Pathogens or Damage-associated Molecular Patterns(DAMPs) Dendritic cell Macrophage Differentiation of T-hel per cells crake 诉FN气扎2 lL-23 ad and/or lL-1β n动w CD4+ T ceA Expansion Dermal yoT cells -C② 引见2 L17 van L-22 Keratinocytes TNF-a 000 3@33 Neutrophils Skin InflamnMED山C的
Langerhans’ce skin injun Epidermis Dermis Interleukin-lo, p TNF-a CLA T-cell activation, Microbial products positive cytoki Dermal T cell production brohl NF-KB-induced activation of endothelial adhesion molecules and chemokines Extravasation Chemokine Endothelial cell ouR Firm adhesion VCAM-1 CAM-1 E-selectin- Blood CLA-PSGL-1 Rolling 网-LFA1 Blood fl Tethering Chemokine VLA-4 CLA negative receptor -CLA-positive T cell Postcapillary venule
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Etiopathogenisis 4. Dysmetabolism CAMP metabolic block of arachidonic acid CGMP polyamines shortened epidermal cell transit time hyperplasia 5. others psychosis, neuroendocrine, climate, medicine, et al may induce or aggravate the disease
Etiopathogenisis 4.Dysmetabolism: cAMP metabolic block of arachidonic acid、 cGMP polyamines shortened epidermal cell transit time, hyperplasia 5.others: psychosis,neuroendocrine,climate,medicine , et al may induce or aggravate the disease
Clinical Presentation Erythematous papules/patches/plaques with SIlvery scales Symmetric Pruritic/ Painful( sometimes Pitting nails Arthritis in 10-20% of patients Exacerbate in winter improve in summer
Clinical Presentation Erythematous papules/patches/plaques with silvery scales Symmetric Pruritic/ Painful（sometimes） Pitting Nails Arthritis in 10-20% of patients Exacerbate in winter ,improve in summer
Clinical Types Psoriasis vulgaris PsoriasIs Arthropathica Psoriasis pustulosa Psoriasis erythrodermic
Clinical Types Psoriasis Vulgaris Psoriasis Arthropathica Psoriasis Pustulosa Psoriasis Erythrodermica