Scanning the Immunopathogenesis of Psoriasis
Abstract
:1. Introduction
2. Main Cell Types Involved in Psoriasis
2.1. T Cells
2.1.1. T Helper and Cytotoxic T Cells
2.1.2. γδ T Cells
2.2. Dendritic Cells
2.2.1. Plasmacytoid DCs
2.2.2. Myeloid DCs
- (i)
- CD11c+CD1c- cells, which are phenotypically immature, produce inflammatory cytokines (TNF and IL-6), and represent the most prevalent CD11c+ subpopulation infiltrating psoriatic skin [80,81,82,83]. These relatively immature mDCs, also known as Tip-DCs or inflammatory mDCs, are considered crucial players in psoriasis pathogenesis [57]. Indeed, they secrete TNF-α, IL-6, IL-20, IL-23 (and IL-12), they express iNOS, producing NO [79,80,81,82,83,84]. Because of this activity, they are able to induce inflammation (through TNF-α and NO), epidermal hyperplasia (through IL-20), and T cell differentiation (through IL-12 and IL-23) [80,81,82,83]. Although mDCs are able to secrete both p40 cytokines, IL-12 and IL-23, that consequently drive T cell differentiation towards a Th/Tc1 and Th/Tc17 phenotype, they mostly release IL-23 that sustains and amplifies the IL-17-mediated response, whereas IL-12 expression is not upregulated in lesional skin compared to non-lesional skin [80,81,82,83]. Dermal Tip-DC infiltration detected in lesional psoriatic skin is estimated as 30-fold greater than normal skin and 10-fold greater than non-lesional psoriatic skin [57,84,85].
- (ii)
- A second population of mDC characterized by the phenotype CD11c+ DC-LAMP+ DEC-205/CD205+BDCA-1+, acts as resident mature antigen-presenting cell and is phenotypically similar to those contained in normal skin. The number of these DCs does not increase in lesional skin compared to uninvolved skin [57,82]. These mature “resident” DCs are likely responsible for the antigen presentation to cutaneous T cells occurring in situ [86], within the dermis rather than following migration to draining lymph nodes [82,87]. CD1c+ “resident” DCs, representing mature (DC-LAMP/CD208+, CD205+, and CD86+) DCs, establish dermal clumps with T cells constituting lymphoid tissue-like structures [80,81,82,83,86,87], though T cells can be stimulated by Tip-DCs (CD11c+, CD1c- mDCs) as well [57]. Therefore, beyond the classic role of antigen-presenting cells, Tip-DCs show a prominent inflammatory activity in psoriasis and their infiltration is increased in lesional skin but normalized during treatment with effective therapies [85,88].
2.3. Neutrophils
2.4. Mast Cells
2.5. NK Cells and NK-T Cells
2.6. Innate Lymphoid Cells
2.7. Keratinocytes
3. Main Cytokines in Psoriasis
3.1. Interferon (IFN)-α
3.2. Interferon (IFN)-γ
3.3. Interleukin (IL)-17
3.4. Interleukin (IL)-22
3.5. Interleukin (IL)-23
3.6. Tumor Necrosis Factor Alpha (TNFα)
3.7. Anti-Inflammatory and Regulatory Signals Involved in Psoriasis
4. The Current Pathogenic Model
4.1. Early Phases
4.1.1. Dendritic Cell Activators
TLR Agonists
Chemerin
Thymic Stromal Lymphopoietin (TSLP)
4.1.2. Autoantigens
LL37
Thrombospondin Type 1 Motif-Like 5 (ADAMTSL5)
Lipid Antigens Generated by Phospholipase A2 Group IVD (PLA2G4D)
4.2. Amplification Phase and Tissue Cell Response
5. The Pathogenic Cascade Compendium
6. Conclusions
Author Contributions
Conflicts of Interest
Abbreviations
β-DEF | β-defenin |
CCL | CC chemokine ligands |
CXCL | chemokine (C-X-C motif) ligand |
CLA | cutaneous lymphocyte antigen |
DCs | dendritic cells |
EGF | epidermal growth factor |
ELAM-1 | endothelial leukocyte adhesion molecule-1 |
GWAS | genetic-wide association studies |
HBEGF | heparin-binding EGF-like growth factor |
HLA | Human leukocyte antigen |
ICAM-1 | intercellular adhesion molecule-1 |
IFN | interferon |
IL | interleukin |
ILC | innate lymphoid cells |
iNOS | intracellular nitric oxide synthase |
KCs | keratinocytes |
mDC | myeloid Dendritic Cell |
MMPs | matrix metalloproteinases |
NKT | natural Killer T cell |
NO | nitric oxide |
pDC | plasmacytoid Dendritic Cells |
STAT | signal transducer and activator of transcription |
TLR | toll-like receptor |
TNF | tumor necrosis factor |
TSLP | thymic stromal lymphopoietin |
VCAM-1 | vascular cell adhesion protein 1 |
VEGF | vascular endothelial growth factor |
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Chiricozzi, A.; Romanelli, P.; Volpe, E.; Borsellino, G.; Romanelli, M. Scanning the Immunopathogenesis of Psoriasis. Int. J. Mol. Sci. 2018, 19, 179. https://doi.org/10.3390/ijms19010179
Chiricozzi A, Romanelli P, Volpe E, Borsellino G, Romanelli M. Scanning the Immunopathogenesis of Psoriasis. International Journal of Molecular Sciences. 2018; 19(1):179. https://doi.org/10.3390/ijms19010179
Chicago/Turabian StyleChiricozzi, Andrea, Paolo Romanelli, Elisabetta Volpe, Giovanna Borsellino, and Marco Romanelli. 2018. "Scanning the Immunopathogenesis of Psoriasis" International Journal of Molecular Sciences 19, no. 1: 179. https://doi.org/10.3390/ijms19010179
APA StyleChiricozzi, A., Romanelli, P., Volpe, E., Borsellino, G., & Romanelli, M. (2018). Scanning the Immunopathogenesis of Psoriasis. International Journal of Molecular Sciences, 19(1), 179. https://doi.org/10.3390/ijms19010179