , 2020, Cell Death & Differentiation.

[32]  Z. Tian,et al.  Functional exhaustion of antiviral lymphocytes in COVID-19 patients , 2020, Cellular & Molecular Immunology.

[33]  Yong-tang Zheng,et al.  Elevated exhaustion levels and reduced functional diversity of T cells in peripheral blood may predict severe progression in COVID-19 patients , 2020, Cellular & Molecular Immunology.

[34]  Dandan Wu,et al.  TH17 responses in cytokine storm of COVID-19: An emerging target of JAK2 inhibitor Fedratinib , 2020, Journal of Microbiology, Immunology and Infection.

[35]  Xiaowei Li,et al.  Molecular immune pathogenesis and diagnosis of COVID-19 , 2020, Journal of Pharmaceutical Analysis.

[36]  P. Mehta,et al.  COVID-19: consider cytokine storm syndromes and immunosuppression , 2020, The Lancet.

[37]  M. Bersanelli,et al.  Controversies about COVID-19 and anticancer treatment with immune checkpoint inhibitors , 2020, Immunotherapy.

[38]  R. Redfield,et al.  Covid-19 — Navigating the Uncharted , 2020, The New England journal of medicine.

[39]  Yuan Shi,et al.  Convalescent plasma as a potential therapy for COVID-19 , 2020, The Lancet Infectious Diseases.

[40]  Bo Diao,et al.  Reduction and Functional Exhaustion of T Cells in Patients With Coronavirus Disease 2019 (COVID-19) , 2020, Frontiers in Immunology.

[41]  Yang Yang,et al.  Applications of genome editing technology in the targeted therapy of human diseases: mechanisms, advances and prospects. , 2020, Signal transduction and targeted therapy.