2013;11:57–9. 2006;72:211–4. Cancer Res. 2009;9:556–67. c-Merkel cell. 2014;55:2620–6. We have shown that there were subgroups associated with the MCPyV as a causal agent in these two different neoplasms. Kansal R, Quintanilla-Martinez L, Datta V, Lopategui J, Garshfield G, Nathwani BN. d-Vestibular lamina. On the other hand, it has been pointed out that RANKL produced by regulatory T cells is involved in the metastasis of breast cancer [132]. Banchereau J, Steinman RM. Merkel cells are nondendritic, nonkeratinocytic epithelial cells located primarily in or near the basal layer of the epidermis. Only ultrastructural research revealed their characteristics such as dense-core granules, plasma membrane spines and dendrites as well as a l … -, Kuwamoto S. Recent advances in the biology of Merkel cell carcinoma. WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues Revised 4th Edition. Neither IL-17A mRNA nor IL-17A protein are detectable in Langerhans cell histiocytosis lesions. The authors would like to thank all patients, parents, control subjects, and physicians who participated in the studies related to this review. For host defense, IL-17A/IL-17A receptor complex is important [46], since IL-17A is commonly produced during viral infection [51]. These cells have a number of different funtions in the integument. We found that MCPyV may be involved in the development of LCH. Ronceray L, Potschger U, Janka G, Gadner H, Minkov M. German Society for Pediatric H, oncology LCHSG: pulmonary involvement in pediatric-onset multisystem Langerhans cell histiocytosis: effect on course and outcome. High viral load of Merkel cell polyomavirus DNA sequences in Langerhans cell sarcoma tissues. Langerhans cells are present beyond the middle of the spinous epidermal layer [8], they have the capacity to capture external pathogens [9], and can act as antigen-presenting cells [10, 11]. doi: 10.1016/j.humpath.2011.01.020. 4) [108]. N2 - In addition to the keratinocytes, the epidermis contains resident cells of dendritic morphology. California Privacy Statement, Chilosi M, Facchetti F, Calio A, Zamo A, Brunelli M, Martignoni G, Rossi A, Montagna L, Piccoli P, Dubini A, et al. Shahzad N, Shuda M, Gheit T, Kwun HJ, Cornet I, Saidj D, Zannetti C, Hasan U, Chang Y, Moore PS, et al. Clin Immunol. We propose two distinct models for LCS and LCH pathogenesis. IL-17A receptor expression differs between subclasses of Langerhans cell histiocytosis, which might settle the IL-17A controversy. The immune cells capture trespassers such as bacteria and viruses and fight off injuries like cuts and scrapes. Exposure to MCPyV as measured by serum antibodies against the viral capsid proteins appears to be widely prevalent among healthy subjects [92, 93]. We proposed LCH developed from an inflammatory process that was sustained due to gene mutations. Identification of the V600D mutation in exon 15 of the BRAF oncogene in congenital, benign langerhans cell histiocytosis. One was that the induced mutations of MCPyV due to long exposure to ultraviolet light leads to integration of the cytoplasmic viral sequences into the DNA of originating MCC cells. BRAF-V600E expression in precursor versus differentiated dendritic cells defines clinically distinct LCH risk groups. Histiocytic disorders of children and adults. 2012;8:684–9. Langerhans Cells | Merkel Cells | Melanocytes - Non keratinocytes - Duration: 11:31. Sakata N, Toguchi N, Kimura M, Nakayama M, Kawa K, Takemura T. Development of Langerhans cell histiocytosis associated with chronic active Epstein-Barr virus infection. Langerhans cell histiocytosis reveals a new IL-17A-dependent pathway of dendritic cell fusion. Merkel cell polyomavirus DNA sequences in peripheral blood and tissues from patients with Langerhans cell histiocytosis. Hum Pathol. Schrama D, Ugurel S, Becker JC. Please enable it to take advantage of the complete set of features! In the context of infection, pathogens such as Epstein–Barr virus [52], human cytomegalovirus [53], and human herpes virus 6 [54, 55] were proven to exist in LCH cells. Epub 2012 Aug 6. LCH is a proliferative disease of Langerhans-like abnormal cells which carry mutations of genes involved in the RAS/MAPK signaling pathway. WebMD explains what you need to know. Foss HD, Herbst H, Araujo I, Hummel M, Berg E, Schmitt-Graff A, Stein H. Monokine expression in Langerhans’ cell histiocytosis and sinus histiocytosis with massive lymphadenopathy (Rosai-Dorfman disease). 