Case Report: Interferon-γ Restores Monocytic Human Leukocyte Antigen Receptor (mHLA-DR) in Severe COVID-19 With Acquired Immunosuppression Syndrome

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Case Report: Interferon-γ Restores Monocytic Human Leukocyte Antigen Receptor (mHLA-DR) in Severe COVID-19 With Acquired Immunosuppression Syndrome
Dickel, S.; Grimm, C.; Amschler, K.; Schnitzler, S. U.; Schanz, J.; Moerer, O. & Payen, D. et al. (2021) 
Frontiers in Immunology12.​

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Authors
Dickel, Steffen; Grimm, Clemens; Amschler, Katharina; Schnitzler, Sebastian Uwe; Schanz, Julie; Moerer, Onnen; Payen, Didier; Tampe, Bjoern; Winkler, Martin Sebastian
Abstract
Background The major histocompatibility complex (MHC) class II characterized by monocytes CD14+ expression of human leukocyte antigen receptors (HLA-DR), is essential for the synapse between innate and adaptive immune response in infectious disease. Its reduced expression is associated with a high risk of secondary infections in septic patients and can be safely corrected by Interferon-y (IFNy) injection. Coronavirus disease (COVID-19) induces an alteration of Interferon (IFN) genes expression potentially responsible for the observed low HLA-DR expression in circulating monocytes (mHLA-DR). Methods We report a case of one-time INFy injection (100 mcg s.c.) in a superinfected 61-year-old man with COVID-19–associated acute respiratory distress syndrome (ARDS), with monitoring of mHLA-DR expression and clinical tolerance. Observations Low mHLA-DR pretreatment expression (26.7%) was observed. IFNy therapy leading to a rapid increase in mHLA-DR expression (83.1%). Conclusions Severe ARDS in a COVID-19 patient has a deep reduction in mHLA-DR expression concomitantly with secondary infections. The unique IFNy injection was safe and led to a sharp increase in the expression of mHLA-DR. Based on immune and infection monitoring, more cases of severe COVID-19 patients with low mHLA-DR should be treated by IFNy to test the clinical effectiveness.
Issue Date
2021
Publisher
Frontiers Media S.A.
Journal
Frontiers in Immunology 
eISSN
1664-3224
Sponsor
Open-Access-Publikationsfonds 2021

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