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Diet and lifestyle could increase the risk of developing psoriasis by 30 per cent

Research being presented this week at the Psoriasis: From Gene to Clinic International Congress in London suggests that diet and lifestyle factors can contribute up to 30 per cent to the risk of psoriasis onset in people with the genetic predisposition to the condition.

Psoriasis is an inflammatory skin condition, affecting around two per cent of the population. Psoriasis occurs when a type of immune cell, called a T-cell, becomes overactive. They attack melanocytes, specialist skin cells that produce the pigment melanin, this immune response causes a growth of skin cells in the form of psoriatic plaques. However, the reason why this happens has been unclear.

Certain alleles (alternative forms of a gene) are linked with a higher risk of developing psoriasis, and HLA-C*06:02 is the main psoriasis risk gene. HLA-C*06:02 positive people are between 9- and 23-fold more likely to develop psoriasis than someone without an allele associated with the disease.

In a recent study the same authors identified that T-cells attack melanocytes in patients with psoriasis HLA-C*06:02 due to reaction against a certain a peptide (a chain of amino acids, the building blocks of proteins, amongst other things). In the skin, this peptide is only found in melanocytes, however similar peptides are also found in our external environment, including in certain foods

T-cell immune reactions are triggered by amino acid patterns. This means that peptides sharing the same amino acid pattern as the peptide in melanocytes may trigger the same psoriasis-inducing reaction. In this study the researchers used a database to find peptides which have the same amino acid pattern as seen in melanocytes. These environmental candidates were then tested for their ability to trigger the reaction that causes psoriasis.

In this way they identified a variety of peptides in proteins from human skin and gut microbiomes, the chlamydia bacterium, and from foods such as wheat, coffee, apples, and spinach, all of which brought on this reaction.

The identification of potential triggers may help to develop strategies for psoriasis prevention in individual patients, these patients and their triggers would have to be verified in clinical practice.

Dr Jörg Prinz, from the Ludwig-Maximilian-University of Munich, one of the authors of the study, said:

“The aim of our study was to get a better understanding the factors at the molecular level that translate the genetic predisposition for psoriasis into the actual manifestation of the disease. Essentially, why do only some of the people who have a genetic tendency towards psoriasis have it, whilst others don’t? Our results show that lifestyle factors may be important.

“These results provide initial evidence that environmental factors may serve as potential triggers for this specific autoimmune response in psoriasis. It may also have implications in understanding how environmental factors affect the risk of autoimmune diseases in general.”

Matthew Gass of the British Association of Dermatologists said:

“This is very interesting research that has the potential to expand our understanding of the mechanisms that drive the development of psoriasis, but also could have practical benefits for potential patients.”

“What we need now is more research that can build on these findings. In an ideal world we would have ways of identifying triggers in individual patients, to help them avoid them.”

-Ends-
Notes to editors:

For more information please contact the media team: comms@bad.org.uk, 0207 391 6084. Website: www.bad.org.uk

The 8th International Congress of Psoriasis from gene to clinic is taking place in London from Thursday 30th November to Saturday 2nd December 2017. For more information, visit: www.psoriasisg2c.com

About us:
The British Association of Dermatologists is the central association of practising UK dermatologists. Our aim is to continually improve the treatment and understanding of skin disease. For further information about the charity, visit www.bad.org.uk 

Environmental antigens may trigger HLA-C*06:02-mediated autoimmunity in psoriasis

Y. Arakawa, A. Arakawa, S. Vural, A. Galinski, S. Vollmer and J. Prinz 

Department of Dermatology, Ludwig-Maximilian-University of Munich, Munich, Germany 

Psoriasis vulgaris is a human leucocyte antigen (HLA)-C*06:02-associated T-cell-mediated autoimmune skin disease that develops upon epidermal infiltration and activation of CD8+ T cells. Environmental and lifestyle factors may trigger disease onset, and account for approximately 30% of disease risk. Using a V?3S1/V?13S1 T cell receptor (TCR) from a pathogenic epidermal psoriatic CD8+ T-cell clone we have recently shown that in psoriasis HLA-C*06:02 mediates an autoimmune response against melanocytes, and we had identified a peptide from ADAMTS-like protein 5 as a melanocytic antigen. In this study, we aim to identify environmental factors at the molecular level that translate the genetic predisposition into disease manifestation. TCRs are polyspecific. They do not recognize specific antigens but react against HLA-presented peptides sharing a particular amino acid pattern specific to this TCR. After defining the amino acid pattern recognized by the V?3S1/V?13S1 TCR in the context of HLA-C*06:02 by peptide library screening we searched environmental proteomes for peptides sharing this particular pattern. Environmental candidate epitopes were tested for their ability to ligate the ADAMTSL5-reactive V?3S1/V?13S1 TCR when presented by HLA-C*06:02. This way we identified a variety of peptides contained in proteins from human skin and gut microbiomes, from infectious pathogens including Chlamydia trachomatis, and from foods (wheat, coffee, apple and spinach) that ligated the V?3S1/V?13S1 TCR. These results provide the first evidence of environmental antigens that may serve as potential triggers of the melanocyte-specific autoimmune response in psoriasis. They suggest that exposure to environmental antigens may drive priming and expansion of potentially self-reactive T cells and thus initiate autoimmune disease responses. Through the unbiased analysis of a pathogenic psoriatic TCR our data furthermore may have important implications in understanding how environmental factors affect the risk for autoimmune diseases in general.
  

