Similarly, lymph node atrophy and the number of lymph nodes decreased, accompanied by necrosis. immune system. strong class=”kwd-title” Keywords: Coronavirus disease 2019 (COVID-19), Cytokine storm, Anti-inflammation treatment Since the sudden outbreak of coronavirus disease 2019 (COVID-19) in Wu Han City, China caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), in just two more months, the epidemic has rapidly spread all over the world. On March 11, 2020, the World Health Organization (WHO) declared the COVID-19 outbreak a pandemic. Till March 22, globally, approximately 303,000 confirmed cases, including more than 12,900 deaths in approximately 150 countries. Data from China have indicated that about 20% of patients developed severe disease, older adults, particularly those with serious underlying health conditions, are at higher risk of death than younger ones. A minority of patients presented with respiratory failure, FLJ34463 septic shock and multi-organ dysfunction resulting in a fatality of 4%. In the past two month, we took part in a serial of remote teleconsultation, discussing WIKI4 several critical COVID-19 patients in intensive care unit (ICU) and clinical pathological conference (CPC). Here, from the perspective of clinical immunologist and rheumatologists, we would like to discuss and share our experience in the treatment of severe COVID-19. 1.?Several important features in critical COVID-19 patients From the point of view of rheumatologists, except for respiratory failure, the critical COVID-19 patients have common features: 1) sudden deterioration of disease around one to two weeks after onset; 2) much lower level of lymphocytes, especially natural killer (NK) cells in WIKI4 peripheral blood; 3) extremely high inflammatory parameters, including C reactive protein (CRP) and pro-inflammatory cytokines (IL-6, TNF, IL-8, et al); 4) destroyed immune system revealed by atrophy of spleen and lymph nodes, along with reduced lymphocytes in lymphoid organs; 5) the majority of infiltrated immune cells in lung lesion are monocytes and macrophages, but minimal lymphocytes infiltration; 6) mimicry of vasculitis, hypercoagulability and multiple organs damage. Based on the above characteristics of COVID-19, we discuss the following points in terms of treatment. 2.?Inflammatory cytokine storm was very common in patients with severe COVID-19 Cytokine storm (CS) refers to excessive and uncontrolled release of WIKI4 pro-inflammatory cytokines. Cytokine storm syndrome can be caused by a variety of diseases, including infectious diseases, rheumatic diseases and tumor immunotherapy. Clinically, it commonly presents as systemic inflammation, multiple organ failure, and high inflammatory parameters. In infectious diseases, CS usually WIKI4 originates from the focal infected area, spreading all over the body through circulation. In coronavirus pneumonia, such as severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), accompanied by rapid virus replication, a large number of inflammatory cell infiltration and CS led to acute lung injury, acute respiratory distress syndrome (ARDS) and death [1,2]. Accumulating evidence revealed that a part of severe COVID-19 patients have a elevated cytokine profile resembling CS in SARS and WIKI4 MERS. Huang et al. reported the level of inflammatory factors in patients with COVID-19. They measured cytokine levels in 41 inpatients (including 13 ICU patients and 28 non ICU patients), IL-1B, IL-1RA, IL-7, IL-8, IL-9, IL-10, fibroblast growth factor (FGF), granulocyte-macrophage colony stimulating factor (GM-CSF), IFN, granulocyte-colony stimulating factor (G-CSF), interferon–inducible protein (IP10), monocyte chemoattractant protein (MCP1), macrophage inflammatory protein 1 alpha (MIP1A), platelet derived growth factor (PDGF), tumor necrosis factor (TNF), vascular endothelial growth factor (VEGF) were increased, among which IL-2, IL-7, IL-10, G-CSF, IP10, MCP1, MIP1A, TNF were higher in severe patients [3,4]. Notably, there was not pronounce difference of serum IL-6 level been the ICU and non ICU patients. However, in another retrospective, multicentre cohort study, the same study group reported a.