Advances in Clinical and Experimental Medicine
2018, vol. 27, nr 6, June, p. 721–725
doi: 10.17219/acem/78020
Publication type: original article
Language: English
Download citation:
The expression of selected molecular markers of immune tolerance in psoriatic patients
1 Department of Dermatology, Venereology and Pediatric Dermatology, Medical University of Lublin, Poland
2 Department of Experimental Hematooncology, Medical University of Lublin, Poland
Abstract
Background. Psoriasis is a chronic autoinflammatory disease whose underlying molecular mechanisms remain unclear. The disease is mediated by the cells and molecules of both the innate and adaptive immune systems. Some T cell surface molecules, including neuropilin-1 (NRP1), programmed death 1 (PD-1) and the human leukocyte antigen G (HLA-G), are known to play a role in the maintenance of immune tolerance.
Objectives. The aim of this study was to investigate HLA-G, NRP1 and programmed cell death gene (PDCD1) mRNA expression in psoriatic patients.
Material and Methods. The study included 72 psoriatic patients and 35 healthy individuals. Twentyone patients (29.17%) suffered from concomitant psoriatic arthritis. The mRNA expression of HLA-G, NRP1, and PDCD1 were determined using quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR). The severity of skin lesions was assessed by means of the Psoriasis Area and Severity Index (PASI), Body Surface Area (BSA), the Patient Global Assessment (PGA), and the Dermatology Life Quality Index (DLQI).
Results. The median value of the PASI was 11.5, and of BSA was 15.8%. The expressions of NRP1 and PDCD1, but not HLA-G, were significantly lower in psoriatic patients in comparison with the control group. The expression of HLA-G, NRP1 and PDCD1 were not significantly different in the psoriatic arthritis and psoriasis vulgaris patients.
Conclusion. The results of this study suggest that the molecular markers of immune tolerance, i.e., HLA-G, NRP1, and PD-1, may be involved in the immune response in psoriatic patients.
Key words
psoriasis, PD-1, HLA-G, NRP1
References (21)
- Deng Y, Chang C, Lu Q. The inflammatory response in psoriasis: A comprehensive review. Clin Rev Allergy Immunol. 2016;50(3):377−389.
- Bardhan K, Anagnostou T, Boussiotis VA. The PD1:PD-L1/2 pathway from discovery to clinical implementation. Front Immunol. 2016;12(7): 550. doi: 10.3389/fimmu.2016.00550
- Oussa NA, Dahmani A, Gomis M, et al. VEGF requires the receptor NRP-1 to inhibit lipopolysaccharide-dependent dendritic cell maturation. J Immunol. 2016;197(10):3927−3935.
- Sarris M, Andersen KG, Randow F, Mayr L, Betz AG. Neuropilin-1 expression on regulatory T cells enhances their interactions with dendritic cells during antigen recognition. Immunity. 2008;28(3):402−413.
- Chen Z, Pang N, Du R, et al. Elevated expression of programmed death-1 and programmed death ligand-1 negatively regulates immune response against cervical cancer cells. Mediators Inflamm. 2016;2016:6891482.
- Urosevic M. HLA-G in the skin − friend or foe? Semin Cancer Biol. 2007;17(6):480−484.
- Amodio G, Sales de Albuquerque R, Gregori S. New insights into HLA-G mediated tolerance. Tissue Antigens. 2014;84(3):255−263.
- Wang Y, Wang L, Yang H, Yuan W, Ren J, Bai Y. Activated circulating T follicular helper cells are associated with disease severity in patients with psoriasis. J Immunol Res. 2016;2016:7346030.
- Smilek DE, Ehlers MR, Nepom GT. Restoring the balance: Immunotherapeutic combinations for autoimmune disease. Dis Model Mech. 2014;7(5):503−513.
- Borghi A, Fogli E, Stignani M, et al. Soluble human leukocyte antigen-G and interleukin-10 levels in plasma of psoriatic patients: Preliminary study on a possible correlation between generalized immune status, treatments and disease. Arch Dermatol Res. 2008;300(10):551−559.
- Han G, Li F, Singh TP, Wolf P, Wang X-J. The pro-inflammatory role of TGFβ1: A paradox? Int J Biol Sci. 2012;8(2):228–235.
- Brenol CV, Veit TD, Chies JA, Xavier RM. The role of the HLA-G gene and molecule on the clinical expression of rheumatologic diseases. Rev Bras Reumatol. 2012;52(1):82–91.
- Moreau P, Flajollet S, Carosella ED. Non-classical transcriptional regulation of HLA-G: An update. J Cell Mol Med. 2009;13(9B):2973–2989.
- Aractingi S, Briand N, Le Danff C, et al. HLA-G and NK receptor are expressed in psoriatic skin: A possible pathway for regulating infiltrating T cells? Am J Pathol. 2001;159(1):71–77.
- Cardili RN, Alves TG, Freitas JC, et al. Expression of human leucocyte antigen-G primarily targets affected skin of patients with psoriasis. Br J Dermatol. 2010;163(4):769–775.
- Sweeney C, Kirby B. Does HLA-G prevent tissue destruction in psoriasis? Br J Dermatol. 2011;164(5):1118–1119.
- Kou K, Nakamura F, Aihara M, et al. Decreased expression of semaphorin-3A, a neurite-collapsing factor, is associated with itch in psoriatic skin. Acta Derm Venereol. 2012;92(5):521–528.
- Henno A, Blacher S, Lambert CA, et al. Histological and transcriptional study of angiogenesis and lymphangiogenesis in uninvolved skin, acute pinpoint lesions and established psoriasis plaques: An approach of vascular development chronology in psoriasis. J Dermatol Sci. 2010;57(3):162–169.
- Ruiz-Bañobre J, García-González J. Anti-PD-1/PD-L1-induced psoriasis from an oncological perspective. J Eur Acad Dermatol Venereol. Epub 2017 Apr 3. doi: 10.1111/jdv.14217
- Kim DS, Je JH, Kim SH, et al. Programmed death-ligand 1, 2 expressions are decreased in the psoriatic epidermis. Arch Dermatol Res. 2015;307(6):531–538.
- Kim JH, Choi YJ, Lee BH, et al. Programmed cell death ligand 1 alleviates psoriatic inflammation by suppressing IL-17A production from programmed cell death 1-high T cells. J Allergy Clin Immunol. 2016; 137(5):1466–1476.