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Inflammation is central to the aetiology of both conditions where variations in immune responses can mitigate or aggravate disease course. Identifying at\u2010risk groups based on immunoinflammatory signatures is valuable in directing personalised care and developing potential targets for precision therapy. This observational study characterised immunophenotypic variation associated with COVID\u201019 severity in T2D. Broad\u2010spectrum immunophenotyping quantified 15 leucocyte populations in peripheral circulation from a cohort of 45 hospitalised COVID\u201019 patients with and without T2D. Lymphocytopenia and specific loss of cytotoxic CD8\n                    <jats:sup>+<\/jats:sup>\n                    lymphocytes were associated with severe COVID\u201019 and requirement for intensive care in both non\u2010diabetic and T2D patients. A morphological anomaly of increased monocyte size and monocytopenia restricted to classical CD14\n                    <jats:sup>Hi<\/jats:sup>\n                    CD16\n                    <jats:sup>\u2212<\/jats:sup>\n                    monocytes was specifically associated with severe COVID\u201019 in patients with T2D requiring intensive care. Increased expression of inflammatory markers reminiscent of the type 1 interferon pathway (IL6, IL8, CCL2, INFB1) underlaid the immunophenotype associated with T2D. These immunophenotypic and hyperinflammatory changes may contribute to increased voracity of COVID\u201019 in T2D. These findings allow precise identification of T2D patients with severe COVID\u201019 as well as provide evidence that the type 1 interferon pathway may be an actionable therapeutic target for future studies.\n                  <\/jats:p>","DOI":"10.15252\/emmm.202013038","type":"journal-article","created":{"date-parts":[[2020,8,20]],"date-time":"2020-08-20T11:15:23Z","timestamp":1597922123000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":49,"title":["Monocytopenia, monocyte morphological anomalies and hyperinflammation characterise severe COVID\u201019 in type 2 diabetes"],"prefix":"10.1038","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3056-3640","authenticated-orcid":false,"given":"Fawaz","family":"Alzaid","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean\u2010Baptiste","family":"Julla","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marc","family":"Diedisheim","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Charline","family":"Potier","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Louis","family":"Potier","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gilberto","family":"Velho","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B\u00e9n\u00e9dicte","family":"Gaborit","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philippe","family":"Manivet","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"St\u00e9phane","family":"Germain","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tiphaine","family":"Vidal\u2010Trecan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ronan","family":"Roussel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean\u2010Pierre","family":"Riveline","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elise","family":"Dalmas","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicolas","family":"Venteclef","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6458-2001","authenticated-orcid":false,"given":"Jean\u2010Fran\u00e7ois","family":"Gautier","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2020,9,11]]},"reference":[{"key":"BFEMMM202013038_CR1","doi-asserted-by":"crossref","first-page":"e88689","DOI":"10.1172\/jci.insight.88689","volume":"1","author":"F Alzaid","year":"2016","unstructured":"Alzaid F, Lagadec F, Albuquerque M, Ballaire R, Orliaguet L, Hainault I, Blugeon C, Lemoine S, Lehuen A, Saliba DG et\u00a0al (2016) IRF5 governs liver macrophage activation that promotes hepatic fibrosis in mice and humans. 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