FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4252968161> ?p ?o ?g. }

• W4252968161 endingPage "929" @default.
• W4252968161 startingPage "929" @default.
• W4252968161 abstract "Pinpointing a single cell type as the sole musketeer securing skin homeostasis is, metaphorically, like rolling a dice: the overall impact of whatever side faces up is in the eye of the beholder. Indeed, the particular relevance of a given cell type under physiological conditions becomes evident only when its function is perturbed or even lost. Using transgenic or knockout animal models selectively targeting a certain cutaneous cell type, we are beginning to understand the critical factors and/or cell types that, once impaired, disturb skin homeostasis. The functional loss or gain of cell-specific proteins might unveil the importance of such cell types, however, only if linked to disease. This means that we have to take a look at skin diseases in order to assess the role of cutaneous cells for the maintenance of physiological conditions. Yet another level of complexity is added by the fact that independent primary disturbances of different cellular functions may ultimately result in the generation of similar uniform pathophysiological reaction patterns. Chronic inflammatory skin disorders, i.e. models of psoriasis, may serve as instructive examples to highlight these points. Fuelled by recently published animal models, there is a lively debate whether psoriatic skin lesions arise from primary keratinocyte abnormalities or from dysregulated immunocytes that secondarily activate otherwise normal keratinocytes. Interestingly, keratinocyte-targeted conditional JunB/c-Jun double knockout mice showed a psoriasis-like phenotype (1). This was further underscored by the phenotype of JunB/c-Jun double mutant mice on a recombination activating gene (RAG)-2-deficient background lacking functional T cells. The authors concluded that immune cells might play a secondary role in the pathogenesis of this disorder, similar to other genetically engineered mouse models with targeted alterations of epidermal molecules such as amphiregulin transgenic (2), I KappaB Kinase beta (IKK2)-deficient (3) or α2-integrin transgenic mice (4). Another example is the specific latent overexpression of transforming growth factor β1 in keratinocytes in mice, a mutation that also led to a psoriasis-like phenotype (5). Yet another mouse model in which activation of a proinflammatory signalling pathway in keratinocytes was forced by transgenic expression of a mutant variant signal transducer and activator of transcription 3 (6) featured a very similar cutaneous phenotype both macroscopically and histopathologically. In these latter animals, however, the pathogenesis of skin lesions was dependent on the co-presence of immunocytes, suggesting that both keratinocytes and T cells were required for the generation of this psoriasiform disorder. Other rodent models which were based on adoptive transfer of dysregulated T cells exhibited a psoriasiform phenotype in the complete absence of primary epithelial abnormalities (7,8). Moreover, disturbances of the cutaneous microvasculature via stimulation of the angiopoietin signalling pathway have also resulted in a cutaneous phenotype that is clinically and histopathologically very similar to the aforementioned psoriasiform models (9). Recent investigations in xenotransplantation models highlight a potential role of resident T cells or plasmacytoid dendritic cells in the pathogenesis and maintenance of chronic hyperproliferative skin changes (10,11). Finally, there are complementary strategies in which certain cell types were depleted to reverse a psoriasis-like phenotype, such as the depletion of neutrophils in the flaky skin mouse model (12) or the depletion of T cells in CD18-hypomorphic mice (13), thus highlighting the contribution of such immigrant cell types for the pathophysiology of the respective phenotype. These examples demonstrate that it is difficult, if not impossible, to reduce the control of skin homeostasis to a single mechanism or cell type. Triggering a complex inflammatory cascade at apparently completely different starting points may result in profound disturbances of the cutaneous equilibrium and result in a rather uniform chronic inflammatory reaction pattern in various different animal models. Similar considerations – without going into detail here – may apply to the pathogenesis of some skin tumors (e.g. regarding the mutually enhancing functions of epithelial alterations and immune dysfunctions in the pathogenesis of non-melanoma skin cancers). Thus, the primary dysfunction of (almost) any given cell type within the skin may eventually lead to a pathological condition, whereby the full-fledged phenotype often depends on ‘bystander’ cells which are secondarily heavily involved in the pathogenesis. Overall, the control of skin immunity is certainly not in the hands of a single cell type, but rather depends on the well-balanced function of several or all cells, that is, picking up on the introductory metaphor ‘All for one, and one for all’." @default.
• W4252968161 created "2022-05-12" @default.
• W4252968161 creator A5016666159 @default.
• W4252968161 creator A5019937386 @default.
• W4252968161 creator A5082322510 @default.
• W4252968161 date "2006-11-01" @default.
