Reinforcing involvement of NK cells in psoriasiform dermatitis animal model

Psoriasis (Ps) is a chronic inflammatory immune-mediated disease with skin and joint manifestations, characterized by abnormal and rapid proliferation of keratinocytes and infiltration of psoriatic lesions with immune cells. Extensive literature suggests that Ps is a T-cell mediated disease its path...

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Bibliographic Details
Published in:Experimental and therapeutic medicine 2019-12, Vol.18 (6), p.4956-4966
Main Authors: Surcel, Mihaela, Munteanu, Adriana Narcisa, Huică, Radu-Ionuț, Isvoranu, Gheorghița, Pîrvu, Ioana Ruxandra, Constantin, Carolina, Bratu, Ovidiu, Căruntu, Constantin, Zaharescu, Isadora, Sima, Lucica, Costache, Marieta, Neagu, Monica
Format: Article
Language:English
Subjects:
Adalimumab
Age
Analysis
Antiviral drugs
Biological response modifiers
Chemokines
Cytokines
Dermatitis
EDTA
Erythema
Family medical history
Inflammation
Interferon
Interferon gamma
Killer cells
Lymphocytes
Medical research
Monoclonal antibodies
Necrosis
Pathogenesis
Patients
Psoriasis
Secukinumab
Skin
Spleen
Splenomegaly
Standard deviation
T cells
Tumor necrosis factor
Tumor necrosis factor-TNF
Tumors
Ustekinumab
Vascular endothelial growth factor
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Summary:Psoriasis (Ps) is a chronic inflammatory immune-mediated disease with skin and joint manifestations, characterized by abnormal and rapid proliferation of keratinocytes and infiltration of psoriatic lesions with immune cells. Extensive literature suggests that Ps is a T-cell mediated disease its pathogenesis being highly related to innate and adaptative immune cells. Although natural killer (NK) cells are involved in the inflammatory process of Ps through pro-inflammatory cytokine secretion (tumor necrosis factor α, interferon γ), their role in this pathology is not yet fully elucidated. In order to study the involvement of NK subpopulations in the pathogenesis of Ps we used the imiquimod-based mouse model of psoriasiform dermatitis and NK cells complex phenotype patterns from peripheral blood (PB) and spleen were investigated. Skin inflammation and the disease severity were assessed using measurements (erythema, desquamation and induration parameters, PASI modified score), splenomegaly assessment and histopathological evaluation. Phenotypic characterization of NK cells in imiquimod (IMQ)-treated mice was performed by flow cytometry, for both PB and spleen cell suspension. A large panel of surface markers was used: maturation and activation markers [cluster of differentiation (CD)49b, CD11b, CD43, CD27, KLRG1, CD335, CD69, CD28, gp49R, CD45R, CD11c] and markers for cytokine receptors (CD25, CD122, CD132). Our experimental data showed important differences in IMQ-treated mouse NK cell phenotype as compared to control group. The maturation markers (CD11b, CD43, CD27, KLRG1) were found increased on NK cells, in periphery and spleen, while CD49b NK1.1 was significantly lower, and the alterations correlated with the severity of the disease. Our findings reflect the immune engagement toward activatory profile of NK cells and draw attention to evaluating Ps intensity correlated with the mature profile of circulating NK cells.
ISSN:1792-0981
1792-1015
DOI:10.3892/etm.2019.7967