Could basement membrane alterations, resembling micro‐wounds at the dermo‐epidermal junction in psoriatic non‐lesional skin, make the skin susceptible to lesion formation?

Abstract

Current data suggest that tissue microenvironment control immune functions. Therefore, understanding the tissue environment in which immune activation occurs will enhance our capability to interfere with abnormal immune pathology. Here, we argue that studying the constitutively abnormal functions of clinically uninvolved psoriatic skin in patients with plaque type psoriasis is very important to better understand psoriasis pathobiology, because non‐lesional skin provides the tissue environment in which the psoriatic lesion develops. A key question in psoriasis is what initiates the abnormal, uncontrolled immune activation in the first place and the answer may lie in the skin. In light of this concept, we summarize abnormalities at the dermal‐epidermal junction region which shows a special “non‐healing‐like” micro‐wound phenotype in the psoriatic non‐lesional skin that may act as a crucial susceptibility factor in the development of the disease.

Relationship between Psoriasis and Prevalence of Cardiovascular Disease in 88 Japanese Patients

“…On the other hand, in Western countries, PsA is associated with a greater rate of CVD complications [13]. These findings were similar to our findings in the Japanese population.…”

Stress-Related Regulation Is Abnormal in the Psoriatic Uninvolved Skin

“…The pathomechanism of this multifactorial disease is not fully understood and with current therapeutic possibilities, recurrence of symptoms cannot yet be prevented [ 3 ]. It is noteworthy that in psoriasis the healthy-looking uninvolved skin has several cellular and extracellular alterations that make the skin susceptible to the development of symptoms [ 4 ]. Therefore, the psoriatic uninvolved skin of patients provides tissue samples where we can search for alterations relative to healthy skin.…”

Nod-Like Receptors in Host Defence and Disease at the Epidermal Barrier

“…The development of psoriatic plaques is caused by the interaction of keratinocytes with these infiltrating immune cells, leading to uncontrolled keratinocyte proliferation and dysfunctional differentiation. However, keratinocytes can have an initiating role in disease development [ 65 , 66 ]. NOD2 is also highly expressed in psoriatic skin [ 67 ] and Nod2 –/– mice are more susceptible to imiquimod-induced psoriasiform disease, suggesting an inflammation-limiting role of Nod2 in murine disease.…”