Is the humoral immunity dispensable for the pathogenesis of psoriasis?
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Is the humoral immunity dispensable for the pathogenesis of psoriasis? / Thomas, J; Küpper, M; Batra, R; Jargosch, M; Atenhan, A; Baghin, V; Krause, L; Lauffer, F; Biedermann, T; Theis, F J; Eyerich, K; Eyerich, S; Garzorz-Stark, N.
In: J EUR ACAD DERMATOL, Vol. 33, No. 1, 01.2019, p. 115-122.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Is the humoral immunity dispensable for the pathogenesis of psoriasis?
AU - Thomas, J
AU - Küpper, M
AU - Batra, R
AU - Jargosch, M
AU - Atenhan, A
AU - Baghin, V
AU - Krause, L
AU - Lauffer, F
AU - Biedermann, T
AU - Theis, F J
AU - Eyerich, K
AU - Eyerich, S
AU - Garzorz-Stark, N
N1 - © 2018 European Academy of Dermatology and Venereology.
PY - 2019/1
Y1 - 2019/1
N2 - BACKGROUND: Imbalances of T-cell subsets are hallmarks of disease-specific inflammation in psoriasis. However, the relevance of B cells for psoriasis remains poorly investigated.OBJECTIVE: To analyse the role of B cells and immunoglobulins for the disease-specific immunology of psoriasis.METHODS: We characterized B-cell subsets and immunoglobulin levels in untreated psoriasis patients (n = 37) and compared them to healthy controls (n = 20) as well as to psoriasis patients under disease-controlling systemic treatment (n = 28). B-cell subsets were analysed following the flow cytometric gating strategy based on the surface markers CD24, CD38 and CD138. Moreover, immunofluorescence stainings were used to detect IgA in psoriatic skin.RESULTS: We found significantly increased levels of IgA in the serum of treatment-naïve psoriasis patients correlating with disease score. However, IgA was only observed in dermal vessels of skin sections. Concerning B-cell subsets, we only found a moderately positive correlation of CD138+ plasma cells with IgA levels and disease score in treatment-naïve psoriasis patients. Confirming our hypothesis that psoriasis can develop in the absence of functional humoral immunity, we investigated a patient who suffered concomitantly from both psoriasis and a hereditary common variable immune defect (CVID) characterized by a lack of B cells and immunoglobulins. We detected variants in three of the 13 described genes of CVID and a so far undescribed variant in the ligand of the TNFRSF13B receptor leading to disturbed B-cell maturation and antibody production. However, this patient showed typical psoriasis regarding clinical presentation, histology or T-cell infiltrate. Finally, in a group of psoriasis patients under systemic treatment, neither did IgA levels drop nor did plasma cells correlate with IgA levels and disease score.CONCLUSION: B-cell alterations might rather be an epiphenomenal finding in psoriasis with a clear dominance of T cells over shifts in B-cell subsets.
AB - BACKGROUND: Imbalances of T-cell subsets are hallmarks of disease-specific inflammation in psoriasis. However, the relevance of B cells for psoriasis remains poorly investigated.OBJECTIVE: To analyse the role of B cells and immunoglobulins for the disease-specific immunology of psoriasis.METHODS: We characterized B-cell subsets and immunoglobulin levels in untreated psoriasis patients (n = 37) and compared them to healthy controls (n = 20) as well as to psoriasis patients under disease-controlling systemic treatment (n = 28). B-cell subsets were analysed following the flow cytometric gating strategy based on the surface markers CD24, CD38 and CD138. Moreover, immunofluorescence stainings were used to detect IgA in psoriatic skin.RESULTS: We found significantly increased levels of IgA in the serum of treatment-naïve psoriasis patients correlating with disease score. However, IgA was only observed in dermal vessels of skin sections. Concerning B-cell subsets, we only found a moderately positive correlation of CD138+ plasma cells with IgA levels and disease score in treatment-naïve psoriasis patients. Confirming our hypothesis that psoriasis can develop in the absence of functional humoral immunity, we investigated a patient who suffered concomitantly from both psoriasis and a hereditary common variable immune defect (CVID) characterized by a lack of B cells and immunoglobulins. We detected variants in three of the 13 described genes of CVID and a so far undescribed variant in the ligand of the TNFRSF13B receptor leading to disturbed B-cell maturation and antibody production. However, this patient showed typical psoriasis regarding clinical presentation, histology or T-cell infiltrate. Finally, in a group of psoriasis patients under systemic treatment, neither did IgA levels drop nor did plasma cells correlate with IgA levels and disease score.CONCLUSION: B-cell alterations might rather be an epiphenomenal finding in psoriasis with a clear dominance of T cells over shifts in B-cell subsets.
KW - Journal Article
U2 - 10.1111/jdv.15101
DO - 10.1111/jdv.15101
M3 - SCORING: Journal article
C2 - 29856508
VL - 33
SP - 115
EP - 122
JO - J EUR ACAD DERMATOL
JF - J EUR ACAD DERMATOL
SN - 0926-9959
IS - 1
ER -