PMC:7402624 / 50537-52517 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7402624","sourcedb":"PMC","sourceid":"7402624","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7402624","text":"More positive values in UMAP Components 1 or 2 captured mainly signals of change or differences in individual immune features in COVID-19 disease compared to HD and RD. UMAP Component 1 captured an immunotype (Immunotype 1) that was characterized by effector or highly activated CD4 T cells, low cTfh, some CD8 TEMRA-like activation, possibly hyperactivated CD8 T cells, and Tbet+ PB, whereas Component 2 or Immunotype 2 captured Tbetbright effector-like CD8 T cells, lacked some of the robust CD4 T cell activation but has some features of proliferating B cells (Fig. 6G and fig. S8). However, the data presented in Figs. 1 to 5 also suggested a subset of patients with minimal activation of T and B cell responses. To investigate this immune signature, we identified 20 patients who had responses more similar to HD and RD for five activated/responding B and T cell populations (Fig. 6J, middle, and fig. S10). If the UMAP Components 1 and 2 captured two distinct “immunotypes” of patient responses to SARS-CoV2 infection, this group of 20 patients represent a third immunotype. Immunotype 3 was negatively associated with UMAP Components 1 and 2 and negatively associated with disease severity, suggesting that a less robust immune response during COVID-19 was associated with less severe pathology (Fig. 6K and fig. S10), despite the fact that these patients were hospitalized with COVID-19 disease. These data further emphasize the different ways patients can present and possibly succumb to COVID-19 disease. These patterns may be related to pre-existing conditions in combination with immune response characteristics. It is likely that additional immune features, such as comprehensive serum cytokine measurements, will improve this model. Nevertheless, the current computational approach integrating deep immune profiling with disease severity trajectory and other clinical information revealed distinct patient immunotypes linked to distinct clinical outcomes (fig. 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