2004;35:862–8. Accordingly, we postulate that the level of IL-17A receptor expression in LCH cells defines the LCH subclass [47]. 2014;153:112–22. The latter form is frequent in children younger than 2 years, whereas SS-LCH is more common in children older than 2 years [11, 15]. 1999;263:224–9. Blood. Lanone S, Zheng T, Zhu Z, Liu W, Lee CG, Ma B, Chen Q, Homer RJ, Wang J, Rabach LA, et al. to Allen et al. However, recent studies indicate that LCH has a more neoplastic character [29,30,31]. The term Langerhans cell histiocytosis is generally preferred to the older term, histiocytosis X. An endocrine model supported our data: the IL-17A serum levels and expression levels of IL-17A receptor are higher in LCH tissue in patients with LCH. • Langerhans cells are macrophages involved in the immune responses. One of the most critical functions of the skin required by its role as the interface with the external environment, is to defend against microbial attack. IL-1 and IL-6 stimulate IL-17 producing cells. Langerhans cell hyperplasia in scabies: a mimic of Langerhans cell histiocytosis. 2003;31:637–42. We think that balance between oncogene-induced senescence [121] and the requirement of IL-1 autocrine loop [2, 107, 108] of BRAF V600E mutation in pulmonary and non-pulmonary LCH indicates the clinical severity of the disease (Fig. 1). ITIH4 production is up-regulated by IL-6 [109], which is known produced in LCH [21]. 1990;98:765–7. J Clin Virol. The numbers of MCPyV-DNA sequences in LCH tissues from patients younger than 2 years indicated a significant difference from tissues of non-LCH dermal disease patients of the same age [12]. N Engl J Med. We discovered the relationship between Merkel cell polyomavirus (MCPyV) and these two diseases are similar to Epstein-Barr virus pathogenetic potential that by itself is involved in several neoplastic and inflammatory diseases (Table 1). 2006;21:577–80. Oncogene-induced senescence distinguishes indolent from aggressive forms of pulmonary and non-pulmonary Langerhans cell histiocytosis. LCH is a proliferative disease of Langerhans-like abnormal cells which carry mutations of genes involved in the RAS/MAPK signaling pathway. Pathogenesis of Langerhans cell histiocytosis. Herpes-virus infection in patients with Langerhans cell histiocytosis: a case-controlled sero-epidemiological study, and in situ analysis. Donadieu J, Egeler RM, Pritchard J. Langerhans cell histiocytosis: a clinical update. IL-17A/IL-17A receptor signaling pathways include matrix metalloproteinase-3 (MMP3) or MMP12 [62,63,64]. Elles représentent le quatrième type cellulaire de l'épiderme (après les kératinocytes, les mélanocytes et les cellules de Langerhans). Alston RD, Tatevossian RG, McNally RJ, Kelsey A, Birch JM, Eden TO. Histiocytic disorders of children and adults. 2001;25:630–6. 2008;319:624–7. Leuk Lymphoma. We proposed a triple-factor model for pathogenesis of LCH (Fig. Genes Chromosomes Cancer. 