Editorial Article

Psoriasis and Lichen Planus as Inflammatory Skin Diseases Mediated By T Cells: Possible Involvement of Cytotoxicity Mechanisms

*Larisa Prpić Massari

Dermatovenerology Clinic and Department of Dermatovenerology, Clinical Hospital Center Rijeka, University of Rijeka, Croatia

*Corresponding Author: Larisa Prpić Massari, Dermatovenerology Clinic and Department of Dermatovenerology, Clinical Hospital Center Rijeka, University of Rijeka, Croatia.
E-mail: larisa.prpic@medri.uniri.hr

Citation: Massari LP (2018) Psoriasis and Lichen Planus as Inflammatory Skin Diseases Mediated By T Cells: Possible Involvement of Cytotoxicity Mechanisms. J Dermatol Surg Res Ther 2018:1-2.

Received Date: 28 September, 2018; Accepted Date: 21 November, 2018; Published Date: 19 December, 2018

Psoriasis is inflammatory disease mediated by T lymphocytes that affects primary skin and joints [1]. Clinically it is characterized by well-demarcated scaly plaques mainly on extensor part of extremities, lumbosacral regions and scalp [2]. Patohistologically, plaques are defined by hyperkeratosis, acanthosis and parakeratosis of epidermis and T cell infiltration in dermis [3]. Apart from a fact that psoriasis is a skin disease, it could affect joints in form of psoriatic arthritis and could cause comorbidities such as cardiovascular disease, diabetes and depression [4].

Similarly, to psoriasis, lichen planus is a T cell mediated inflammatory disease clinically characterized by violaceus plaques on flexural parts of arms and lumbosacral regions as well as mucosa affections mainly on oral and genital mucosa [5]. Patohistologically, lichen planus lesions are labeled by hyperkeratosis and acanthosis of epidermis and band-like infiltration of T lymphocytes along the epidemodermal junction [6]. Apart from severe mucosal forms, disease is generally self-limiting in the period of two to three years [6].

Immunopathogenesis of psoriasis and lichen planus is quite similar [7,8]. In psoriasis, different agents such viruses, bacteria, systemic drugs or stress damage basal keratinocytes releasing mediators such as cathelicidin or LL-37 molecule, defensins and S-100 proteins [9,10]. LL-37 molecules bind to self-DNA that is also released from damaged keratinocytes and forms complexes [9,10]. Those complexes activate antigen presenting cells (APCs) mainly plasmacytoid DC to secrete IFN-alpha [9,10].

Furthermore, APC drain to regional lymph nodes where they present antigens to naive T lymphocytes that differentiate into Th1, Th17 and Th22 cells [10,11]. Migration of those cells back to skin and production of type 1, type 17 and type 22 cytokines are key stimuli for epidermal cell proliferation, accumulation of new inflammatory cells in dermis and epidermis and formation of psoriatic plaque [10].

In lichen planus lesions, different antigen stimuli especially viruses, drugs, or contact sensitivity antigen alter the basal keratinocytes releasing chemokines, such as CXCR3/CCL20/CCR6 that attract new lymphocytes into developing lesion [12,13]. Plasmacytoid DCs could amplify this effect by IFN-alpha production [13]. Activated APCs present antigen to T lymphocytes in regional lymph nodes and stimulate differentiation towards Th1 and Th17 direction [13]. However, in lichen planus activated basal keratinocytes present antigen that are bind to MHC class I molecule to CD8+ cytotoxic T cells [14]. Cytotoxic T cells express FasL or secrete perforin, granzyme B, granulysin or TNF-alpha that trigger basal keratinocyte apoptosis histopathologically seen as vacuolar degeneration of epidermis in form of Civatte bodies [15,16].

In psoriasis, the upregulation of cytotoxic molecules such as perforin, grenzyme B and FasL is demonstrated in peripheral blood of psoriasis patients and in psoriatic skin lesions, however the exact mode of action and target cells are still unknown [17,18].

Psoriasis and lichen planus are both T-cell mediated skin disease with very similar immunopathogenesis scenario. However, cytotoxicity mechanisms in lichen planus are well determined and undoubtedly play an important role while those mechanisms in psoriasis are still to be investigated in future.

References

 

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