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      Possible Implication of Local Immune Response in Darier's Disease: An Immunohistochemical Characterization of Lesional Inflammatory Infiltrate

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          Abstract

          Cell-mediated immunity is considered to be normal in Darier's Disease (DD), an inherited skin disorder complicated by skin infections. To date, there are no investigations on the local inflammatory infiltrate in DD skin lesions. In this immunohistochemical study we characterized and quantified it, making comparisons with two other inflammatory skin disorders, that is, pemphigus vulgaris (PV) and lichen ruber planus (LRP), and with the normal skin (NSk). We found a significant ( P < .05) decrease of CD1a+ Langerhans cells (LCs) in DD, compared to PV, LRP, and NSk, and of CD123+ plasmacytoid dendritic cells (pDCs), compared to PV and LRP. We hypothesize that the genetic damage of keratinocytes might result in a loss of some subsets of dendritic cells and, consequently, in an impaired local immune response, which might worsen the infections that inevitably occur in this disease.

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          Type I interferon in systemic lupus erythematosus and other autoimmune diseases.

          Jacques Banchereau, Virginia Pascual (2006)
          Different genetic alterations may lead to type I interferon (IFN) overproduction in human systemic lupus erythematosus (SLE). The increased bioavailability of type I IFN contributes to peripheral tolerance breakdown through the activation of immature myeloid dendritic cells (mDCs). IFN-matured mDCs activate autoreactive T cells. These cells, together with plasmacytoid DCs, help expand autoreactive B cells. IFN-matured DCs also activate cytotoxic CD8+ T cells, possibly increasing apoptotic cell availability. The capture of apoptotic cells by mDCs and of nucleic acid-containing immune complexes by plasmacytoid DCs and B cells amplifies the autoimmune reaction leading to disease manifestations. Genetic alterations in lineages other than B cells might explain other autoimmune syndromes where type I IFNs appear to be involved.
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            Intrinsic and cooperative antigen-presenting functions of dendritic-cell subsets in vivo.

            Petra Schnorrer, José Villadangos (2007)
            Dendritic cells (DCs) comprise several subsets, and their roles in the presentation of antigens derived from pathogens, vaccines and self tissues are now beginning to be elucidated. Differences in location, life cycle and intrinsic abilities to capture, process and present antigens on their MHC class I and class II molecules enable each DC subset to have distinct roles in immunity to infection and in the maintenance of self tolerance. Unexpected interactions among DC subsets have also been revealed. These interactions, which allow the integration of the intrinsic abilities of different DC types, enhance the ability of the DC network to respond to multiple scenarios of infection.
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              Langerhans cell (LC) proliferation mediates neonatal development, homeostasis, and inflammation-associated expansion of the epidermal LC network

              Laurent Chorro, Aurelien Sarde, Mei-Mei Li … (2010)
              Most tissues develop from stem cells and precursors that undergo differentiation as their proliferative potential decreases. Mature differentiated cells rarely proliferate and are replaced at the end of their life by new cells derived from precursors. Langerhans cells (LCs) of the epidermis, although of myeloid origin, were shown to renew in tissues independently from the bone marrow, suggesting the existence of a dermal or epidermal progenitor. We investigated the mechanisms involved in LC development and homeostasis. We observed that a single wave of LC precursors was recruited in the epidermis of mice around embryonic day 18 and acquired a dendritic morphology, major histocompatibility complex II, CD11c, and langerin expression immediately after birth. Langerin+ cells then undergo a massive burst of proliferation between postnatal day 2 (P2) and P7, expanding their numbers by 10–20-fold. After the first week of life, we observed low-level proliferation of langerin+ cells within the epidermis. However, in a mouse model of atopic dermatitis (AD), a keratinocyte signal triggered increased epidermal LC proliferation. Similar findings were observed in epidermis from human patients with AD. Therefore, proliferation of differentiated resident cells represents an alternative pathway for development in the newborn, homeostasis, and expansion in adults of selected myeloid cell populations such as LCs. This mechanism may be relevant in locations where leukocyte trafficking is limited.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Mediators Inflamm
                Journal ID (publisher-id): MI
                Title: Mediators of Inflammation
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 0962-9351
                ISSN (Electronic): 1466-1861
                Publication date (Print): 2010
                Publication date (Electronic): 30 June 2010
                Volume: 2010
                Electronic Location Identifier: 350304
                Affiliations
                1Section of Pathological Anatomy, Department of Human Pathology and Oncology, University of Siena, Policlinico Santa Maria alle Scotte, Via delle Scotte, 6, 53100 Siena, Italy
                2Section of Dermatology, Department of Clinical Medicine and Immunological Science, University of Siena, 53100 Siena, Italy
                3Unit of Rheumatology, Interdepartmental Research Center of Systemic Autoimmune and Autoinflammatory Diseases, University of Siena, Policlinico Le Scotte, 53100 Siena, Italy
                4Department of Odontostomatological and Ophthalmological Science, University of Siena, 53100 Siena, Italy
                Author notes
                *Clelia Miracco: miracco@ 123456unisi.it

                Academic Editor: Philip W. Wertz

                Article
                DOI: 10.1155/2010/350304
                PMC ID: 2910469
                PubMed ID: 20671948
                SO-VID: 8686cc40-4821-4339-944a-5564b9559282
                Copyright © Copyright © 2010 Clelia Miracco et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 30 March 2010
                Date accepted : 17 May 2010
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Immunology
                Data availability:
                ScienceOpen disciplines: Immunology

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