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Thursday, June 2, 2011

Psoriasis and atopic dermatitis: The same, only different

In the May issue of JACI, Guttman-Yassky et al. (J Allergy Clin Immunol 2011;127:1110-1118), in part 1 of a 2-part review, covered the clinical and pathological similarities and differences between psoriasis and atopic dermatitis (AD) with AD as the point of reference. They finish up in this month’s issue (J Allergy Clin Immunol 2011;127:1420-1432) with a broad discussion comparing the immune phenotypes and therapies for AD and psoriasis.

In part 1, Guttman-Yassky et al. pointed out that psoriasis and AD both present with defects in skin barrier function, skin lesions infiltrated by increased numbers of T cells and dendritic cells and upregulation of epidermal proliferation genes. They note that the chronic phase of AD is more similar to psoriasis than the acute phase. There are distinct differences though. AD patients are susceptible to bacterial and viral skin infections, which is not true for psoriasis patients. Also, AD skin is characterized by decreases in keratinocyte differentiation, cornification, moisture and lipid content. Though lipid depletion is also observed for psoriasis, it is characterized by increased differentiation and cornification. Cytokine milieu in AD is dominated by TH2 cells, while psoriasis is associated with TH1 and TH17 cytokines. Additionally, AD is associated with structural protein anomalies (e.g., filaggrin dysfunction) that are not observed in psoriasis.

The authors discuss in part 2 how the disorders were thought to be mediated by polarized T helper cell responses with TH2 dominance seen in AD; however, this simple dichotomy did not account for all observations, such as hyperkeratinization, seen in chronic AD. They point out that the discovery that TH17 and T22 cells affected epidermal activation eventually led to a new working model wherein psoriasis is mediated by TH1 and TH17 immunity, and AD is mediated by TH2 and T22 cell effects. Production of anti-microbial peptides (AMP) is known to be compromised in AD compared to psoriasis. This was originally attributed to the TH2 environment, but the authors comment that IL-17 deficiency as well as excessive TH2 cytokines can explain the decreased AMP production found in AD. Guttman-Yassky et al note that the impaired AMP production would explain increased susceptibility to skin infections in AD. In contrast, psoriasis is characterized by increased AMP production. The authors also discuss basic differences between AD and psoriasis with regard to differences in dendritic cell populations, AD-associated eosinophilia, barrier defects and inflammation, and mast cell production of interferon gamma (IFN-γ) in psoriasis.

Guttman-Yassky et al. finish up part II with a discussion of the prognosis and intervention for psoriasis and AD. Unlike AD, they note that active psoriasis can be completely resolved and treatment time is short. The authors comment that, in spite of their differences, both AD and psoriasis share epidermal hyperplasia, aberrant immunity, and skin barrier anomalies. This would suggest that immune-based strategies to correct barrier defects that have been developed for psoriasis might be effective for AD. Guttman-Yassky et al. detail current AD treatments and make a case for psoriasis therapies as intervention for AD.

Tell us what you think. Please feel free to post your own comments and/or predictions below.

9 comments:

  1. I don't know, there is much different option to try to heal your symptoms of psoriasis, but from your text I'm under impressions P it's not so dangerous disease, I'm not saying it's dangerous but it's quite ugly and something now one would have to have.

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  2. Personally I think that all these skin disorders are sun related..... exacerbated by some other skin irratant. When a person is diagnosed with psoriasis...this is such a broad term. I believe any person can develope psoriasis if exposed to the right catalysts....I also believe that many people develope actinic dermatitis in concert with other skin irratants(atopic dermatitis) and are just lumped into the "psoriasis" heap. From my personal experience "psoriasis" is a normal natural response to "something"

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  3. Fighting psoriasis can be a lifelong battle to find the right cure for psoriasis for you and one of the ways to fight psoriasis is to make important lifestyle changes as well as use home remedies for psoriasis. It is important to not lose hope in the fight against psoriasis which can happen after trying various approaches that may have worked for someone else but fail to work for you. You just need to keep experimenting until you find the right psoriasis treatment that works for you.

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  4. Hello,

    I appreciate your idea here. Th17 lineage is a recently described subset of memory T cells that is characterized by its CD4+ status and its ability to make a constellation of cytokines including interleukin-17A, IL-17F, IL-22, and in humans, IL-26. Definitely it has a good content. Thank you for imparting more of your own thoughts...

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  5. This is very educational content and written well for a change. It's nice to see that some people still understand how to write a quality post!
    How to get rid of psoriasis

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