Recruitment of dendritic cells in oral lichen planus

Santoro, Amerigo; Majorana, Alessandra; Roversi, L; Gentili, Francesca; Marrelli, Simona; Vermi, William; Bardellini, Elena; Sapelli, Pierluigi; Facchetti, Fabio

doi:10.1002/path.1699

Cited by 99 publications

(110 citation statements)

References 54 publications

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“…Over time, the spectra of effects of LCs on peripheral T cells, activation of skin resident memory T lymphocytes, a defense function against pathogens and tissue repair were explored [72,73]. In our study, immunohistochemical results of S100 staining observed in the case of classic LPP and LP, both intraepithelial LCs and dermal DCs, are consistent with the results of Santoro et al [49]. However, significant differences between the groups were not found by us, and this might indicate the similarity existing between clinical forms of LP.…”

Section: Discussionsupporting

confidence: 81%

“…Acting as paracrine and autocrine mediators, these have been shown to be involved in numerous intracellular and extracellular functions, such as regulation of cell proliferation and survival or, alternatively, apoptosis, chemotaxis, inflammation, immune responses, Ca 2+ homeostasis, differentiation of keratinocytes and dynamics of cytoskeleton constituents [45,46,47]. S100 proteins are expressed in normal and diseased skin [48,49], and the subcellular distribution of these proteins in keratinocytes is heterogeneous [50,51]. S100-positive dendritic cells (DCs), involved in antigen presentation, phagocytosis, healing and repair processes, have been demonstrated to be significantly increased in LP [52].…”

Section: Introductionmentioning

confidence: 99%

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Eradication of damaged keratinocytes in cutaneous lichen planus forms demonstrated by evaluation of epidermal and follicular expression of CK15, indices of apoptosis and regulatory protein S100

Upeniece

Groma

Skuja

et al. 2016

pjp

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The study of cytoskeleton arrangement and its contribution to survival of cell-tocell contacts appears to be essential for understanding of numerous cellular and tissue processes. Applying CK15, S100 labeling and TUNEL reaction to cutaneous lichen planus subtypes, we found CK15 expression in the outer and inner root sheath of hair follicles, the basal epidermal layer, and eccrine glands. Its follicular expression was decreased in nearby inflammatory infiltrates. The CK15 immunopositivity was mostly described as weak (92.3%) for lichen planus but equally subdivided into weak, moderate and strong in lichen planopilaris (χ 2 = 32.514; df = 4; p < 0.001). The greatly varying apoptotic index was the highest in the lichen planopilaris involving the scalp: 81.2 ±10.7; 87.8 ±10.7 and 88.0 ±10.5 for the basal, spinous and upper epidermal layers, respectively. S100 positive epidermal and follicular cells did not differ in the lesions demonstrated in the study groups; still immunoreactivity was more pronounced in the scalp region of lichen planopilaris. Damage of cell-to-cell contacts was confirmed by electron microscopy. Apart from immunocyte-mediated keratinocyte death, cytoskeleton-based injury and loss of cellto-cell and matrix contacts may be of great importance, leading to eradication of degrading cells and thus contributing to the pathogenesis of lichen planus.

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Section: Discussionsupporting

confidence: 81%

Section: Introductionmentioning

confidence: 99%

Eradication of damaged keratinocytes in cutaneous lichen planus forms demonstrated by evaluation of epidermal and follicular expression of CK15, indices of apoptosis and regulatory protein S100

Upeniece

Groma

Skuja

et al. 2016

pjp

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“…Appropriate Texas red-and FITC-conjugated isotype-specific secondary antibodies were used to reveal the primary antibodies, as previously described. 18,24 Immunostained sections were analyzed and photographed using an Olympus BX60 fluorescence microscope, equipped with the Olympus DP-70 digital camera. Pictures were analyzed by Analysis 3.2 soft imaging system GMBH and Adobe Photoshop 5.0, limited edition.…”

Section: Tissues and Reagentsmentioning

confidence: 99%

“…24 Since the number of ChemR23 ϩ cells regularly outnumbered CD56 ϩ and CD94 ϩ cells, the expression of ChemR23 by DCs was also investigated. Figure 6 shows that OLP lesions presented an elevated number of CD123 ϩ , BDCA2 ϩ plasmacytoid DCs, and DC-SIGN ϩ myeloid DCs.…”

Section: Role Of Chemerin In the Colocalization Of Nk Cells And DC Inmentioning

confidence: 99%

The role of chemerin in the colocalization of NK and dendritic cell subsets into inflamed tissues

