In recent years, it is believed that the susceptibility genes of psoriasis are gradually identified; smoking, alcohol consumption, improper diet, mental stress and infectious factors may be important environmental factors that induce and aggravate psoriasis; autoimmune inflammation and new angiogenesis are the pathological basis of the disease, and cytokines and chemokines involved in mediating and maintaining the inflammatory network are gradually elucidated. 1.Psoriasis-related genes Psoriasis is a polygenic genetic disease, and a variety of genes are associated with the development of psoriasis. Human leukocyte-associated antigen (HLA): located in the human chromosome 6p21.3 region, is the first genetic factor found to be associated with psoriasis. Among them, HLA-Cw*6 is the most relevant allele for psoriasis, and HLA-Cw*6 and -B*57 may be susceptibility gene markers for psoriasis. HLA-DRB 1 *0701, HLA-DQA1 *0201 and DQB 1 *0303 are expressed in type I psoriasis. The allele β of octameric transcription factor 3B was more closely associated with psoriasis vulgaris than HLA-Cw*0602. cDSN (corneodesmosin) gene: located at 160 kb from the telomeric end of HLA-C on 6p21, is expressed in differentiated keratin-forming cells and encodes a protein homologous to a component of the granulosa cell layer. ameen et al. found that Caucasian psoriasis patients were closely associated with CDSN allele 5 (+619T, +1240G, +1243C) and HLA-Cw6. The human endogenous retroviral K deoxyuridase (HERV.KdUTP) gene: a member of the tandem repeat virus HML-2 family and a susceptibility gene for psoriasis, is expressed in normal skin, lesions and peripheral blood in psoriasis. p63 gene: this gene encodes six different proteins of the homologous tumor suppressor protein factor p53 that play a key role in the normal development of ectoderm-derived structures. The p63 gene plays a key role in the normal development of ectoderm-derived structures. KIR gene: The relationship between the KIR gene and psoriasis susceptibility is extremely complex and the mechanism needs to be further investigated. 2. Autoimmunity 2.1 Major cells involved in the development of psoriasis The cells involved in the immune response at the site of psoriasis lesions mainly involve lymphocytes, keratinocytes, antigen-presenting cells, etc., while cytokines and chemokines are the hubs of the interaction between various immune cells. In psoriasis, the natural immunity mediated by antigen-presenting cells and natural killer cells and the acquired immunity mediated by T cells are disrupted, and cytokines, chemokines and growth factors are produced under the synergistic effect of the two, which leads to the infiltration of inflammatory cells in the lesion and the stepwise amplification of the inflammatory network, eventually leading to the development of the infiltrative scaly erythema characteristic of psoriasis. The keratinocytes (KC) are involved in the local immune response by secreting a variety of cytokines, and are both important cytokine producers and targets for the action of many cytokines. Langerhans cells (LC): LC are closely related to the occurrence, development and prognosis of psoriasis. The mature LC plays an important role in the immune response in psoriatic lesions. Mast cells: A certain number of mast cell aggregates are present at the site of inflammatory lesions in psoriasis. The antiallergic drug cetirizine can significantly reduce the fibrin-positive mast cells in psoriasis lesions and improve the efficacy of clinical treatment of psoriasis erythematous lesions, suggesting that antihistamines play a pluripotent and immunopharmacological role in the pathogenesis of psoriasis, which may be exerted by regulating mast cells.6 Other cells: HLA-DR, CD1α, CD16 The expression levels of HLA-DR, CD1α, CD16, CD57, TNF and ICAM-1 in psoriatic lesions decreased significantly or even disappeared after treatment. This suggests that dendritic cells and natural killer cells play an important role in the pathogenesis of psoriasis. In addition, peripheral blood leukocyte counts, especially neutrophil counts, were increased and peripheral blood erythrocyte counts were decreased in psoriasis patients. 2.2 Major inflammatory mediators IL-1: an important regulator of plaque psoriasis development. mRNA levels of IL-1α were reduced in a small proportion of psoriasis patients, while IL-1β mRNA levels were significantly increased. IL-10 is secreted by Th2 cells and induces the differentiation of Th0 cells into Th2 cells, thus promoting the production of Th2 cytokines and inhibiting Th1 cytokines; IL-10 also reduces the level of IL-8/CXCR2 in epidermal cells, thus normalizing the abnormal proliferation and differentiation of keratinocytes. IL-17: It inhibits the secretion of TNF-γ-induced chemokine CCL27 and its mRNA expression and NF-kappaB activation in keratinocytes. By inhibiting the production of CCL27, T cell-derived IL-17 was able to alleviate T cell infiltration in skin inflammation. In addition, IL-17 alone or in synergy with TNF-α increased COX2 mRNA levels and COX2 protein content in keratinocytes, enhanced COX2 initiation factor activation and COX2 mRNA stability. IL-22: produced from and activated by Th1 and NK cells, mainly acts on epithelial cells and may play an important role in natural immunity and epithelial tissue regeneration. IL-22 can improve the body’s antimicrobial defense and limit cell differentiation by regulating gene expression. The elevated IL-22 in psoriatic epidermis was associated with the upregulation of S100A7, S100A8, S100A9 and MMP1 expression.IL-23: IL-23 was significantly increased in psoriatic lesions. Low levels of IL-23 protein heterodimers were detected in the supernatant and lysate products of KCs from both lesions and non-lesioned areas of psoriasis patients in culture. 5-Hydroxytryptamine (5-HT): 5-HT was significantly elevated in spiny cells, sweat cells, sebaceous cells and hair roots of lesions in patients with progressive psoriasis, and was not significantly elevated between pustular psoriasis and psoriasis vulgaris. There was no significant difference between pustular psoriasis and psoriasis vulgaris. 