Japanese patients with psoriasis and atopic dermatitis show distinct personality profiles.

Personality and emotional factors are supposed to influence the course of skin diseases, such as psoriasis and atopic dermatitis. Few reports exist, however, showing distinct personality traits among patients with psoriasis, atopic dermatitis patients and healthy controls. The aim of the present study was to examine personality differences among psoriasis patients, atopic dermatitis patients and healthy controls in Japan. A total number of 51 psoriasis patients, 97 atopic dermatitis patients and 48 healthy individuals were enrolled in the study. Questionnaires of Yatabe-Guilford Personality Inventory were administered individually. These groups were evaluated by 12 dimensions of temperaments. According to the dimension scores, personality was defined as five groups. Atopic dermatitis patients showed significantly higher scores regarding temperaments of depression, feelings of inferiority, nervousness and lack of objectivity than psoriasis patients. Regarding a temperament of cyclic tendency and lack of cooperativeness, female atopic dermatitis patients showed significantly higher scores than female psoriasis patients. Regarding general activity, female atopic dermatitis patients showed significantly lower scores than those of female psoriasis patients. No significant difference in scores of temperaments of lack of agreeableness, rhathymia, thinking extraversion, ascendance and social extraversion were detected among psoriasis patients, atopic dermatitis patients and healthy controls. The personalities of male psoriasis patients were significantly different from those of atopic dermatitis patients and healthy controls. Female psoriasis patients showed a significantly different personality profile from that of atopic dermatitis patients, but not from healthy controls. Japanese psoriasis and atopic dermatitis patients show distinct personality profiles suggesting that specific a psychosomatic approach may be required during the treatment.

CD4+ T-cells from peripheral blood of a patient with psoriasis recognize keratin 14 peptide but not 'homologous' streptococcal M-protein epitope.

Psoriasis has been recognized as an immunologically mediated inflammatory skin disease that has been associated with group A, beta-haemolytic streptococcal infections. Notably cross-reactive autoimmune mechanism, which is mediated by T cells reacting to epitopes that are common to streptococcal M-protein and keratin, has been proposed in psoriasis. In order to investigate this possibility, peptides corresponding to M-protein and human epidermal keratin, which share some amino acid sequence between them, were synthesized and tested for their ability to stimulate T-cells of patients with psoriasis. Among five cases examined, we isolated a CD4(+) T-cell line that recognized the type I keratin (K14)(p168-181) when it was presented by the patient's HLA-DR molecules from a single psoriatic patient, whose MHC allele was HLA-A2/A26, -B27/B16, -DR4/DR8, -DQ8. Further analysis disclosed that the critical peptide recognized by the T-cell line was 10-mer keratin(p171-180) (DLRNKILTAT). However, corresponding M6 protein with homology to K14 did not stimulate the T-cell response and no evidence for cross-reactivity was obtained. The K14-responsive T cell line produced IFN-gamma, but little IL-4 when stimulated with irradiated autologous PBMC pulsed with this peptide. Thus, the finding that human epidermal keratin peptide is immunogenic in a psoriasis patient may provide the evidence that T lymphocytes play an important role in the pathogenesis of psoriasis as an autoimmune disorder participated with Th1 like cells. However, the keratin-responsive T cell line was detected in only one of five cases of psoriasis examined, suggesting that such T cell line appears to be not so popular in psoriatic patients. No evidence for cross-reactivity to streptococcal M protein also suggests that the contribution of streptococci may simply be inducing proliferation of various repertoire of T cells (including K14-responsive T cells) possibly through a superantigen-dependent process.