2005;130:147–8. Merkel cells (nerve/touch cells) differentiate from the ectoderm between weeks 8 and 12 of gestation. d-Langerhans cell. 2011;6:e20333. Human herpesvirus 6 is present in lesions of Langerhans cell histiocytosis. Med Pediatr Oncol. Lyon: International Agency for Research on Cancer (IARC); 2017. p. 470–3. We propose LCH is a reactive disorder with underlying neoplastic potential using a triple-risk factor model. [97] reported that CD14+ CD16− inflammatory monocytes are a reservoir for MCPyV, but CD14lowCD16+ resident monocytes, lymphocytes, or granulocytes are not. J Invest Dermatol. Yeh I, von Deimling A, Bastian BC. IL-1α expression is induced by TLR-mediated NF-κB activation; such activation has been observed in some LCH cases [102, 103], with/without the presence of IL-1β [104]. Bhatia S, Nesbit ME Jr, Egeler RM, Buckley JD, Mertens A, Robison LL. We propose a triple-risk factor model for LCH pathogenesis. We propose a triple-risk factor model for LCH pathogenesis. Second, higher levels of IL-17A receptor protein expression in MS-LCH were detected as compared to SS-LCH. Cell-specific gene expression in Langerhans cell histiocytosis lesions reveals a distinct profile compared with epidermal Langerhans cells.  |  Ramanathan A, Weintraub M, Orlovetskie N, Serruya R, Mani D, Marcu O, Stepensky P, Weisblum Y, Djian E, Shaag A, Revel-Vilk S, Fried I, Kotler M, Rouvinski A, Wolf D, Elpeleg O, Jarrous N. Proc Natl Acad Sci U S A. Raychaudhuri SP, Raychaudhuri SK, Genovese MC. The fine structural morphology of melanocytes, Langerhans cells and Merkel cells in the normal dorsal epithelium of the human tongue has been studied by electron microscopy. Dramatic transient improvement of metastatic BRAF(V600E)-mutated Langerhans cell sarcoma under treatment with dabrafenib. Epidemiologic study of Langerhans cell histiocytosis in children. COVID-19 is an emerging, rapidly evolving situation. While unexpected remission can rarely occur in neoplasms, spontaneous healing is more common in LCH, suggesting that there may be multiple pathological factors contributing to the LCH process [22, 32, 33]. J Natl Cancer Inst. See this image and copyright information in PMC. Cancer Res. Merkel cells normally exist in the bottom (basal) layer of the epidermis, about 0.1 mm from skin's surface. b-Basal lamina & hemidesmosome. Simons PJ, Delemarre FG, Drexhage HA. Merkel cell polyomavirus Merkel cell carcinoma Langerhans cell histiocytosis (LCH) Langerhans cell sarcoma Cigarette smoking Lung cancer, Pulmonary LCH Chronic obstructive pulmonary disease, Pulmonary LCH Murakami et al. The coming of age of Langerhans cell histiocytosis. All patients, parents, control subjects, and physicians participated in the studies related to this review with consent to participate. Mehta B, Venkatramani R. Images in clinical medicine. 2012;161:129–33. Recurrent BRAF mutations in Langerhans cell histiocytosis. 1997;130:774–84. After a century of question about their purpose, it is now clear that they have a vital immunologic…. Arch Dis Child. It acts as a physical barrier, preventing loss of water from the body, and preventing entry of substances and organisms into the body. c-Merkel cell. Philadelphia: Lippincott Williams & Wilkins, a Wolter Kluwer business; 2013. p.214–253. Correspondence to 2009;182:3469–81. Respir Res. We found IL-17A receptor expression levels in LCH cells are important for defining LCH subclasses. The principal pathological characteristics of LCH include the morphologic aspects of activated Langerhans cells adjoined to inflammatory granuloma. 2013;462:219–28. Eur J Immunol. Fields Virology. Bone. 2011;42:1063–77. Detection of IL-17A-producing peripheral blood monocytes in Langerhans cell histiocytosis patients. These cells determine the appropriate adaptive immune response (inflammation or tolerance) by interpreting the microenvironmental context in which they encounter foreign substances. Though Allen et al. On the contrary, LCH is a reactive disorder with underlying neoplastic potential. Murakami I, Gogusev J, Fournet JC, Glorion C, Jaubert F. Detection of molecular cytogenetic aberrations in langerhans cell histiocytosis of bone. Generally, no response is observed after secondary viral infection [111]. Matsushita M, Kuwamoto S, Iwasaki T, Higaki-Mori H, Yashima S, Kato M, Murakami I, Horie Y, Kitamura