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• W2890136542 abstract "Editorial note: Welcome to the Journal of Investigative Dermatology (JID) SnapshotDx Quiz. In this monthly online-only quiz, the first question (“What is your diagnosis?”) relates to the clinical images above, while additional questions concern the findings reported in the JID article by Lauffer et al (https://doi.org.com/10.1016/j.jid.2018.02.034). Detailed answers and a list of relevant references are available following the Quiz Questions below. 1.A 40-year-old African American female presents with erythematous scaly plaques with hypopigmentation, hyperpigmentation, and scarring alopecia on her scalp. A biopsy demonstrates which of the following characteristic histologic patterns?a.Interface dermatitisb.Superficial and deep perivascular infiltratec.Parakeratosisd.Spongiotic dermatitise.Pseudoepitheliomatous hyperplasia2.As proposed by Lauffer et al., what mechanism causes keratinocyte cell death in interface dermatitis?a.Necroptosisb.Apoptosis (intrinsic pathway)c.Apoptosis (extrinsic pathway)d.Pyroptosise.Granulysin-induced cell death3.As proposed by Lauffer et al., which of the following inflammatory cytokines are required for necroptosis in interface dermatitis?a.Interferon (IFN)-γ and tumor necrosis factor (TNF)-αb.TNF-α onlyc.Interleukin (IL)-17 and IL-22d.IL-4 and IL-13e.IL-22 See following pages for detailed answers. 1.A 40-year-old African American female presents with erythematous scaly plaques with hypopigmentation, hyperpigmentation, and scarring alopecia on her scalp. A biopsy demonstrates which of the following characteristic histologic patterns?Correct answer: a. Interface dermatitisThe above images represent discoid lupus erythematosus (DLE) and interface dermatitis. Interface dermatitis is a major inflammatory skin reaction pattern. Interface dermatitis is composed of inflammatory cell infiltrates at the dermal-epidermal junction and vacuolar degeneration of the basal cell layer of the epidermis due to cell injury and death (Sontheimer, 2009Sontheimer R.D. Lichenoid tissue reaction/interface dermatitis: clinical and histological perspectives.J Invest Dermatol. 2009; 129: 1088-1099https://doi.org/10.1038/sj.jid.2009.42Abstract Full Text Full Text PDF PubMed Scopus (89) Google Scholar).Discussion of incorrect answers:b.Superficial and deep perivascular lymphocytic infiltrateThe biopsy does not show significant features of superficial and deep perivascular lymphocytic infiltrates. The differential diagnosis for this reaction pattern includes lymphocytoma cutis, lymphoma, lymphocytic infiltrate of Jessner, polymorphous light eruption, deep subtype of erythema annulare centrifugum, and syphilis.c.ParakeratosisThe presence of corneocytes with retained nucleus, or parakeratosis, is not seen in this biopsy. Nonetheless, parakeratosis can appear with interface dermatitis in skin conditions such as benign lichenoid keratosis, lichenoid drug eruption, and graft-versus-host disease.d.Spongiotic dermatitisIntercellular edema within keratinocytes is a hallmark of spongiotic dermatitis, but it is not present in the biopsy. Spongiotic dermatitis is classically seen in pityriasis rosea, viral exanthems, contact dermatitis, and atopic dermatitis. Diagnoses that combine varying degrees of vacuolar interface changes and spongiosis include early erythema multiforme, polymorphic light eruption, drug eruptions, and Gianotti-Crosti syndrome.e.Pseudoepitheliomatous hyperplasiaThe biopsy does not show features of pseudoepitheliomatous hyperplasia. Pseudoepitheliomatous