TY  - JOUR
A1  - Wunsch, Marie
A1  - Hohmann, Christopher
A1  - Milles, Bianca
A1  - Rostermund, Christina
A1  - Lehmann, Paul V.
A1  - Schroeter, Michael
A1  - Bayas, Antonios
A1  - Ulzheimer, Jochen
A1  - Mäurer, Mathias
A1  - Ergün, Süleyman
A1  - Kuerten, Stefanie
T1  - The Correlation between the Virus- and Brain Antigen-Specific B Cell Response in the Blood of Patients with Multiple Sclerosis
JF  - Viruses
N2  - There is a largely divergent body of literature regarding the relationship between Epstein-Barr virus (EBV) infection and brain inflammation in multiple sclerosis (MS). Here, we tested MS patients during relapse (n = 11) and in remission (n = 19) in addition to n = 22 healthy controls to study the correlation between the EBV- and brain-specific B cell response in the blood by enzyme-linked immunospot (ELISPOT) and enzyme-linked immunosorbent assay (ELISA). Cytomegalovirus (CMV) was used as a control antigen tested in n = 16 MS patients during relapse and in n = 35 patients in remission. Over the course of the study, n = 16 patients were untreated, while n = 33 patients received immunomodulatory therapy. The data show that there was a moderate correlation between the frequencies of EBV- and brain-reactive B cells in MS patients in remission. In addition we could detect a correlation between the B cell response to EBV and disease activity. There was no evidence of an EBV reactivation. Interestingly, there was also a correlation between the frequencies of CMV- and brain-specific B cells in MS patients experiencing an acute relapse and an elevated B cell response to CMV was associated with higher disease activity. The trend remained when excluding seronegative subjects but was non-significant. These data underline that viral infections might impact the immunopathology of MS, but the exact link between the two entities remains subject of controversy.
KW  - B cells
KW  - CMV
KW  - EBV
KW  - ELISPOT
KW  - MS
Y1  - 2016
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-146946
VL  - 8
IS  - 4
ER  - 
TY  - JOUR
A1  - Alrefai, Hani
A1  - Muhammad, Khalid
A1  - Rudolf, Ronald
A1  - Pham, Duong Anh Thuy
A1  - Klein-Hessling, Stefan
A1  - Patra, Amiya K.
A1  - Avots, Andris
A1  - Bukur, Valesca
A1  - Sahin,, Ugur
A1  - Tenzer, Stefan
A1  - Goebeler, Matthias
A1  - Kerstan, Andreas
A1  - Serfling, Edgar
T1  - NFATc1 supports imiquimod-induced skin inflammation by suppressing IL-10 synthesis in B cells
JF  - Nature Communications
N2  - Epicutaneous application of Aldara cream containing the TLR7 agonist imiquimod (IMQ) to mice induces skin inflammation that exhibits many aspects of psoriasis, an inflammatory human skin disease. Here we show that mice depleted of B cells or bearing interleukin (IL)-10-deficient B cells show a fulminant inflammation upon IMQ exposure, whereas ablation of NFATc1 in B cells results in a suppression of Aldara-induced inflammation. In vitro, IMQ induces the proliferation and IL-10 expression by B cells that is blocked by BCR signals inducing NFATc1. By binding to HDAC1, a transcriptional repressor, and to an intronic site of the Il10 gene, NFATc1 suppresses IL-10 expression that dampens the production of tumour necrosis factor-α and IL-17 by T cells. These data indicate a close link between NFATc1 and IL-10 expression in B cells and suggest NFATc1 and, in particular, its inducible short isoform, NFATc1/αA, as a potential target to treat human psoriasis.
KW  - B cells
KW  - psoriasis
KW  - interleukins
KW  - inflammation
Y1  - 2016
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-173053
VL  - 7
ER  -