Y, Hayashi K. Detection of Merkel cell polyomavirus in the human tissues from 41 Japanese autopsy cases using polymerase chain reaction. NW, JN, MI, and MT participated in pathological analyses. Blood. Among patients with LCH-RO (−) (MS-LCH and SS-LCH), MCPyV-DNA was restricted to lesional LCH cells [12], thus we predicted that primary MCPyV infection may influence the LCH subtype involving cells in an early-activated state [27]. J Clin Invest. Yu RC, Chu C, Buluwela L, Chu AC. LCH cells that are in an active state [50] can induce IL-17A producers in a similar manner as activated Langerhans cells promote Th17 polarization [44]. 2004;163:536–9. 2011;108:18055–60. Epub 2020 Aug 25. These are principally the Langerhans cell, Merkel cell and melanocyte. NIH [37,38,39]. Acute-phase ITIH4 levels distinguish multi-system from single-system Langerhans cell histiocytosis via plasma peptidomics. Shimakage M, Sasagawa T, Kimura M, Shimakage T, Seto S, Kodama K, Sakamoto H. Expression of Epstein-Barr virus in Langerhans’ cell histiocytosis. Merkel cell polyomavirus and Langerhans cell neoplasm Ichiro Murakami, Noriko Wada, Junko Nakashima, Mitsuko Iguchi, Makoto Toi, Yumiko Hashida, Tomonori Higuchi, Masanori Daibata, Michiko Matsushita, Takeshi Iwasaki, Satoshi Kuwamoto, Yasushi Horie, Keiko Nagata, Kazuhiko Hayashi, Takashi Oka , Tadashi Yoshino , Toshihiko Imamura, Akira Morimoto, Shinsaku Imashuku, Jean Gogusev Show … We propose two distinct models for LCS and LCH pathogenesis. Loiarro M, Ruggiero V, Sette C. Targeting TLR/IL-1R signalling in human diseases. 3rd ed. investigated the presence of IL-17A-producing cells among peripheral blood mononuclear cells isolated from LCH patients and observed a high percentage of IL-17A(+) monocytes in peripheral blood of LCH patients compared to controls [61]. 2011;117:7099–101. also showed that CD3-positive cells in tonsils produced IL-17A [37, 39]. 2014;45:119–26. Eur J Intern Med. [85] reported that patients with LCH-RO (+) carried the BRAF V600E mutation in circulating CD11c+ and CD14+ cellular fractions as well as in bone marrow CD34+ hematopoietic cell progenitors, whereas the mutation was restricted to lesional LCH cells in patients with LCH-RO (−). © 2021 BioMed Central Ltd unless otherwise stated. Cookies policy. Langerhans cells (LCs) are epidermal immune cells of myeloid origin. 2002;27:474–82. Our study about IL-17 [47] resulted in three major findings. In 1868, Paul Langerhans discovered the epidermal dendritic cells that now bear his name. de Graaf JH, Tamminga RY, Dam-Meiring A, Kamps WA, Timens W. The presence of cytokines in Langerhans’ cell histiocytosis. J Virol. Overlapping and enzyme-specific contributions of matrix metalloproteinases-9 and -12 in IL-13-induced inflammation and remodeling. 2016;47:1785–96. Feng H, Shuda M, Chang Y, Moore PS. Chest. Langerhans cells are tissue-resident dendritic cells of the skin, and contain organelles called Birbeck granules. Structure and signalling in the IL-17 receptor family. 1). Langerhans cell histiocytosis (LCH) is currently considered a rare neoplastic disease with an inflammatory component, driven by genomic alterations in the mitogen-activating protein kinase (MAPK) pathway, including BRAF V600E, MAP2K1 mutations and BRAF deletions [1, 2]. Found largely in the epidermis, the outer layer of the skin, as well as in lymph nodes, Langerhans cells are an important element of the immune system.They are classified as dendritic cells because they grow projections called dendrites as they develop. Science. eCollection 2014. J Immunol. 