Psoriasis is a chronically relapsing skin inflammation affecting about 2% the population worldwide. Plaque psoriasis, also known as psoriasis vulgaris, is the most common form of the disease. However there is now accumulating evidence of important systemic manifestations of psoriasis including cardiovascular disorders and metabolic syndrome. About 30% of patients also develop psoriatic arthritis (PsA), which manifests as an inflammation of the synovium, entheses and spine. Therefore, the term Psoriatic Disease has been recently introduced to encompass the different clinical manifestations of this disorder.
At the skin level, psoriasis pathogenesis involves a complex interplay between T cells, dendritic cells and keratinocytes in which autoreactive CD8+ T lymphocytes have been suggested to be involved in the early phase, whereas IL-17-producing T cells play a central role in the amplification phase by enhancing the inflammatory response of keratinocytes and creating a positive feedback loop around the IL-23/IL-17 axis. A marked enhancement of IFN? and Th1 T cell infiltration also occurs in psoriatic plaques, although the specific role of this infiltration in the pathogenesis of psoriasis is currently unclear.
Despite our progress in understanding the pathogenesis of plaque psoriasis, the immune mechanisms involved in the development of systemic disease manifestations and psoriatic arthritis remain poorly understood. As an explanation for the development of extra-cutaneous manifestations, psoriasis has been viewed as a state of systemic inflammation that progressively leads to the involvement of other organs, besides skin, via the systemic circulation. Currently, there is only limited knowledge of the soluble and cellular components that mediate this process and can lead to the development of cardiovascular manifestations and joint inflammation.
This Research Topic will focus on the immune and inflammatory mechanisms that may link psoriasis with its comorbidities. We aim to provide an overview of the immunological mechanisms involved in (i) plaque psoriasis formation, (ii) in the development of systemic manifestations, such as atherosclerosis, and (iii) in the development of joint inflammation. This integrated view aims to enhance our understanding of the immune mechanisms that mediate the progression of inflammation from the skin to systemic circulation and to synovial tissue in patients with psoriatic disease.
We welcome the submission of Review, Original Research articles and Clinical Trial data that cover, but are not limited to, the following topics:
1. Immune and cytokine networks in psoriatic skin lesions.
2. Immune and cytokine networks in atherosclerotic plaques found in psoriasis patients and/or mouse models of psoriasis.
3. Immune and cytokine networks in synovial tissues from patients with PsA.
4. Immunogenetics of psoriasis and PsA.
5. Autoimmune aspects of psoriasis and PsA.
6. Systemic inflammation in psoriatic disease.
Psoriasis is a chronically relapsing skin inflammation affecting about 2% the population worldwide. Plaque psoriasis, also known as psoriasis vulgaris, is the most common form of the disease. However there is now accumulating evidence of important systemic manifestations of psoriasis including cardiovascular disorders and metabolic syndrome. About 30% of patients also develop psoriatic arthritis (PsA), which manifests as an inflammation of the synovium, entheses and spine. Therefore, the term Psoriatic Disease has been recently introduced to encompass the different clinical manifestations of this disorder.
At the skin level, psoriasis pathogenesis involves a complex interplay between T cells, dendritic cells and keratinocytes in which autoreactive CD8+ T lymphocytes have been suggested to be involved in the early phase, whereas IL-17-producing T cells play a central role in the amplification phase by enhancing the inflammatory response of keratinocytes and creating a positive feedback loop around the IL-23/IL-17 axis. A marked enhancement of IFN? and Th1 T cell infiltration also occurs in psoriatic plaques, although the specific role of this infiltration in the pathogenesis of psoriasis is currently unclear.
Despite our progress in understanding the pathogenesis of plaque psoriasis, the immune mechanisms involved in the development of systemic disease manifestations and psoriatic arthritis remain poorly understood. As an explanation for the development of extra-cutaneous manifestations, psoriasis has been viewed as a state of systemic inflammation that progressively leads to the involvement of other organs, besides skin, via the systemic circulation. Currently, there is only limited knowledge of the soluble and cellular components that mediate this process and can lead to the development of cardiovascular manifestations and joint inflammation.
This Research Topic will focus on the immune and inflammatory mechanisms that may link psoriasis with its comorbidities. We aim to provide an overview of the immunological mechanisms involved in (i) plaque psoriasis formation, (ii) in the development of systemic manifestations, such as atherosclerosis, and (iii) in the development of joint inflammation. This integrated view aims to enhance our understanding of the immune mechanisms that mediate the progression of inflammation from the skin to systemic circulation and to synovial tissue in patients with psoriatic disease.
We welcome the submission of Review, Original Research articles and Clinical Trial data that cover, but are not limited to, the following topics:
1. Immune and cytokine networks in psoriatic skin lesions.
2. Immune and cytokine networks in atherosclerotic plaques found in psoriasis patients and/or mouse models of psoriasis.
3. Immune and cytokine networks in synovial tissues from patients with PsA.
4. Immunogenetics of psoriasis and PsA.
5. Autoimmune aspects of psoriasis and PsA.
6. Systemic inflammation in psoriatic disease.