hyperplasia (PEH) is a nonspecific pattern of endophytic epidermal hyperplasia secondary to irritant, inflammatory, or neoplastic processes. Irregular acanthotic epidermal processes arising from the epithelium of adnexal structures is characteristic of this pattern and can mimic well-differentiated squamous cell carcinoma.2.As proposed by Lauffer et al., what mechanism causes keratinocyte cell death in interface dermatitis?Correct answer: a. NecroptosisLauffer et al. report that necroptosis, or programmed necrosis, could be a mechanism of keratinocytic cell death in interface dermatitis. The activation of necroptosis requires receptor-interacting serine/threonine-protein kinase 3 (RIP3)/RIP1 complex mediated phosphorylation of mixed lineage kinase domain-like protein (MLKL) at T357 and S358 (Sun et al., 2012Sun L. Wang H. Wang Z. He S. Chen S. Liao D. Wang X. Mixed lineage kinase domain-like protein mediates necrosis signaling downstream of RIP3 kinase.Cell. 2012; 148: 213-227https://doi.org/10.1016/j.cell.2011.11.031Abstract Full Text Full Text PDF PubMed Scopus (1679) Google Scholar, Wang et al., 2014Wang H. Sun L. Su L. Rizo J. Liu L. Wang L.F. et al.Mixed lineage kinase domain-like protein MLKL causes necrotic membrane disruption upon phosphorylation by RIP3.Mol Cell. 2014; 54: 133-146Abstract Full Text Full Text PDF PubMed Scopus (993) Google Scholar). Phosphorylated MLKL oligomers bind to and broadly permeabilize cellular and intracellular membranes leading to necrosis. Necroptosis is typically inhibited by the competing activation of apoptosis through caspase-8 degradation of RIP3 and RIP1 (Lin et al., 1999Lin Y. Devin A. Rodriguez Y. Liu Z. Cleavage of the death domain kinase RIP by Caspase-8 prompts TNF-induced apoptosis.Genes Dev. 1999; 13: 2514-2526Crossref PubMed Scopus (680) Google Scholar). The investigators demonstrated elevated RIP3 expression in the epidermis of lichen planus (LP) and cutaneous lupus erythematosus as compared to psoriasis (Figure 4). These results are consistent with previous findings showing the activation of RIP3 and MLKL in toxic epidermolysis necrosis, a strikingly fulminant form of interface dermatitis (Kim et al., 2015Kim S.K. Kim W.J. Yoon J.H. Ji J.H. Morgan M.J. Cho H. Kim Y.S. Upregulated RIP3 Expression Potentiates MLKL Phosphorylation-Mediated Programmed Necrosis in Toxic Epidermal Necrolysis.J Invest Dermatol. 2015; 135: 2021-2030https://doi.org/10.1038/jid.2015.90Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar, Lauffer et al., 2018Lauffer F. Jargosch M. Krause L. Garzorz-Stark N. Franz R. Roenneberg S. Eyerich K. Type I Immune Response Induces Keratinocyte Necroptosis and Is Associated with Interface Dermatitis.J Invest Dermatol. 2018; https://doi.org/10.1016/j.jid.2018.02.034Abstract Full Text Full Text PDF Scopus (36) Google Scholar).Discussion of incorrect answers:b.Apoptosis (intrinsic pathway)After exposure to various cytotoxic insults, oligomerization of Bak and Bax on the outer mitochondrial membrane leads the release of cytochrome c. Cytochome c, Apaf-1, dATP, assembles into a macromolecular complex termed the “apoptosome”, which recruits and cleaves pro-caspase-9. Caspase-9 activates effector caspases-3 and 7, leading to cell death. UVB-induced keratinocyte apoptosis appears to require caspase-9 activity and the intrinsic pathway (Sitailo et al., 2002Sitailo L.A. Tibudan S.S. Denning M.F. Activation of caspase-9 is required for UV-induced apoptosis of human keratinocytes.J Biol Chem. 2002; 277: 19346-19352https://doi.org/10.1074/jbc.M200401200Crossref PubMed Scopus (138) Google Scholar).c.Apoptosis (extrinsic pathway)Members of the tumor necrosis factor (TNF) family ligate their corresponding death receptors, which leads to the assembly of death-inducing signaling complex and pro-caspase-8 cleavage. Caspase-8 plays an analogous role as caspase-9 in activating effector caspases. Fas-ligand induced apoptosis is critical for the maturation of T-cells and cytotoxic T-cell mediated killing, which has been implicated in the development of eczematous dermatitis (Trautmann et al., 2000Trautmann A. Akdis M. Kleemann D. Altznauer F. Simon H.U. Graeve T. Akdis C.A. T cell-mediated Fas-induced keratinocyte apoptosis plays a key pathogenetic role in eczematous dermatitis.J Clin Invest. 2000; 106: 25-35https://doi.org/10.1172/jci9199Crossref PubMed Google Scholar). In contrast, TNF-α-mediated apoptosis is complicated by the activation of a competing inflammatory pathway that drives NF-κB expression. When the death pathway is selected, RIP1 is a required component of the TNF-α-associated apoptotic machinery and is therefore poised to facilitate crosstalk with the necrosis pathway (Micheau and Tschopp, 2003Micheau O. Tschopp J. Induction of TNF receptor I-mediated apoptosis via two sequential signaling complexes.Cell. 2003; 114: 181-190Abstract Full Text Full Text PDF PubMed Scopus (2008) Google Scholar).d.PyroptosisPyroptosis is a caspase-1- or 4/5/11-dependent, inflammatory cell death pathway. In the presence of pathogen-associated molecular patterns, members of the AIM2-like receptors (ALRs) and NOD-like receptors (NLR) oligomerize into an “inflammasome,” which leads to the activation of caspase-1 and recruitment of T-cells through the secretion of IL-1β and IL-18. Caspases-4/5/11 can directly bind to lipopolysaccharide and autocatalyze self-cleavage. Caspases-1/4/5/11 all cleave gasdermin D, which perforates the cell by forming large pores on the cytoplasmic membrane (Shi et al., 2017Shi J. Gao W. Shao F. Pyroptosis: Gasdermin-Mediated Programmed Necrotic Cell Death.Trends Biochem Sci. 2017; 42: 245-254https://doi.org/10.1016/j.tibs.2016.10.004Abstract Full Text Full Text PDF PubMed Scopus (1334) Google Scholar).e.Granulysin-induced cell deathCytotoxic T-cells and NK cells secrete soluble granulysin, which directly lyses keratinocytes in Stevens-Johnson syndrome/toxic epidermal necrolysis, and is the predominant mediator of cell death in these conditions (Chung et al., 2008Chung W.H. Hung S.I. Yang J.Y. Su S.C. Huang S.P. Wei C.Y. Chen Y.T. Granulysin is a key mediator for disseminated keratinocyte death in Stevens-Johnson syndrome and toxic epidermal necrolysis.Nat Med. 2008; 14: 1343-1350https://doi.org/10.1038/nm.1884Crossref PubMed Scopus (561) Google Scholar).3.As proposed by Lauffer et al., which of the following inflammatory cytokines are required for necroptosis in interface dermatitis?Correct answer: a. IFN-γ and TNF-αLauffer et al. demonstrated that soluble cytokines produced by lymphocytes isolated from lesional skin of interface dermatitis are sufficient to induce RIP3 expression, MLKL phosphorylation, and necrotic changes in 3-D keratinocyte culture (Figure 4). Depletion of both IFN-γ and TNF-α did not lead to cell necrosis. Recombinant IFN-γ and TNF-α are also capable of inducing keratinocyte necrosis (Figure 3c). The current findings are consistent with the well-established findings of TNF-α-induced necroptosis, which also requires the concurrent inhibition of caspase-dependent apoptosis (Sun et al., 2012Sun L. Wang H. Wang Z. He S. Chen S. Liao D. Wang X. Mixed lineage kinase domain-like