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      Granzyme B: A novel therapeutic target for treatment of atopic dermatitis

      Author(s): , , 1
      Publication date Created:
      Publication date (Electronic):
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      Journal: Indian Journal of Dermatology, Venereology and Leprology
      Publisher: Scientific Scholar

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          Abstract

          Granzyme B is a serine protease that can play multiple roles in intracellular and extracellular perforin-dependent or non-perforin-dependent mechanisms. Granzyme B has been found to be an important factor involved in the pathogenesis of atopic dermatitis and is increased in both skin lesions and peripheral blood of atopic dermatitis patients. In this article, we review the correlation between granzyme B and atopic dermatitis to provide a novel therapeutic targeting option for clinical treatment of the latter.

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          Intracellular versus extracellular granzyme B in immunity and disease: challenging the dogma

          Wendy Boivin, Dawn Michelle Cooper, Paul Ryan Hiebert … (2009)
          The cytotoxic granzyme B (GrB)/perforin pathway has been traditionally viewed as a primary mechanism that is used by cytotoxic lymphocytes to eliminate allogeneic, virally infected and/or transformed cells. Although originally proposed to have intracellular and extracellular functions, upon the discovery that perforin, in combination with GrB, could induce apoptosis, other potential functions for this protease were, for the most part, disregarded. As there are 5 granzymes in humans and 11 granzymes in mice, many studies used perforin knockout mice as an initial screen to evaluate the role of granzymes in disease. However, in recent years, emerging clinical and biochemical evidence has shown that the latter approach may have overlooked a critical perforin-independent, pathogenic role for these proteases in disease. This review focuses on GrB, the most characterized of the granzyme family, in disease. Long known to be a pro-apoptotic protease expressed by cytotoxic lymphocytes and natural killer cells, it is now accepted that GrB can be expressed in other cell types of immune and nonimmune origin. To the latter, an emerging immune-independent role for GrB has been forwarded due to recent discoveries that GrB may be expressed in nonimmune cells such as smooth muscle cells, keratinocytes, and chondrocytes in certain disease states. Given that GrB retains its activity in the blood, can cleave extracellular matrix, and its levels are often elevated in chronic inflammatory diseases, this protease may be an important contributor to certain pathologies. The implications of sustained elevations of intracellular and extracellular GrB in chronic vascular, dermatological, and neurological diseases, among others, are developing. This review examines, for the first time, the multiple roles of GrB in disease pathogenesis.
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            A systematic review and meta-analysis of the regional and age-related differences of atopic dermatitis clinical characteristics

            Yik Weng Yew, Jacob Thyssen, Jonathan I Silverberg (2018)
            Previous studies found conflicting results about the commonality of different atopic dermatitis (AD) signs and symptoms.
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              Granzyme B in injury, inflammation, and repair.

              David Granville, P Hiebert (2012)
              Fragile skin and susceptibility to skin tearing are major problems among the elderly and can be complicated further by impaired wound healing. Non-healing wounds fail to progress through the normal stages of healing and enter a state of chronic inflammation featuring increased proteolytic activity. Increased expression of the serine protease granzyme B is observed during prolonged inflammation and is implicated in the pathogenesis of several chronic inflammatory diseases. Although its role in cytotoxic lymphocyte-mediated apoptosis is well established, granzyme B can also degrade extracellular matrix proteins and alter inflammation if present in the extracellular milieu. The present review focuses on the emerging evidence for the involvement of granzyme B in chronic inflammation, impaired wound healing, and age-related skin fragility. Copyright © 2012 Elsevier Ltd. All rights reserved.
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                Author and article information

                Journal
                Title: Indian Journal of Dermatology, Venereology and Leprology
                Abbreviated Title: IJDVL
                Publisher: Scientific Scholar
                ISSN (Electronic): 0973-3922
                ISSN (Print): 0378-6323
                Publication date Created: 2022
                Publication date (Electronic): October 31 2022
                Publication date (Electronic): March 20 2023
                Volume: 89
                Pages: 166-169
                Affiliations
                [1 ]Department of Dermatology & Venerology, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, Chengdu, China,
                Article
                DOI: 10.25259/IJDVL_260_2022
                SO-VID: a29c9c84-2eb6-432d-938c-f6c2a5d1b6ba
                Copyright © © 2023
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