Interestingly, psoriasis is the only chronic inflammatory disease that has a strong association with HLA-C, and about two-thirds of the patients carry the HLA-Cw 0602 allele compared to 10 15 in the population at large. It is therefore tempting to argue that the priming of the effector and memory T cells that cause psoriasis, especially the guttate variant, may at least to some extent take place in the tonsils, which interestingly is the only mucosal lymphoid organ lined with stratified epithelium 28. There are five sub-types of psoriasis: plaque, guttate, inverse, pustular, and erythrodermic, with the most common sub-type being plaque psoriasis. As psoriasis is known to be a T-cell mediated disease, it has been proposed that certain T cells primed against streptococcal M proteins in the tonsils may cross-react with epitopes from human keratins to cause exacerbations of psoriasis (7). This patient cohort was enriched for cases in which tonsillitis may have served as a trigger of skin disease, as 9 of the 14 patients reported multiple episodes of acute tonsillitis and 8 of these patients had exacerbations of psoriasis during tonsillitis episodes. Interestingly, tonsillectomy has been reported to improve the extracutaneous and cutaneous manifestations of some of these PPP-associated disorders. Guttate psoriasis is characterized by the rapid and generalized development of many small papules, which resolve spontaneously in about half the cases, and progress to chronic plaque psoriasis in the rest.
Sufferers may experience itch, pain, and/or psoriasis-related nail disease and arthritis. Histological appearance of the chronic psoriatic plaque (d) reveals acanthosis (white arrow head), elongated epidermal rete ridges (two-headed arrow), and hyperkeratosis (black arrow head). T cells primed against streptococcal proteins in the palatine tonsils 5. Interestingly, and a key feature of chronic plaque psoriasis, is the normal appearing uninvolved skin immediately adjacent to psoriatic plaques of affected individuals. Several recent studies have demonstrated that uninvolved tissue may contain a unique signature of genes, that when activated may account for the conversion of uninvolved skin to involved plaque. However, given the myriad cell types known to participate in this conversion, isolation of a single triggering factor is unlikely (Figure 1). Guttate psoriasis is a form of psoriasis that often starts in childhood or young adulthood. Interestingly, in contrast to sub-cutaneous treatment, epicutaneously applied YopM did not enter systemic distribution, mainly remained in the epidermis, dermis, and subcutis, and couldn’t be found in local lymph nodes. In a particular embodiment, the YopM variant may also retain the property of full length YopM protein to allow translocation into the cytosol and/or nucleus of a target cell.
Figure 1 Clinical presentation of severe plaque psoriasis (A) and histochemical staining of a plaque biopsy (B) (A) Clinical presentation of a patient with severe plaque psoriasis, the commonest form of psoriasis. Combinations of functional changes associated with the variants of these genes could favour the early steps of the plaque-inducing immune response (Figure 2). These T-cells may be activated by resident APCs and keratinocytes in the dermis and epidermis respectively. The role of streptococcal infection in the initiation of guttate psoriasis. 0012 Guttate psoriasis is a form of psoriasis that often starts in childhood or young adulthood.
Lifting The Silver Flakes: The Pathogenesis And Management Of Chronic Plaque Psoriasis
Within each body site, the composition of the microbiome may change rapidly, but community features can remain constant for years 5, 6.