protein mediates necrosis signaling downstream of RIP3 kinase.Cell. 2012; 148: 213-227https://doi.org/10.1016/j.cell.2011.11.031Abstract Full Text Full Text PDF PubMed Scopus (1679) Google Scholar). The mechanism to bypass caspase inhibition of necroptosis in interface dermatitis is unclear. In addition, co-activation of IFN-γ and TNF-α signaling could suppress TNF-α-associated NF-κB expression and promote cell death pathways in certain contexts (Suk et al., 2001Suk K. Chang I. Kim Y.H. Kim S. Kim J.Y. Kim H. Lee M.S. Interferon gamma (IFNgamma) and tumor necrosis factor alpha synergism in ME-180 cervical cancer cell apoptosis and necrosis. IFNgamma inhibits cytoprotective NF-kappa B through STAT1/IRF-1 pathways.J Biol Chem. 2001; 276: 13153-13159https://doi.org/10.1074/jbc.M007646200Crossref PubMed Scopus (132) Google Scholar).Discussion of incorrect answers:b.TNF-α onlyThe combination of both IFN-γ and TNF-α was necessary and sufficient for the induction of RIP3 expression in keratinocytes (Figure 4c and 4d). Depletion of TNF-α only or IFN-γ only in mixed T cell supernatant still produced induction of RIP3 and pMLKL. However, depletion of both IFN-γ and TNF-α inhibited RIP3 and pMLKL activation. Physiologically, TNF-α exerts pleotropic effects in both inflammation and cell death. Factors that influence the selection of these fates are largely undefined.c.IL-17 and IL-22Stimulation of 3-D skin culture with IL-17 and IL-22 was not sufficient to induce cell death (Figure 3). TH17 T-cells secrete IL-17 and are also a significant source of IL-22. TH17 cells are important for defense against infections by orchestrating inflammatory responses of epithelial cells and TH1 cells. In psoriasis, both IL-17 and IL-22 have been shown to play a significant role in pathogenesis (Eyerich et al., 2017Eyerich K. Dimartino V. Cavani A. IL-17 and IL-22 in immunity: Driving protection and pathology.Eur J Immunol. 2017; 47: 607-614https://doi.org/10.1002/eji.201646723Crossref PubMed Scopus (207) Google Scholar).d.IL-4 and IL-13Stimulation of 3-D skin culture with IL-4 and IL-13 was not sufficient to induce cell death (Figure 3). IL-4 and IL-13 are key mediators of type 2 immunity in the production of IgE and M2 macrophage polarization (Van Dyken and Locksley, 2013Van Dyken S.J. Locksley R.M. Interleukin-4- and interleukin-13-mediated alternatively activated macrophages: roles in homeostasis and disease.Annu Rev Immunol. 2013; 31: 317-343https://doi.org/10.1146/annurev-immunol-032712-095906Crossref PubMed Scopus (460) Google Scholar).e.IL-22Stimulation of 3-D skin culture with IL-22 was not sufficient to induce cell death (Figure 3). IL-22 is produced predominantly by TH22, TH1 CD4 cells, and TH17 cells. Transgenic mice overexpressing IL-22 produce skin pathology reminiscent of psoriasis, and serum levels of IL-22 appear to correlate with disease activity in patients with psoriasis (Dudakov et al., 2015Dudakov J.A. Hanash A.M. van den Brink M.R. Interleukin-22: immunobiology and pathology.Annu Rev Immunol. 2015; 33: 747-785https://doi.org/10.1146/annurev-immunol-032414-112123Crossref PubMed Scopus (528) Google Scholar). Download .pdf (.05 MB) Help with pdf files Quiz and brief explanation of correct answers Download .pdf (.25 MB) Help with pdf files Detailed discussion of all quiz answers" @default.
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• W2890136542 date "2018-10-01" @default.
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• W2890136542 title "SnapshotDx Quiz: October 2018" @default.
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