TY  - JOUR
A1  - Schön, Michael P.
A1  - Berking, Carola
A1  - Biedermann, Tilo
A1  - Buhl, Timo
A1  - Erpenbeck, Luise
A1  - Eyerich, Kilian
A1  - Eyerich, Stefanie
A1  - Ghoreschi, Kamran
A1  - Goebeler, Matthias
A1  - Ludwig, Ralf J.
A1  - Schäkel, Knut
A1  - Schilling, Bastian
A1  - Schlapbach, Christoph
A1  - Stary, Georg
A1  - von Stebut, Esther
A1  - Steinbrink, Kerstin
T1  - COVID‐19 and immunological regulations – from basic and translational aspects to clinical implications
JF  - JDDG: Journal der Deutschen Dermatologischen Gesellschaft
N2  - The COVID‐19 pandemic caused by SARS‐CoV‐2 has far‐reaching direct and indirect medical consequences. These include both the course and treatment of diseases. It is becoming increasingly clear that infections with SARS‐CoV‐2 can cause considerable immunological alterations, which particularly also affect pathogenetically and/or therapeutically relevant factors.
Against this background we summarize here the current state of knowledge on the interaction of SARS‐CoV‐2/COVID‐19 with mediators of the acute phase of inflammation (TNF, IL‐1, IL‐6), type 1 and type 17 immune responses (IL‐12, IL‐23, IL‐17, IL‐36), type 2 immune reactions (IL‐4, IL‐13, IL‐5, IL‐31, IgE), B‐cell immunity, checkpoint regulators (PD‐1, PD‐L1, CTLA4), and orally druggable signaling pathways (JAK, PDE4, calcineurin). In addition, we discuss in this context non‐specific immune modulation by glucocorticosteroids, methotrexate, antimalarial drugs, azathioprine, dapsone, mycophenolate mofetil and fumaric acid esters, as well as neutrophil granulocyte‐mediated innate immune mechanisms.
From these recent findings we derive possible implications for the therapeutic modulation of said immunological mechanisms in connection with SARS‐CoV‐2/COVID‐19. Although, of course, the greatest care should be taken with patients with immunologically mediated diseases or immunomodulating therapies, it appears that many treatments can also be carried out during the COVID‐19 pandemic; some even appear to alleviate COVID‐19.
KW  - COVID-19
KW  - SARS-CoV-2
KW  - immunology
Y1  - 2020
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-218205
VL  - 18
IS  - 8
SP  - 795
EP  - 807
ER  - 
TY  - JOUR
A1  - Herster, Franziska
A1  - Bittner, Zsofia
A1  - Codrea, Marius Cosmin
A1  - Archer, Nathan K.
A1  - Heister, Martin
A1  - Löffler, Markus W.
A1  - Heumos, Simon
A1  - Wegner, Joanna
A1  - Businger, Ramona
A1  - Schindler, Michael
A1  - Stegner, David
A1  - Schäkel, Knut
A1  - Grabbe, Stephan
A1  - Ghoreschi, Kamran
A1  - Miller, Lloyd S.
A1  - Weber, Alexander N. R.
T1  - Platelets Aggregate With Neutrophils and Promote Skin Pathology in Psoriasis
JF  - Frontiers in Immunology
N2  - Psoriasis is a frequent systemic inflammatory autoimmune disease characterized primarily by skin lesions with massive infiltration of leukocytes, but frequently also presents with cardiovascular comorbidities. Especially polymorphonuclear neutrophils (PMNs) abundantly infiltrate psoriatic skin but the cues that prompt PMNs to home to the skin are not well-defined. To identify PMN surface receptors that may explain PMN skin homing in psoriasis patients, we screened 332 surface antigens on primary human blood PMNs from healthy donors and psoriasis patients. We identified platelet surface antigens as a defining feature of psoriasis PMNs, due to a significantly increased aggregation of neutrophils and platelets in the blood of psoriasis patients. Similarly, in the imiquimod-induced experimental in vivo mouse model of psoriasis, disease induction promoted PMN-platelet aggregate formation. In psoriasis patients, disease incidence directly correlated with blood platelet counts and platelets were detected in direct contact with PMNs in psoriatic but not healthy skin. Importantly, depletion of circulating platelets in mice in vivo ameliorated disease severity significantly, indicating that both PMNs and platelets may be relevant for psoriasis pathology and disease severity.
KW  - psoriasis
KW  - neutrophil
KW  - platelet
KW  - platelet-neutrophil complexes (PNCs)
KW  - imiquimod
Y1  - 2019
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-320175
VL  - 10
ER  -