Prof. Dr. Rolland Gyulai
Department of Dermatology and Allergology, University of Szeged, Szeged, Csongrád, Hungary
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Academic Career Length
33Years (1994-Present)
(Calculated once Scilit publication data is synced: current year − year of first publication + 1)
Representative Publications
View All Publications1 January 2005 in The Journal of Immunology
Journal Article
HSHideaki Sugiyama
Hideaki Sugiyama
Rolland GyulaiETEiko Toichi
Eiko Toichi
EGEdina Garaczi
Edina Garaczi
SSShinji Shimada
Shinji Shimada
KCKevin D. Cooper
Kevin D. Cooper +2
The balance between regulatory and effector functions is important for maintaining efficient immune responses, while avoiding autoimmunity. The inflammatory skin disease psoriasis is sustained by the ongoing activation of pathogenic effector T cells. We found that a CD4+ T lymphocyte subpopulation in peripheral blood, phenotypically CD25high, CTLA-4+, Foxp3high (regulatory T (Treg) cells), is deficient in its suppressor activity in psoriasis. This was associated with accelerated proliferation of CD4+ responder T cells in psoriasis, the majority of which expressed CXCR3. Nevertheless, criss-cross experiments isolated the defect to psoriatic Treg cells. To examine Treg cells in a nonlymphoid tissue of a human T cell-mediated disease, Treg cells were also analyzed and isolated from the site of inflammation, psoriatic lesional skin. At the regulatory vs effector T cells ratios calculated to be present in skin, however, the psoriatic Treg cell population demonstrated decreased suppression of effector T cells. Thus, dysfunctional blood and target tissue CD4+CD25high Treg cell activity may lead to reduced restraint and consequent hyperproliferation of psoriatic pathogenic T cells in vivo. These findings represent a critical component of human organ-specific autoimmune disease and may have important implications with regard to the possible therapeutic manipulation of Treg cells in vivo.
6 March 2019 in Scientific Reports
Journal Article
Szabina HorváthRKRita Komlódi
Rita Komlódi
APAnikó Perkecz
Anikó Perkecz
EPErika Pintér
Erika Pintér
Rolland GyulaiKÁKemény Ágnes
Kemény ÁgnesImiquimod (IMQ)-induced skin inflammation is currently the most widely accepted psoriasis animal model, however, it features several limitations. We have modified the IMQ-model to minimize its systemic effects towards effectively maintaining the characteristic skin reactions. The original protocol (OP) uses 62.5 mg Aldara cream (or vaseline) on the shaved back skin of mice for 4 days. In contrast, in our modified protocol (MP) 25 mg Aldara and vaseline are applied simultaneously in separate Finn chambers over the dorsal skin of mice. In both the OP and MP groups, histology showed unequivocal hallmarks of psoriasiform dermatitis. Additionally, skin scaling and blood perfusion values were similar. While Aldara elicited significantly increased skin thickness in the MP group, significant weight loss, spleen enlargement, increased inflammatory cytokine levels in plasma, and treatment related death were only observed in the OP group. Our new method reproduces psoriatic skin alterations highlighting considerably reduced systemic inflammatory reactions. Possessing psoriasiform and control skin areas on the same mouse also reduces inter-individual differences. Additionally, the new method permits prolonged IMQ treatment studies to mimic the chronic nature of psoriasis. Finally, our experimental approach may also be used in other mouse models, to prevent the undesired systemic effects of topically applied drugs.
1 August 2018 in Journal of Investigative Dermatology
Journal Article
ÁKÁgnes Kemény
Ágnes Kemény
XKXenia Kodji
Xenia Kodji
Szabina HorváthRKRita Komlódi
Rita Komlódi
ÉSÉva Szőke
Éva Szőke
Rolland Gyulai +9
1 September 2003 in British Journal of Dermatology
Journal Article
JOJ. Olah
J. Olah
Rolland GyulaiIKI. Korom
I. Korom
EVE. Varga
E. Varga
ADA. Dobozy
A. Dobozy
11 December 2019 in Expert Review of Clinical Immunology
Journal Article
SDSzandra Dalmády
Szandra Dalmády
Lajos KeményMAMárk Antal
Márk Antal
Rolland GyulaiIntroduction: Psoriasis is a chronic autoimmune skin disease with strong genetic background and environmental triggers. Patients with psoriasis and psoriatic arthritis are at greater risk of developing other chronic and potentially severe comorbidities, such as psoriatic arthritis, hyperlipidemia, type 2 diabetes mellitus, obesity, metabolic syndrome, cardiovascular diseases or depression. Recently, accumulating epidemiologic, genetic and pathogenetic evidence indicates that psoriasis is also associated with periodontitis, a chronic progressive inflammatory disease, which may result in tooth loss without early and adequate therapy. Areas covered: In this review article we summarize and discuss in detail the available epidemiologic, genetic, microbiological and immunological links between psoriasis and periodontitis. Expert opinion: Periodontitis, via the immunomodulatory effect of the oral microbiota, may play both a direct and indirect role in the development or exacerbation of psoriasis, and may influence the efficacy of antipsoriatic therapy. These new findings indicate a need for increased awareness, early recognition and focus on prevention of periodontitis for patients with psoriasis.
22 February 1996 in New England Journal of Medicine
Journal Article
Rolland GyulaiLajos KeményMKMária Kiss
Mária Kiss
ÉÁÉva Ádám
Éva Ádám
FNFerenc Nagy
Ferenc NagyADAttila Dobozy
Attila Dobozy
Recent studies have demonstrated the presence of a new gamma herpesvirus–like DNA sequence, designated Kaposi's sarcoma–associated herpesvirus (KSHV) or human herpesvirus-8, in different forms of Kaposi's sarcoma in patients infected with the human immunodeficiency virus (HIV)1 and in uninfected patients.2 KSHV sequences were also detected in proliferative lesions other than Kaposi's sarcoma (AIDS-related body-cavity–based lymphomas,3 Castleman's disease,4 and various proliferative skin lesions5) in immunocompromised patients. Nador et al. (Oct. 5 issue)6 reported finding KSHV DNA in a body-cavity–based lymphoma in an HIV-negative patient. We report detecting the KSHV sequence in another non–Kaposi's sarcoma tumor from a nonimmunocompromised patient.
About Me
Prof. Rolland Gyulai, MD, PhD, DSc is the director and chair of the Department of Dermatology and Allergology, University of Szeged, Hungary. Dr. Gyulai finished medical school and completed his residency programs in dermatology and clinical oncology at the University of Szeged, Hungary. His main clinical interest is immunodermatology and oncodermatology. He received his PhD from the University of Szeged in 1998. Dr. Gyulai has spent 3 years at Case Western Reserve University, Cleveland, OH, USA, as a postdoctoral fellow in immunodermatology, and one year at the Institute of Immunobiology, Heinrich Heine University, Düsseldorf, Germany. He is the author of more than 60 scientific papers, 8 book chapters, holder of 4 patents, and the recipient of several prestigious honors and awards, including the Young Scientists Award of the Hungarian Academy of Sciences and the Moritz Kaposi Award of the Hungarian Dermatological Society. Dr. Gyulai became the Doctor of the Hungarian Academy of Sciences in 2017. Dr. Gyulai is the former president of the Hungarian Dermatological Society, and the past-president of the German-Hungarian Dermatological Society (DUDG). He is member of the Scientific Board of the Skin Inflammation & Psoriasis International Network (SPIN), and the European Dermatology Forum (EDF), and the Hungarian representative of Euroderm Excellence. Dr. Gyulai is the associate editor of the Journal of the European Academy of Dermatology and Venereology (JEADV).
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