1999;115:1452–5. MCPyV-DNA in PBMC correlated with LCH-RO (+) [12]. HHS Serum of patients with LCH can show an upregulation of IL-17A receptor in LCH cells but also in healthy monocyte-derived DCs. Innate lymphoid populations can rapidly produce IL-17A [44], which is maintained at low levels in the absence of external stimulation [45]. This study was approved by the Institutional Review Board of Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan, Faculty of Medicine, Tottori University, Tottori, Japan, and Kochi Medical School, Kochi University, Kochi, Japan. In the future, stimuli that govern IL-17A or IL-17A receptor production might serve as therapeutic targets to stop LCH progression, similar to cessation of smoking which induces pulmonary LCH regression [11, 68], which is almost always a disease of smokers [2]. Department of Pathology, Kochi Medical School, Kochi University, Kohasu, Okoh, Nankoku, Kochi, 783-8505, Japan, Ichiro Murakami, Junko Nakashima & Mitsuko Iguchi, Department of Pathology, Kochi University Hospital, 185-1 Kohasu, Okoh, Nankoku, Kochi, 783-8505, Japan, Ichiro Murakami, Noriko Wada, Junko Nakashima, Mitsuko Iguchi & Makoto Toi, Department of Microbiology and Infection, Kochi Medical School, Kochi University, Kohasu, Okoh, Nankoku, Kochi, 783-8505, Japan, Yumiko Hashida, Tomonori Higuchi & Masanori Daibata, Department of Pathobiological Science and Technology, School of Health Science, Faculty of Medicine, Tottori University, 86 Nishi, Yonago, Tottori, 683-8503, Japan, Department of Anatomic Pathology, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, Fukuoka, 812-8582, Japan, Department of Pathology, Tottori University Hospital, 86 Nishi, Yonago, Tottori, 683-8503, Japan, Division of Molecular Pathology, Faculty of Medicine, Tottori University, 86 Nishi, Yonago, Tottori, 683-8503, Japan, Satoshi Kuwamoto, Keiko Nagata & Kazuhiko Hayashi, Department of Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata, Kita-ku, Okayama, Okayama, 700-8558, Japan, Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata, Kita-ku, Okayama, Okayama, 700-8558, Japan, Department of Pediatrics, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, 465 Kajii, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, Kyoto, 602-8566, Japan, Department of Pediatrics, Jichi Medical University School of Medicine, 3311-1 Yakushiji, Shimotsuke, Tochigi, 329-0498, Japan, Division of Laboratory Medicine, Uji-Tokushukai Medical Center, 145 Ishibashi, Makishima, Uji, Kyoto, 611-0041, Japan, Inserm U507 and U1016, Institut Cochin, 75014, Paris, France, AP-HP Hôpital Necker-Enfants Malades, University Paris Descartes (Paris 5), 75006, Paris, France, You can also search for this author in In pulmonary LCH, the removal of stimuli, i.e. Merkel cells are found in the epidermis epidermis The outermost layer of the two main layers that make up the skin (the dermis is the deeper layer). USA.gov. Complete resolution of roentgenographic changes in a patient with pulmonary histiocytosis X. Akira S, Yamamoto M, Takeda K. Role of adapters in toll-like receptor signalling. Article  Martel-Jantin C, Pedergnana V, Nicol JT, Leblond V, Tregouet DA, Tortevoye P, Plancoulaine S, Coursaget P, Touze A, Abel L, Gessain A. Merkel cell polyomavirus infection occurs during early childhood and is transmitted between siblings. Mertz et al. Hall CB, Weinberg GA, Iwane MK, Blumkin AK, Edwards KM, Staat MA, Auinger P, Griffin MR, Poehling KA, Erdman D, et al. Chen K, Pociask DA, McAleer JP, Chan YR, Alcorn JF, Kreindler JL, Keyser MR, Shapiro SD, Houghton AM, Kolls JK, Zheng M. IL-17RA is required for CCL2 expression, macrophage recruitment, and emphysema in response to cigarette smoke. 2). Chest. J Clin Invest. A Langerhans cell is a specific kind of white blood cell. 2009;206:299–311. 2014;9:15. Mechanistically, MCPyV-induced oncogenesis is considered to be induced by MCPyV large T (LT) antigen through molecular binding with the retinoblastoma protein [3]. Peters TL, McClain KL, Allen CE. Many immune system cytokines are involved in bone metabolism, such as involvement of IL-1, IL-6 in the heightening of bone resorption by osteoclasts also producing a cytokine storm. Pulmonary Langerhans’ cell histiocytosis: radiologic resolution following smoking cessation. 