Immunohistochemical Comparison of IL-36 and the IL-23/Th17 Axis of Generalized Pustular Psoriasis and Acute Generalized Exanthematous Pustulosis
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Background: Cutaneous pustular disorders include generalized pustular psoriasis (GPP) and acute generalized exanthematous pustulosis (AGEP). Objective: To identify differences between GPP and AGEP, here we immunohistochemically evaluated interleukin (IL)-36 and the IL-23/Th17 axis. Methods: This retrospective comparative immunohistochemical study was completed using 11 biopsies of 11 cases of GPP and 11 biopsies of 11 cases of AGEP. Through staining with the anti-IL-36-alpha (IL-36α), anti-IL-36 receptor antagonist (IL-36Ra), anti-nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), anti-IL-23, anti-IL-17, and anti-IL-8 antibodies, main expression location and intensity were visualized in the epidermis and dermis. Results: In both diseases, diffuse IL-36α expression was observed in the epidermis. IL-36Ra expression was observed in the dermal perivascular area as well as in the epidermis. NF-κB expression was observed in the epidermis and perivascular dermal area. Diffuse IL-23 and IL-17 expression was seen in the whole epidermis and the perivascular dermal area. IL-8 was expressed in the subcorneal pustules and parakeratotic area. Contrary to other cytokines, IL-23 expression in the epidermis of patients with GPP was more intense than only that in patients with AGEP. Conclusion: Common pathomechanisms might exist in the development of GPP and AGEP based on these immunohistochemical results, but further studies are needed.
Abstract
Background: Cutaneous pustular disorders include generalized pustular psoriasis (GPP) and acute generalized exanthematous pustulosis (AGEP). Objective: To identify differences between GPP and AGEP, here we immunohistochemically evaluated interleukin (IL)-36 and the IL-23/Th17 axis. Methods: This retrospective comparative immunohistochemical study was completed using 11 biopsies of 11 cases of GPP and 11 biopsies of 11 cases of AGEP. Through staining with the anti-IL-36-alpha (IL-36α), anti-IL-36 receptor antagonist (IL-36Ra), anti-nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), anti-IL-23, anti-IL-17, and anti-IL-8 antibodies, main expression location and intensity were visualized in the epidermis and dermis. Results: In both diseases, diffuse IL-36α expression was observed in the epidermis. IL-36Ra expression was observed in the dermal perivascular area as well as in the epidermis. NF-κB expression was observed in the epidermis and perivascular dermal area. Diffuse IL-23 and IL-17 expression was seen in the whole epidermis and the perivascular dermal area. IL-8 was expressed in the subcorneal pustules and parakeratotic area. Contrary to other cytokines, IL-23 expression in the epidermis of patients with GPP was more intense than only that in patients with AGEP. Conclusion: Common pathomechanisms might exist in the development of GPP and AGEP based on these immunohistochemical results, but further studies are needed.