• W4252968161 modified "2023-10-12" @default.
• W4252968161 title "Commentary 2" @default.
• W4252968161 cites W1502820929 @default.
• W4252968161 cites W1991062077 @default.
• W4252968161 cites W2020845827 @default.
• W4252968161 cites W2034654881 @default.
• W4252968161 cites W2067117198 @default.
• W4252968161 cites W2074360288 @default.
• W4252968161 cites W2086296240 @default.
• W4252968161 cites W2095395089 @default.
• W4252968161 cites W2124846094 @default.
• W4252968161 cites W2129016683 @default.
• W4252968161 cites W2140118273 @default.
• W4252968161 cites W2159996176 @default.
• W4252968161 cites W2169758620 @default.
• W4252968161 doi "https://doi.org/10.1111/j.1600-0625.2006.00506_9.x" @default.
• W4252968161 hasPublicationYear "2006" @default.
• W4252968161 type Work @default.
• W4252968161 citedByCount "1" @default.
• W4252968161 crossrefType "journal-article" @default.
• W4252968161 hasAuthorship W4252968161A5016666159 @default.
• W4252968161 hasAuthorship W4252968161A5019937386 @default.
• W4252968161 hasAuthorship W4252968161A5082322510 @default.
• W4252968161 hasConcept C102230213 @default.
• W4252968161 hasConcept C104317684 @default.
• W4252968161 hasConcept C127716648 @default.
• W4252968161 hasConcept C141035611 @default.
• W4252968161 hasConcept C1491633281 @default.
• W4252968161 hasConcept C164659718 @default.
• W4252968161 hasConcept C169760540 @default.
• W4252968161 hasConcept C182704531 @default.
• W4252968161 hasConcept C189014844 @default.
• W4252968161 hasConcept C203014093 @default.
• W4252968161 hasConcept C2777074287 @default.
• W4252968161 hasConcept C2780564577 @default.
• W4252968161 hasConcept C2781085546 @default.
• W4252968161 hasConcept C54355233 @default.
• W4252968161 hasConcept C81885089 @default.
• W4252968161 hasConcept C86339819 @default.
• W4252968161 hasConcept C86803240 @default.
• W4252968161 hasConcept C95444343 @default.
• W4252968161 hasConceptScore W4252968161C102230213 @default.
• W4252968161 hasConceptScore W4252968161C104317684 @default.
• W4252968161 hasConceptScore W4252968161C127716648 @default.
• W4252968161 hasConceptScore W4252968161C141035611 @default.
• W4252968161 hasConceptScore W4252968161C1491633281 @default.
• W4252968161 hasConceptScore W4252968161C164659718 @default.
• W4252968161 hasConceptScore W4252968161C169760540 @default.
• W4252968161 hasConceptScore W4252968161C182704531 @default.
• W4252968161 hasConceptScore W4252968161C189014844 @default.
• W4252968161 hasConceptScore W4252968161C203014093 @default.
• W4252968161 hasConceptScore W4252968161C2777074287 @default.
• W4252968161 hasConceptScore W4252968161C2780564577 @default.
• W4252968161 hasConceptScore W4252968161C2781085546 @default.
• W4252968161 hasConceptScore W4252968161C54355233 @default.
• W4252968161 hasConceptScore W4252968161C81885089 @default.
• W4252968161 hasConceptScore W4252968161C86339819 @default.
• W4252968161 hasConceptScore W4252968161C86803240 @default.
• W4252968161 hasConceptScore W4252968161C95444343 @default.
• W4252968161 hasIssue "11" @default.
• W4252968161 hasLocation W42529681611 @default.
• W4252968161 hasOpenAccess W4252968161 @default.
• W4252968161 hasPrimaryLocation W42529681611 @default.
• W4252968161 hasRelatedWork W1514229478 @default.
• W4252968161 hasRelatedWork W1546309763 @default.
• W4252968161 hasRelatedWork W1854224221 @default.
• W4252968161 hasRelatedWork W1989514551 @default.
• W4252968161 hasRelatedWork W2089273599 @default.
• W4252968161 hasRelatedWork W2195257333 @default.
• W4252968161 hasRelatedWork W2369646821 @default.
• W4252968161 hasRelatedWork W2417555070 @default.
• W4252968161 hasRelatedWork W2888371630 @default.
• W4252968161 hasRelatedWork W4386894844 @default.
• W4252968161 hasVolume "15" @default.
• W4252968161 isParatext "false" @default.
• W4252968161 isRetracted "false" @default.
• W4252968161 workType "article" @default.