Psoriasis is not an autoimmune disease?

Abstract

The concept that psoriasis is an autoimmune disease needs to be questioned. The autoimmune label has been based on molecular mimicry between streptococcal and keratin proteins and the existence of homologous peptides between these proteins. However, it is only peripheral blood CD8, and not CD4, T lymphocytes that respond to the homologous peptides. This ignores the fact that it is CD4 T cells which are necessary to initiate psoriasis. Recent studies on skin bacterial microbiota have found a variety of bacteria in both normal skin and psoriatic lesions. In biopsy specimens, the most common phylum was Firmicutes and the most common genus streptococcus in both psoriasis and normal skin. The innate immune system is activated in psoriasis, and recent genetic findings have shown the majority of susceptibility loci are associated with innate immunity. There is a known clinical relationship between both Crohn's disease (CD) and periodontitis, and psoriasis, and patients with psoriasis share mutations in some innate immunity genes with individuals with CD. It is now accepted that CD is due to a breakdown of immune tolerance (dysbiosis) to bacteria in the intestine. These findings suggest that psoriasis is initiated by an abnormal response to bacteria in the skin due to genetic factors.

Interleukin-22 and Its Correlation with Disease Activity in Plaque Psoriasis

“…It has been known for a long time that patients with CD and their first-degree relatives have increased risk of developing psoriasis and vice versa (Egeberg et al 2016). Very recently, it was proposed that similar to CD (Øyri et al 2015), psoriasis could be a result of breakdown of immune tolerance (dysbiosis) to cutaneous bacteria (Fry et al 2013, 2015). According to the aforementioned theory, genetic abnormalities affecting especially innate immune response facilitate initiation of inflammatory response to cutaneous microbiota (Skroza et al 2013; Terziroli Beretta-Piccoli et al 2017; Vlachos et al 2016; Wu et al 2012).…”

Microbial elements as the initial triggers in the pathogenesis of polymorphic light eruption?

“…), and in turn, these AMPs could contribute to the induction of PLE. Similarly, damage to commensals may give rise to commensal‐associated molecular patterns (CAMPS) (S18, S19), resulting in microbial signals, altering the skin's microbial landscape and contributing to abnormal immune responses in inflammatory diseases such as psoriasis and beyond. In this regard, studies indicate that photoprovoked PLE patients show an upregulation of certain AMPs (S20).…”

Unexplored diversity and strain-level structure of the skin microbiome associated with psoriasis

“…13 Five types of psoriasis have been described with chronic plaque psoriasis (psoriasis vulgaris) by far the most common form responsible for approximately 90% of cases. 13 Most of the genetic loci predisposing an individual to psoriasis have been identified by genome-wide linkage analysis and are involved with both acquired and innate immunity, 13, 14 and it has been demonstrated that an aberrant immune response to antimicrobial peptide LL-37 is likely involved in psoriasis immunopathogenesis. 15 It is becoming increasingly evident that psoriasis has a microbial component and that infections may cause disease exacerbation.…”