3, environmental factors Smoking can stimulate neutrophil activation and release peroxidase, peroxide and enzyme systems play an important role in the pathogenesis of psoriasis, which can change the oxidative metabolism of phagocytes and increase the oxidative metabolism of inflammatory reactions and the release of enzymes, leading to the occurrence or aggravation of skin lesions. In addition, many harmful components in tobacco smoke can affect the deformability of red blood cells, reduce the ability of hemoglobin to bind oxygen and lead to vascular endothelial cell damage. Alcohol consumption can stimulate or aggravate psoriasis. Alcohol can cause vasodilation and increase vascular permeability, which facilitates neutrophil outflow and infiltration into the epidermis (rash); it can also increase the content of arachidonic acid, the precursor of biologically active substances such as prostaglandins and leukotrienes in the blood, which in turn inhibits adenylate cyclase in the epidermis and reduces cAMP and increases cGMP, leading to rapid proliferation of epidermal cells. Scarpa et al. reported that in patients with progressive psoriasis vulgaris and arthritic psoriasis without abdominal clinical symptoms, colonoscopy revealed redness and congestion of the colonic mucosa in 40% of patients, mucosal edema and granulomatous hyperplasia in 20% of each patient; multisite colonic mucosal biopsies revealed microstructural changes in all patients: small focal plasma cell and lymphocyte Infiltration, lymphoid follicle formation, active inflammation, and glandular atrophy were observed in all patients. In addition, the low incidence of psoriasis in Africa is explained by unique dietary factors (maize is a major component of their diet) in addition to genetic factors. Michaelsson et al. reported the presence of anti-gluten antibodies IgA or/and IgG in the serum of 16% of patients with common psoriasis, who showed significant clinical improvement after 3 months of a simple gluten-free diet, and The previously increased number of Ki67+ cells in the lesions was significantly reduced and the overexpression of transglutaminase was significantly decreased. Another controlled study showed that a low-fat diet for 4 weeks resulted in a significant improvement in psoriasis and a decrease in blood lipids. Psychological stress can trigger and exacerbate psoriasis, suggesting that neuroendocrine factors play a role in the pathogenesis of psoriasis. Patients with psoriasis often have different degrees of depression and anxiety, which can affect the central nervous system and lead to the occurrence and development of the disease through the regulation of the network of chemical information molecules and receptors common to the three major systems: neurological, endocrine and immune. It has been confirmed that the level of α-endorphin is obviously increased and related to the severity of psoriasis, and the neuropeptide may induce the change of immune cell subpopulation through some cytokines, and then secrete immunomodulatory cytokines. 4, viral infection Some viral persistent infection may have a certain relationship with psoriasis. Adenovirus has a certain affinity for keratin-forming cells, and after infection, it can make the cells enter the S phase from the quiescent phase, and adenovirus E1A and E1B proteins can inhibit apoptosis, so that the affected T cells or keratin-forming cells are in an activated state, which becomes the reason for the persistence of psoriasis. Human microvirus B19 (PVB19) is a single-stranded DNA virus that can cause various clinical symptoms. Yazici et al. demonstrated that PVB19 DNA is mainly associated with antibody IgG, suggesting the existence of subclinical activation of PVB19 in psoriasis patients and that PVB19 infection may play an important role in the pathophysiology of psoriasis. Human endogenous retroviruses (HERVs) are genomic traces left by the infestation of active retroviruses in ancient times, and are part of the normal human genome. Moles et al. reported that the detection rate of HERVs sequences in psoriasis lesions was significantly higher. 5. Neoangiogenesis Microangiogenic abnormalities are closely related to the occurrence, persistence and recurrence of psoriasis and play an important role in the pathogenesis of psoriasis. Under the effect of endogenous angiogenesis inhibitors, the normal skin microvascular system is in quiescence and no proliferation occurs; however, in psoriatic lesions, the original balance is disrupted by the increase of pro-angiogenic factors, which leads to abnormal proliferation of microvessels. Vascular endothelial growth factor (VEGF), which promotes vascular neovascularization, was expressed at an increased level in plaque psoriasis lesions, and VEGF+405 and -460 were associated with the progressive phase of psoriasis. On the basis of genetic factors, various environmental factors induce abnormalities in the body’s neuro-endocrine system and deregulation of various immune cells in the skin, leading to the release of inflammatory cytokines, which further impairs the innate and acquired immune function of the body, and more inflammatory cytokines are released to induce relevant inflammatory cell infiltration. This cascading amplification of the neuro-endocrine-immune-inflammatory network ultimately leads to the formation and maintenance of the chronic inflammatory process unique to psoriasis. Various factors such as infection, trauma, and trauma may trigger the unique immune-inflammatory mechanisms of psoriasis through a common pathway (neuroendocrine-immune). However, many aspects of the pathogenesis of psoriasis are still unclear: for example, which specific neuroendocrine changes are associated with psoriasis? What are the mechanisms by which the neuroendocrine system regulates immune cells in the skin? It is believed that these links will be elucidated one by one as research progresses.