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Caffeine can reduce inflammation in patients with eczema and psoriasis

Doctors at the Psoriasis: From Gene to Clinic International Congress in London have today presented their findings on the use of caffeine to reduce inflammation in patients with atopic dermatitis and psoriasis – two of the most common chronic skin conditions worldwide.

Their review has found that caffeine acts in a number of ways to improve symptoms of inflammation, making it an effective therapy to complement primary treatments for eczema or psoriasis, namely topical corticosteroids.

The research has suggested several ways in which caffeine reduces inflammation. Conditions such as atopic dermatitis and psoriasis result in decreased levels of a molecule called cyclic adenosine monophosphate (cAMP) in skin cells*. These cAMP molecules act as messengers within the cells, and low levels have been found to increase inflammatory pathways and suppress anti-inflammatory ones. Caffeine has been shown to inhibit the enzyme that degrades cAMP, phosphodiesterase, and so raise the levels of this molecule back to normal and counter the inflammation.

Caffeine also plays a helpful role in cell death to reduce inflammation. There are two ways in which cells can die: apoptosis is usually the beneficial process by which a cell is programmed to die in response to certain triggers, while necrosis is when the cell dies due to external forces, such as injury or infection – and this can lead to further inflammation in the body. Caffeine encourages damaged cells to promptly trigger apoptosis and has effects which prevent cells from dying prematurely from necrosis when damaged by oxidative stress (the harmful effect of free radicals when not enough antioxidants are present to fight them off). These properties, in addition to further anti-oxidising (free radical fighting) effects of the caffeine’s metabolites, may also reduce inflammation.

The researchers, from Alfaisal University, Riyadh and Mount Sinai Health System, New York, emphasised that although oral intake may have a positive effect, a topical approach is much more likely to produce greater improvement. This would involve adding caffeine to steroid creams and then applying the cream to the skin.

Dr Mais Alashqar, one of the researchers, said:

“This review on the potential for caffeine to reduce inflammation in skin disease patients has been a long time coming. Initial studies in the 1970s first demonstrated this, but 40 years later this knowledge has, in a sense, faded. We still don’t add caffeine to topical steroids that patients use daily. It is a simple step that could significantly benefit the many patients around the world that suffer from inflammatory skin conditions like eczema or psoriasis. We hope that our review will help bring this knowledge back into the consciousness of doctors and patients.”

Matthew Gass of the British Association of Dermatologists said:

“Research such as this review is important. Such is the scale of the scientific literature that is available to modern experts that it is easy for some of it to not to be acted upon, or even forgotten. In the case of using caffeine in steroid creams, it seems that even if it has not been entirely forgotten there is certainly room to research this option in more depth. There are so many patients out there who are struggling to manage inflammatory skin conditions and so research avenues such as this should be thoroughly explored.”

-Ends-

Notes to editors:

* Keratinocytes and leukocytes specifically

Psoriasis is a common inflammatory skin disease affecting two per cent of the population. It occurs equally in men and women, can appear at any age, and tends to come and go unpredictably. Atopic eczema is a very common skin condition due to skin inflammation. It may start at any age, but the onset is often in childhood. One in every five children in the UK is affected by eczema at some stage. It may also start later in life in people who did not have atopic eczema as a child.

For more information please contact the media team: comms@bad.org.uk, 0207 391 6084. Website: www.bad.org.uk

The 8th International Congress of Psoriasis from gene to clinic is taking place in London from Thursday 30th November to Saturday 2nd December 2017. For more information, visit: www.psoriasisg2c.com

About us:
The British Association of Dermatologists is the central association of practising UK dermatologists. Our aim is to continually improve the treatment and understanding of skin disease. For further information about the charity, visit www.bad.org.uk

Caffeine in the treatment of atopic dermatitis and psoriasis: a review

M. Alashqar1 and N. Goldstein2 

1Alfaisal University, Riyadh, Saudi Arabia and 2Mount Sinai Health System, New York, NY, U.S.A. 

Atopic dermatitis (AD) and psoriasis are inflammatory skin diseases. AD is characterized by immune dysregulation and barrier impairment, while psoriasis shows immune dysfunction and resultant keratinocyte hyperproliferation. Caffeine has shown efficacy in ameliorating the symptoms of both diseases, but it is not conclusive through which pathways. The aim of this study was to provide a detailed discussion of the available work on this topic, as well as known modes of action of caffeine that are relevant to these two conditions. After an extensive review of the literature, we found that both diseases have decreased intracellular cAMP levels in cutaneous leucocytes, so it is very likely that being a methylxanthine, and hence a phosphodiesterase inhibitor, caffeine raises intracellular cAMP levels, which suppresses inflammatory pathways and potentiates anti-inflammatory ones. Moreover, caffeine is known to be an ATR (ataxia-telangiectasia mutated) kinase inhibitor and an ATM (ATM- and Rad3-related) kinase inhibitor, which promotes prompt apoptosis of damaged cells. It was also found to have antinecrotic effects in cells damaged by reactive oxygen species (ROS). These proapoptotic and antinecrotic properties may also be reducing the inflammation. Finally, caffeine’s metabolites have shown antioxidizing effects against ROS, which certainly would reduce inflammation caused by lipid peroxidation, DNA damage and organelle destruction. We find that caffeine acts in a number of ways to improve symptoms of inflammation and that it is an effective adjunct to therapy in AD and psoriasis.
  

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