To date there are no reasonable explanations for

To date, there are no reasonable explanations for the successive distribution of a lesion over the skin cleavage lines. Some scholars believed that it might involve hematogenic dissemination of somehow activated leukocytes in its pathogenesis. Others suggested that Koebner\'s phenomenon may play a pivotal role in the pathogenesis of LPPI. We propose that stimulation of sweat, friction, a moist environment, or other external stimuli to the intertriginous area could be at least partially responsible. Accumulation of similar cases is necessary to further explore the profound characteristics of this rare presentation.
Funding/support The study was financially supported in part by the National Natural Science Foundation of China (grant no. 81173400).
Psoriasis is a common skin disorder that often flares upon exposure to external stressors. Although a number of therapeutic approaches are available for psoriasis, the preventive regimen is limited, largely due to its uncertain pathogenesis. Psoriasis has long been considered to be an immunologically initiated disorder based on bench and clinical evidence. Genetically, some psoriasis susceptibility loci are associated with immune function such as cytokine production and T cell differentiation; psoriasis and autoimmune diseases share some susceptibility energy metabolism (2p16 near the REL locus encoding c-Rel with rheumatoid arthritis; 5q33.1 encoding TNIP1 with systemic lupus erythematosus). Clinically, psoriatic lesions are featured by inflammation including increased cytokine expression, and both T cell and dendritic cell infiltration. However, some evidence suggests that psoriasis could be by a primary defect in epidermal permeability barrier function. This concept is drawn from: (1) psoriasis susceptibility genes, PSORS4 is located on chromosome 1q21, within the epidermal differentiation complex, which encodes numerous proteins required for epidermal differentiation and the formation of the cornified envelope, a structure that is critical for the permeability barrier; (2) psoriasis often occurs on the sites vulnerable to epidermal trauma, such as the extensors of the extremities and the scalp; (3) psychological stress, which compromises the epidermal permeability barrier, can trigger psoriasis, and psychological intervention has been considered as an approach to prevent and/or alleviate psoriasis; (4) higher prevalence of psoriasis in Caucasians than in Africans, the latter displaying a superior barrier; (5) Koebner phenomenon; and (6) improvement of epidermal permeability barrier function by occlusion alone can alleviate psoriasis. Although this “abnormal epidermal permeability barrier-driven” hypothesis can partially illustrate the pathogenesis of psoriasis, it is a fact that majority of psoriasis cases worsen or flare in low humidity seasons, not in high humidity, when psoriasis patients suffer from psychological stress, and/or when their skin is subjected to external trauma. Therefore, the pathogenesis of psoriasis is still a puzzle. However, our recent study along with other studies strongly suggest that psoriasis could be the result of genetic defects together with multiple epidermal function abnormalities, based on current knowledge about the regulatory role of epidermal function in skin. Among psoriasis susceptibility genes, PSORS4 at chromosome 1q21 region contains genes encoding epidermal differentiation complex, controlling loricrin, involucrin, filaggrin and small proline-rich protein transcription, all of which are critical structural proteins required for epidermal permeability barrier formation. In particular, deletion of the late cornified envelope 3B and 3C gene is strongly associated with psoriasis in Europeans, Americans, as well as in Chinese. In psoriatic patients, the lower expression levels of filaggrin, a protein of known importance for the barrier, and loricrin in uninvolved skin sites of psoriasis are likely to be attributable to the genetic defects. Pertinent to these genetic alterations, we recently found that epidermal permeability barrier recovery is delayed in uninvolved skin sites of psoriasis. Moreover, the uninvolved skin sites also display higher skin surface pH, possibly in part due to reduction of filaggrin. Furthermore, reduction of filaggrin can result in lower levels of natural moisturizing factor in the stratum corneum. Taken together, patients bearing psoriasis susceptibility genes could display multiple alterations of epidermal function.