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Psoriatic Arthritis
Published in Jason Liebowitz, Philip Seo, David Hellmann, Michael Zeide, Clinical Innovation in Rheumatology, 2023
Elena Ciofoaia, Ana-Maria Orbai, Jason Liebowitz
In addition to anti-LL-37, elevated levels of anti-ADAMTSL5 IgG were also increased in PsA patients and both correlated with disease severity. This again suggests a contribution to systemic inflammation and a potential causal pathogenic relationship. Interestingly, anti-LL-37 was found to be presented by HLA-C*06:02, and it also plays a role in secretion of the pro-inflammatory cytokines TNF, IL-23, and IL-12. ADAMTSL5 is also well presented by HLA-C*06:02, and it triggers the expression of IFN-γ and IL-17. Therefore, not surprisingly, in patients treated with IL-17 and TNF blockade, both ADAMTSL5 and LL-37 levels have been reported to decrease. Keratin-17 is considered a hallmark of psoriasis. Keratin 17-reactive CD8+ T cells elicit significant IFN-γ responses, and it induces T cell proliferation only in patients with the HLA-Cw*06:02 allele. Other potential autoantigens studies have mentioned hnRNP-A1, which plays a role in autoimmunity and has also been elevated in patients with psoriasis.
Epithelial and fibroepithelial tumors
Published in Eckart Haneke, Histopathology of the NailOnychopathology, 2017
The histopathological differential diagnosis may be difficult in very early lesions. It comprises arsenical keratosis, Bowen's disease, and squamous cell carcinoma.164 However, some authors called them all superficial squamous cell carcinoma and vehemently rejected the terms carcinoma in situ or KIN.165,166 When there is a lichenoid inflammatory infiltrate, it may be similar to lichen planus-like keratosis. This, however, shows rather dissolution of the basal cell layer than atypical cells. The keratoses seen in organ transplant recipients are histologically often different in that they are characterized by epithelial proliferations of large cells that initially show surprisingly little atypia but once they transform, they rapidly progress to invasive squamous cell carcinoma. They exhibit early keratin 17 expression.167
Hair dysplasias
Published in Pierre Bouhanna, Eric Bouhanna, The Alopecias, 2015
Juan Ferrando, L. Alheli Niebla, Gerardo A. Moreno-Arias
In those cases associated with type 2 congenital pachionychia, a structural alteration of keratin 17 has been observed.28 Mutation of the ST14 gene (Cr 11q24.3-q.25) that encodes a protease (type II transmembrane serine protease matriptase) has been identified in cases of pili torti associated with hypotrichosis and ichthyosis.29 When associated with congenital hypotrichosis and juvenile macular dystrophy mutation has been identified in 16q22.1.30,31 Other mutations have also been identified in CDH3.
Berberine modulates Keratin 17 to inhibit cervical cancer cell viability and metastasis
Published in Journal of Receptors and Signal Transduction, 2021
Luping Liu, Li Sun, Jing Zheng, Li Cui
Keratin (KRT) is a protein family that is critical for hair formation and is the essential cellular structural material in forming the cornified layer which protects cells against damage or physical stress [10]. Keratin 17 (KRT17) is a kind of type I KRT [10], and upregulation of KRT17 expression is associated with lesion progression as well as poor prognosis in a number of epithelial cancers [11]. For example, overexpression of KRT17 was related to poor prognosis in epithelial ovarian cancer [12]. KRT17 performs an immunomodulatory function in skin by polarizing the immune response through up-regulating epithelial proliferation and tumor growth [13]. In addition, it is worth noting that an up-regulated KRT17 expression level was found in advanced cervical cancer tissue, and is closely associated with the poor survival of patients with this disease [14]. However, whether KRT17 could be regulated by BBR in cervical cancer cells remains elusive.
Keratinocyte differentiation antigen-specific T cells in immune checkpoint inhibitor-treated NSCLC patients are associated with improved survival
Published in OncoImmunology, 2021
Fiamma Berner, Rebekka Niederer, Jolien J. Luimstra, Oltin Tiberiu Pop, Ann-Kristin Jochum, Mette-Triin Purde, Omar Hasan Ali, David Bomze, Jens Bauer, Lena Katharina Freudenmann, Ana Marcu, Eva-Maria Wolfschmitt, Sebastian Haen, Thorben Gross, Marissa Lisa Dubbelaar, Marie-Therese Abdou, Petra Baumgaertner, Christina Appenzeller, Caroline Cicin-Sain, Tobias Lenz, Daniel E. Speiser, Burkhard Ludewig, Christoph Driessen, Markus Jörger, Martin Früh, Wolfram Jochum, Antonio Cozzio, Hans-Georg Rammensee, Juliane Walz, Jacques Neefjes, Lukas Flatz
The PBMCs of patients that showed an IFN-γ+ T cell response to the epitope pools were then stimulated with the single peptides, which lead to the identification of several HLA-A 03:01 and HLA-C 04:01 specific CD8 epitopes. Surprisingly, no epitopes for HLA-A 02:01 were identified. Interestingly, seven of the identified peptide epitopes induced a CD8+ IFN-γ+ T cell response in at least two patients. Four peptides were shared among HLA-A 03:01-positive patients (Figure 2a) and three were shared among HLA-C 04:01-positive patients (Figure 2b). A summary of the shared and non-shared epitopes identified is presented in Supplementary Table S4. Epitopes were identified for all keratinocyte differentiation antigens with the exception of keratin 17. Representative flow cytometry plots of the identified epitopes are shown in Supplementary Fig. S5. When comparing survival between patients harboring T cells specific for the identified epitopes, and patients where we failed to identify such T cells, we observed better overall survival (OS) (HR = 0.37 [95% CI, 0.20–0.68]; log-rank p-value =0.01) and progression-free survival (PFS) (HR = 0.37 [95% CI, 0.20–0.68]; log-rank p-value = 0.01) for patients with CD8+ IFN-γ+ T cell responses to the predicted epitope(s) (Figure 2c-d).
The value of desmosomal plaque-related markers to distinguish squamous cell carcinoma and adenocarcinoma of the lung
Published in Upsala Journal of Medical Sciences, 2020
Inmaculada Galindo, Mercedes Gómez-Morales, Inés Díaz-Cano, Álvaro Andrades, Mercedes Caba-Molina, María Teresa Miranda-León, Pedro Pablo Medina, Joel Martín-Padron, María Esther Fárez-Vidal
The novel markers described here showed a heterogeneous staining of SCC, which was observed in the membranes and cytoplasm of more differentiated cells, marking the intercellular junctions, with staining of nuclei more frequently detected in areas of more immature appearance. In AC samples, focal staining with these novel markers was detected in nucleus and cytoplasm, but never in membrane. In addition to their role in cell adhesion, plakophilins, including PKP1, have been reported to localize to the cytoplasm and nucleus, where they are thought to have several functions that are not completely understood (18). This explains the nuclear and cytoplasmic positivity observed, mainly in SCC in our series. In a few cases and in a few cells, we have also seen occasional nuclear staining for CKT15 and DSG3. Although nuclear localization of CKT15 and DSG3 has not been reported (22,23) and non-specific staining cannot be ruled out, it has been shown that several cytoskeletal proteins, formerly thought to be exclusively cytoplasmic, and including some keratins (keratins 7, 8, 17, and 18), are components of the nuclear matrix, where they may have multiple functions. Some studies of skin and cervical tumours indicated that keratin 17 has a role in the cell cycle and in gene expression regulation (44). These data and the fact that KRT15 and DSG3 are not routinely used in most laboratories prompted our assessment of nuclear staining. Further investigation is warranted to explore the significance of our findings.