참고문헌 (28)
- Choon SE., "Clinical profile, morbidity, and outcome of adult-onset generalized pustular psoriasis : analysis of 102 cases seen in a tertiary hospital in Johor, Malaysia", Int J Dermatol, 53, pp.676~684 (2014)
- Varman KM., "Acute generalized pustular psoriasis, von Zumbusch type, treated in the burn unit. A review of clinical features and new therapeutics", Burns, 40, pp.e35~e39 (2014)
- Raison-Peyron N, ""Cutaneous adverse drug reactions"are not always drug-induced", Eur J Dermatol, 23, pp.439~442 (2013)
- Abbas M., "Pustular psoriasis complicated with acute generalized exanthematous pustulosis", J Dermatol Case Rep, 8, pp.42~45 (2014)
- 최민지, "Clinicopathologic Manifestations of 36 Korean Patients with Acute Generalized Exanthematous Pustulosis: A Case Series and Review of the Literature", Annals of Dermatology, 22(2), pp.163~169 (2010), 대한피부과학회
- Kardaun SH., "The histopathological spectrum of acute generalized exanthematous pustulosis(AGEP)and its differentiation from generalized pustular psoriasis", J Cutan Pathol, 37, pp.1220~1229 (2010)
- Chang SL., "A comparison of Ki-67 antigen presentation in acute generalized exanthematous pustulosis and pustular psoriasis", Arch Dermatol Res, 302, pp.525~529 (2010)
- Schmid S., "Acute generalized exanthematous pustulosis : role of cytotoxic T cells in pustule formation", Am J Pathol, 161, pp.2079~2086 (2002)
- Duan H., "Interleukin-8-positive neutrophils in psoriasis", J Dermatol Sci, 26, pp.119~124 (2001)
- Yilmaz SB., "Serum and tissue levels of IL-17 in different clinical subtypes of psoriasis", Arch Dermatol Res, 304, pp.465~469 (2012)
- Lowes MA., "The IL-23", T17 pathogenic axis in psoriasis is amplified by keratinocyte responses, 2013, pp.34, 174~181
- Sugiura K., "The majority of generalized pustular psoriasis without psoriasis vulgaris is caused by deficiency of interleukin-36 receptor antagonist", J Invest Dermatol, 133, pp.2514~2521 (2013)
- Kabashima R., "Increased circulating Th17 frequencies and serum IL-22 levels in patients with acute generalized exanthematous pustulosis", J Eur Acad Dermatol Venereol, 25, pp.485~488 (2011)
- 송효상, "Gene Mutation Analysis in a Korean Patient with Early-Onset and Recalcitrant Generalized Pustular Psoriasis", Annals of Dermatology, 26(3), pp.424~425 (2014), 대한피부과학회
- Onoufriadis A., "Mutations in IL36RN", IL1F5 are associated with the severe episodic inflammatory skin disease known as generalized pustular psoriasis, 2011, pp.89, 432~437
- Navarini AA., "Rare variations in IL36RN in severe adverse drug reactions manifesting as acute generalized exanthematous pustulosis", J Invest Dermatol, 133, pp.1904~1907 (2013)
- Kanazawa N., "Novel IL36RN mutation in a Japanese case of early onset generalized pustular psoriasis", J Dermatol, 40, pp.749~751 (2013)
- Sidoroff A., "Acute generalized exanthematous pustulosis(AGEP)--a clinical reaction pattern", J Cutan Pathol, 28, pp.113~119 (2001)
- Naldi L., "The clinical spectrum of psoriasis", Clin Dermatol, 25, pp.510~518 (2007)
- Towne JE., "IL-36 in psoriasis", Curr Opin Pharmacol, 12, pp.486~490 (2012)
- Debets R., "Two novel IL-1 family members, IL-1 delta and IL-1 epsilon, function as an antagonist and agonist of NF-kappa B activation through the orphan IL-1 receptor-related protein2", J Immunol, 167, pp.1440~1446 (2001)
- Teraki Y., "A case of generalized psoriasiform and pustular eruption induced by infliximab : evidence for skin-homing Th17 in the pathogenesis", Br J Dermatol, 163, pp.1347~1351 (2010)
- Bissonnette R., "Increased expression of IL-17A and limited involvement of IL-23 in patients with palmo-plantar(PP)pustular psoriasis or PP pustulosis;results from a randomised controlled trial", J Eur Acad Dermatol Venereol, 28, pp.1298~1305 (2014)
- Ueda T., "Acute generalized exanthematous pustulosis due to allylisopropylacetylurea : role of IL-17-producing T cells", Eur J Dermatol, 21, pp.140~141 (2011)
- Koch AE., "Interleukin-8 as a macrophage-derived mediator of angiogenesis", Science, 258, pp.1798~1801 (1992)
- Larsen CG., "The neutrophil-activating protein(NAP-1)is also chemotactic for T lymphocytes", Science, 243, pp.1464~1466 (1989)
- Britschgi M., "Acute generalized exanthematous pustulosis, a clue to neutrophil-mediated inflammatory processes orchestrated by T cells", Curr Opin Allergy Clin Immunol, 2, pp.325~331 (2002)
- Keller M., "T cell-regulated neutrophilic inflammation in autoinflammatory diseases", J Immunol, 175, pp.7678~7686 (2005)