Parolini

Santoro

Marcenaro

et al. 2007

Blood

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333

282

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IntroductionNatural killer (NK) cells represent a minor population (5%-20%) of peripheral blood lymphocytes that is also present in secondary lymphoid organs, such as spleen, and lymph nodes, as well as in liver, bone marrow, and maternal uterus. [1][2][3] The function of NK cells in humans is regulated by a balance between opposite signals delivered by a set of HLA class I-specific inhibitory receptors and by a number of activating receptors and coreceptors responsible for NK cell triggering. By the combined use of these receptors, NK cells can discriminate between normal HLA class I ϩ cells and cells that have lost the expression of HLA class I molecules as a consequence of tumor transformation or viral infection. [4][5][6][7] Most NK cells in peripheral blood express the CD56 low CD16 ϩ phenotype, whereas the remainders are CD56 high CD16 Ϫ cells. It was proposed that CD56 high NK cells represent a primary source of immunoregulatory cytokines, whereas the CD56 low C16 ϩ subset represents the principal cytotoxic population. 8 During inflammation, viral infection and tumor growth, NK cells are rapidly recruited from the blood into injured tissues. 9-11 NK cell recruitment is governed by integrated signals, which include adhesion molecules and chemotactic factors. CD56 low CD16 ϩ NK cells express both ␤1 and ␤2 integrins, as well as the ligands for E-and P-selectins. In addition to these molecules, CD56 high NK cells also express high levels of L-selectin, a pivotal molecule for the interaction with lymph node high endothelial venules. 12-14 With respect to chemokine receptors, CD56 low CD16 ϩ NK cells express high levels of CXCR1 and CX3CR1. 9,15 By contrast, CD56 high NK cells express CCR7 as well as CCR5 and CXCR3. 8,9,15 It is likely that the different expression profile of adhesion molecules and chemokine receptors between the 2 major blood NK cell subsets is responsible for the preferential migration of CD56 low CD16 ϩ and CD56 high CD16 Ϫ NK cells into inflamed tissues and secondary lymphoid organs, respectively. 16 In fact, the CD56 high CD16 Ϫ NK cell subset although poorly represented in peripheral blood constitutes the only type of NK cells present in secondary lymphoid tissues. 2,3 We have recently identified a novel protein, chemerin, as the natural ligand of the previously orphan receptor ChemR23. 17 ChemR23 exhibits a unique expression profile among leukocyte populations being expressed preferentially by monocyte/macrophages and by immature myeloid and plasmacytoid dendritic cells (DCs). 18 Chemerin, originally isolated from inflamed biologic fluids, such as ovarian cancer ascites and rheumatoid arthritis synovial fluids, is synthesized as a secreted precursor protein.Prochemerin is poorly active but can be rapidly converted into a full ChemR23 agonist by the proteolytic removal of the last 6 amino acids by neutrophil-derived proteases (elastase and cathepsin G), mast cell products (triptase), and proteases of the coagulation cascade. 19,20 Therefore, prochemerin represents a "ready to The online ...

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“…In this work, we focused our analysis on two representative oral areas: the buccal mucosa, covering the inside of the cheek, and the lining mucosa anterior to the murine incisors, including the gingival papilla and the mucosa toward the midline of the lower lip (hereinafter termed lining mucosa). These anatomically distinct tissues contain DC subsets that were found to be involved in various oral diseases such as lichen planus and periodontitis (29,30). We believe that by studying these oral DCs, we can increase our understanding of their role during disease and harness their capacity for eliciting protective oral immunity.…”

mentioning

confidence: 99%

Dendritic Cells in Distinct Oral Mucosal Tissues Engage Different Mechanisms To Prime CD8+ T Cells

Nudel

Elnekave

Furmanov

et al. 2011

The Journal of Immunology

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Although oral dendritic cells (DCs) were shown to induce cell-mediated immunity, the identity and function of the various oral DC subsets involved in this process is unclear. In this study, we examined the mechanisms used by DCs of the buccal mucosa and of the lining mucosa to elicit immunity. After plasmid DNA immunization, buccally immunized mice generated robust local and systemic CD8+ T cell responses, whereas lower responses were seen by lining immunization. A delayed Ag presentation was monitored in vivo in both groups; yet, a more efficient presentation was mediated by buccal-derived DCs. Restricting transgene expression to CD11c+ cells resulted in diminished CD8+ T cell responses in both oral tissues, suggesting that immune induction is mediated mainly by cross-presentation. We then identified, in addition to the previously characterized Langerhans cells (LCs) and interstitial dendritic cells (iDCs), a third DC subset expressing the CD103+ molecule, which represents an uncharacterized subset of oral iDCs expressing the langerin receptor (Ln+iDCs). Using Langerin-DTR mice, we demonstrated that whereas LCs and Ln+iDCs were dispensable for T cell induction in lining-immunized mice, LCs were essential for optimal CD8+ T cell priming in the buccal mucosa. Buccal LCs, however, failed to directly present Ag to CD8+ T cells, an activity that was mediated by buccal iDCs and Ln+iDCs. Taken together, our findings suggest that the mechanisms engaged by oral DCs to prime T cells vary between oral mucosal tissues, thus emphasizing the complexity of the oral immune network. Furthermore, we found a novel regulatory role for buccal LCs in potentiating CD8+ T cell responses.

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Recruitment of dendritic cells in oral lichen planus

Cited by 99 publications

References 54 publications

Eradication of damaged keratinocytes in cutaneous lichen planus forms demonstrated by evaluation of epidermal and follicular expression of CK15, indices of apoptosis and regulatory protein S100

Eradication of damaged keratinocytes in cutaneous lichen planus forms demonstrated by evaluation of epidermal and follicular expression of CK15, indices of apoptosis and regulatory protein S100

The role of chemerin in the colocalization of NK and dendritic cell subsets into inflamed tissues

Dendritic Cells in Distinct Oral Mucosal Tissues Engage Different Mechanisms To Prime CD8+ T Cells

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