Psoriasis represents a chronic inflammatory skin disorder and etiologically results from immune system dysregulation. Across the globe, the condition afflicts approximately 125 million individuals [1]. Previous studies have demonstrated regional and age-related disparities in psoriasis incidence, with the prevalence being higher in areas farther from the equator [2]. Some factors, such as stress, infections, and certain medications can trigger or exacerbate this condition [3]. Clinically, psoriasis manifests as thick, red, scaly plaques on the skin and is accompanied by pruritus in 60–90 % of patients [4]. Some cases characteristically had pustular and erythrodermic eruptions. Pathophysiologically, the psoriasis involves accelerated multiplication of keratinocytes (KCs) and infiltration of immune cells, especially T cells, in affected skin samples [1].

In fact, psoriasis is more than a skin condition, which is a systemic inflammatory disease associated with a number of comorbidities. Clinical observations have revealed that incidences of anxiety, depression, sleep disorders, impaired adjustment, and even suicidal tendency are higher in psoriasis patients than in healthy people [3,[5], [6], [7], [8]]. These comorbidities severely affect patients’ quality of life. Furthermore, individuals with pre-existing mental disorders appear more susceptible to psoriasis and are more likely to trigger or exacerbate psoriasis. This suggests a potential bidirectional interaction between the skin and the brain [5,8], and we provide a summary of the primary psychiatric disorders that are commonly found in individuals with psoriasis, as well as the typical psychiatric disorders predisposing psoriasis (Table 1). Animal experiments also demonstrated that imiquimod-induced psoriasis-like mouse model exhibited changes in brain regions compared to controls, along with anxiety-like and social avoidance-like behaviors [9]. In contrast, mice that were initially under stress exhibited increased psoriasis-like epidermal hyperplasia [10]. Nonetheless, results of some studies suggested otherwise. Several experiments failed to reveal any association between psoriasis and cognition or dementia [11,12]. Since the available results are not entirely consistent, further research is necessary to validate them.

With regard to the connection between the skin and the brain, the concept of the ‘skin-brain axis’ has been proposed [46,47]. As for the specific mechanisms, the link is substantiated by the involvement of typical T cell subsets and cytokines in the pathogenesis of both psoriasis and mental disorders [47]. Along this axis, T cells and related cytokines may disrupt and cross the blood-brain barrier (BBB) directly [48], or interact with the hypothalamic-pituitary-adrenal axis (HPA axis) and the sympathetic nervous system (SNS) [[49], [50], [51], [52]]. This led to the hypothesis that the psoriasis and mental comorbidities might, engage in a bidirectional interplay, with skin inflammation potentially leading to psychiatric comorbidities, in turn, exacerbating skin inflammation [46].

Understanding the intricate interaction between the skin and the brain is crucial to prevent the development and progression of these comorbidities [53], work out interventions that avert mutual exacerbation, and ultimately enhance the quality of life for affected individuals. Research efforts are urgently needed to look into this complex relationship and further develop efficacious treatments and holistic care for them.

In this review, we summarized several pivotal T cell subsets and associated cytokines involved in the skin-brain axis, along with the essential pathways facilitating communication between the skin and the brain, with attempt to enhance our understanding of the relationship between psoriasis and mental disorders.