6th ed. Hogarty MD. Article  We propose a triple-risk factor model for…, Proposed reaction model in LCH activity. 1986;140:543–6. 2020 Sep 8;117(36):22113-22121. doi: 10.1073/pnas.2009947117. Weiss LM, Jaffe R, Facchetti F. Tumours derived from Langerhans cells. 1994;343:767–8. These cells later develop into melanocytes—the pigment forming cells in the epidermis. Langerhans cell histiocytosis is a rare disorder that can look like some types of cancer. 2009;15:483–4. Glotzbecker MP, Dormans JP, Pawel BR, Wills BP, Joshi Y, Elkan M, Hodinka RL. PubMed Central  Hashida Y, Kamioka M, Tanaka M, Hosokawa S, Murakami M, Nakajima K, Kikuchi H, Fujieda M, Sano S, Daibata M. Ecology of Merkel cell Polyomavirus in healthy skin among individuals in an Asian cohort. Mertz KD, Junt T, Schmid M, Pfaltz M, Kempf W. Inflammatory monocytes are a reservoir for Merkel cell polyomavirus. Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. For example, we believe that the pathogenetic potential of the Merkel cell polyomavirus (MCPyV), the resident virus in skin, is variable and depends from the degree of individual's reactivity. Matrix metalloproteinase-12 (MMP-12) in osteoclasts: new lesson on the involvement of MMPs in bone resorption. Langerhans cell histiocytosis (LCH) is a disorder that primarily affects children, but is also found in adults of all ages. 2005;17:1–14. Proposed role of MCPyV in the development of LCH and LCS. Generally, stimuli are recognized by receptors such as Toll-like receptors (TLRs) in Langerhans cells [44, 49]. 1872 – The first eponymous association with Langerhans was proposed separately by Theodor Eimer (1843-1898) and Enrico Sertoli (1842-1910), who described the cells as ‘Langerhans’sche Körperchen‘ and ‘corpuscoli di Langerhans’, respectively, which translates to ‘Langerhans bodies’. Immunity. Therefore, LCH is also classified as involving at least one high-risk organ [LCH-RO (+)] or a no high-risk organ [LCH-RO (−)] [19] (Table 2) [21]. LCH is a proliferative disease of Langerhans-like abnormal cells which carry mutations of genes involved in the RAS/MAPK signaling pathway. Proposed triple-factor model for LCH pathogenesis. Morimoto A, Oh Y, Shioda Y, Kudo K, Imamura T. Recent advances in Langerhans cell histiocytosis. In general, cytokines work throughout autocrine or paracrine mechanisms; however, IL-3 and some other proinflammatory cytokines exhibit endocrine mechanisms [47, 48]. 2010;11:45. These are principally the Langerhans cell, Merkel cell and melanocyte. Our data suggest that LCH is a reactive disorder with an underlying oncogenic potential. Epidermis is the uppermost or epithelial layer of the oral mucosa in disease. Were detected as compared to controls with no significant differences among LCH subclasses, MCPyV triggered! 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Histiocytosis lesions reveals a distinct profile compared with epidermal Langerhans cells are macrophages involved in non-specific, immune... Of respiratory syncytial virus indolent from aggressive forms of LCS developed according the same mechanism involved the! A reactive disorder with underlying neoplastic potential potential using a triple-risk factor for. Data we use in the UK and Ireland Shioda Y, Moore PS cunningham al, Kasel JA DC! Caused by multifocal histiocytosis X adjoined to inflammatory granuloma Signal 16 langerhans and merkel cells Article:... Chang Y, Ishigame H, Thiele J, Egeler RM, Pritchard histiocytosis. Ultrastructural observations of the V600D mutation in Exon 15 of the following serves as a source of the Langerhans! For Research on Cancer ( IARC ) ; 2017. p. 470–3 3 ] patients, parents, subjects. Hallmark of the junctional epithelium is: a-Basement membrane Colby TV, Chen WG, LM. Il-1Beta target IL-1alpha for secretion as opposed to surface expression is indicated on the contrary LCH...

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