PhD Scientific Days 2020

Budapest, 31 August-1 September 2020

Clinical Medicine III. Posters

Investigation of splice-variants in keratinocyte immune mechanisms

Előadó neve

Dr. Kelemen, Evelyn

Előadó munkahelye

Department of Dermatology and Allergology, University of Szeged, Szeged, Hungary

Előadó e-mail címe

kelemenevy09@gmail.com

Az előadás címe

Investigation of splice-variants in keratinocyte immune mechanisms

Szerző(k) neve és munkahelye

Evelyn Kelemen1, Judit Danis1,2, Anikó Göblös1,2, Zsuzsanna Bata-Csörgő1,2, Lajos Kemény1,2, Éva Ádám3, Márta Széll2,3
1 Department of Dermatology and Allergology, University of Szeged, Szeged, Hungary
2 MTA- SZTE Dermatological Research Group, Szeged, Hungary
3 Department of Medical Genetics, University of Szeged, Szeged, Hungary

Szekció

Clinical Medicine III. Posters

Language of the presentation

English

Összefoglaló szövege

Psoriasis is a multifactorial, chronic inflammatory skin disease affecting 2% of the population, caused by the hyperproliferation of keratinocytes.

We are examining the molecular background of psoriasis and previously performed large-scale gene-expression studies to compare non-lesional psoriatic epidermis to healthy epidermis. These experiments highlighted the importance of inflammatory and mRNA maturation processes in the disease. Since the presence and function of splice-variants in keratinocyte immune mechanisms are poorly studied, we aimed to identify splice-variants in the immune response of keratinocytes.

Excess cytosolic nucleic acids are known to play a role in psoriasis pathogenesis by inducing keratinocyte immune responses, thus transfection of the synthetic dsDNA-analogue poly(dA:dT) and dsRNA-analogue poly(I:C) or psoriasis-specific inflammatory cytokines (tumor-necrosis-factor-α (TNFα), interleukin (IL) -12, IL-23, IL-17) were used to model psoriasis-associated inflammatory reactions in human keratinocytes. By performing a qPCR-array gene-expression was studied, and splice variants were detected by PCR.

The genes with highest induction in keratinocytes, as determined by the qPCR-array, were already described to express splice-variants in professional immune cells, e.g. fractalkine (CX3CL1) and Z-DNA binding protein (ZBP1). We identified four splice variants of the ZBP1 molecule and two of the CX3CL1, with different expression during the poly(I:C) and poly(dA:dT) treatment. At the same time treatment with psoriasis-specific cytokines did not induced the expression of any of these genes.

We assume that some of the examined splice variants occur in the psoriatic epidermis. In further experiments we will analyze the function of these variants in keratinocytes and in the pathogenesis of psoriasis.

Key words: psoriasis, splice-variants, non-lesional epidermis, cytokines, keratinocytes

The project was supported by the ÚNKP-19-3-SZTE-133 New National Excellence Program of The Ministry for Innovation and Technology

Bemutatás módja

Poszter

Kind

Szabad

Status

elfogadva

Accepted presentation method

poszter

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

5132

Start

12:49

End

12:52

Authors (legacy)

Evelyn Kelemen1, Judit Danis1,2, Anikó Göblös1,2, Zsuzsanna Bata-Csörgő1,2, Lajos Kemény1,2, Éva Ádám3, Márta Széll2,3
1 Department of Dermatology and Allergology, University of Szeged, Szeged, Hungary
2 MTA- SZTE Dermatological Research Group, Szeged, Hungary
3 Department of Medical Genetics, University of Szeged, Szeged, Hungary