Open research questions in Psoriasis: Treatment and Pathogenesis

What the literature leaves open

• This sparse evidence structure may reduce the precision of some estimates and the stability of SUCRA rankings, especially for dose-specific regimens. Short- term increases in adverse events do not necessarily predict long- term harm; however, they warrant careful monitoring, particularly when long-term safety data remain limited.

  Efficacy and safety of interleukin inhibitors in the treatment of moderate-to-severe plaque psoriasis: a systematic review and network meta-analysis · 2026 · DOI

• Per- and polyfluoroalkyl substances (PFAS) are persistent toxicants with immunological, metabolic and epithelial effects, but their relevance to inflammatory skin disease remains unclear.

  Integrative computational toxicology reveals PFOS and PFHxS associated inflammatory keratinocyte niches in psoriasis through exposure transcriptomics, single-cell spatial mapping and token-aware virtual perturbation · 2026 · DOI

• Metabolic immunology research on psoriasis and AD has made significant progress over the past decade, but numerous unresolved questions remain. First, spatiotemporal heterogeneity: scRNA-seq and spatial transcriptomics have revealed extreme heterogeneity in cell types and states within skin lesions (117, 231–233). We stress that single- cell and spatial methods have already mapped many disease-specific cellular states in both psoriasis and AD, including at the sebaceous gland (109, 118, 227, 229, 231); the open gap is therefore not whether such methods can find new cell states, but that these atlases remain almost entirely transcriptional and rarely report metabolic activity. The concrete priority is to overlay metabolic readouts onto the existing maps—by inferring pathway activity from transcriptomes (for example with scMetabolism or Compass), by spatial metabolomics and mass-spectrometry imaging, and by flux measurements on sorted lesional subsets—so as to build a genuinely metabolic, rather than merely transcriptional, single-cell atlas of the two diseases. Second, disease subtypes and personalization: AD has been subdivided into multiple phenotypes (intrinsic vs. extrinsic, Asian vs. Western, pediatric vs. adult) (132, 234–236); psoriasis also exhibits phenotypic stratification (237, 238); metabolic signatures may differ significantly across these phenotypes, which is critical for the precise application of metabolite-targeted drugs. Third, the interaction between the skin microbiome and me- tabolism: Staphylococcus aureus overgrows in AD lesions (239, 240), and its metabolites can directly influence epidermal metabo- lism and immunity; the skin microbiome in psoriasis also exhibits an imbalance (241, 242). The microbiome-metabolism-immunity triangle represents an important future research direction. Fourth, treatment integration: Combining metabolism-targeted drugs (metformin, statins, PPAR agonists, AhR modulators, JAK inhibitors) with traditional biologics (anti-IL-17, anti-IL-13) to achieve more profound disease control in certain refractory patients is a clinical question worthy of validation (243–245). Fifth, new metabolic targets: Novel metabolic pathways such as histone lactylation, serine-glycine metabolism, glutamine metabo- lism, and ferroptosis have garnered attention in inflammatory diseases (96, 246–249), but their roles in dermatology remain to be systematically explored. Sixth, multi-omics integration and computational/AI ap- proaches: psoriasis and AD are now among the most intensively profiled inflammatory skin diseases, and dedicated multi-omics comparisons of the two—integrating genomics, epigenomics, trans- criptomics, proteomics, and metabolomics—already exist (72). The value of the immunometabolic framework proposed here is that it offers a biological scaffold on which such multi-omics layers can be aligned: the shared-node/divergent-pathway model predicts, for each node, the direction in which a given omics readout should move in each disease, turning the comparison into a set of testable, quantitative hypotheses rather than parallel descriptive catalogues. Machine-learning and other computational methods are increas- ingly used in this setting—for lesion classification and severity scoring, for molecular subtyping and endotyping, and for bio- marker and drug-target discovery from high-dimensional omics data (250)—and are well suited to detecting metabolic patterns that distinguish the two diseases but are not apparent from any single assay. We see three concrete near-term applications: (i) supervised models that separate psoriasis from AD on the basis of lesional metabolic signatures and that flag the mixed or overlapping cases highlighted in Section 1; (ii) unsupervised clustering of metabolic- omics data to define metabolically distinct endotypes that may predict response to metabolism-directed drugs; and (iii) integrative models that link the systemic metabolic axis (Section 8), including the gut microbiome, to lesional metabolic state. Realising this will require harmonised, openly shared multi-omics datasets and careful external validation across skin phototypes and populations, without which model performance may not generalise.

  Divergent immunometabolic reprogramming in psoriasis and atopic dermatitis: a tale of two inflammatory skin diseases · 2026 · DOI

• Based on these observations, this review further proposes that “compartment-specific bidirectional calcium dysregulation” may represent an underrecognized pathological pattern in psoriasis, characterized by the coexistence of impaired epidermal calcium signaling and persistent immune calcium hyperactivation.

  Calcium signaling in psoriasis: from pathogenesis to therapeutic opportunities · 2026 · DOI

• Psoriasis is a chronic autoimmune skin disorder marked by IL-17 producing gamma delta T cell ({gamma}{delta}T17) and pruritus, but immunoregulatory roles of itch-inducing neurons in this context remain unclear.

  Sensory neurons shape γδ T cell effector programs to control Psoriasiform Inflammation. · 2026 · DOI

• Abstract Prurigo nodularis (PN) is a chronic, highly pruritic inflammatory skin disease that, until recently, was poorly understood.

  The evolving understanding of prurigo nodularis · 2026 · DOI

• In conclusion, psoriasis and Crohn’s disease are linked by partial immune convergence rather than by complete disease identity. Epidemiological, clinical, genetic, transcriptomic, spatial, and therapeutic evidence supports overlap at the level of selected upstream inflammatory programs, especially TNF-a signaling and IL-23-centered type 17 immunity. However, these shared programs are interpreted differently by skin and gut tissue ecologies, including barrier architecture, resident immune niches, microbial exposure, trafficking programs, and repair demands. This explains why similar upstream pathways can produce distinct tissue outcomes and divergent therapeutic responses. Therapeutically, TNF inhibition, IL-12/23 blockade, and selective IL-23 inhibition currently provide the strongest rationale for dual- organ compatibility in selected patients, whereas IL-17 blockade and paradoxical psoriasiform reactions illustrate the limits of directly translating shared immune pathways into interchangeable treatment targets. Therefore, coexisting cutaneous psoriasis and Crohn’s disease should not automatically be managed as a single shared phenotype. Treatment decisions should be guided by dominant organ burden, synchronized or discordant disease activity, prior biologic exposure, psoriatic arthritis status, and objective inflammatory assessment. Future studies should identify which patients with psoriasis and Crohn’s disease actually share a cross-organ inflammatory phenotype, rather than assuming that pathway overlap applies to all coexisting cases. This will require validated biomarkers, tissue-based profiling, longitudinal monitoring of skin and intestinal activity, and prospective studies specifically designed for patients with coexisting disease. This evidence is needed before shared immune biology can be used reliably to guide treatment in individual patients.

  Shared inflammatory architecture and therapeutic tensions between psoriasis and Crohn’s disease · 2026 · DOI

• Key references TNF inhibitors Block TNF-a, an upstream inflammatory amplifier linking myeloid activation, leukocyte recruitment, barrier inflammation, and tissue damage.

  Shared inflammatory architecture and therapeutic tensions between psoriasis and Crohn’s disease · 2026 · DOI

• Traditionally, systemic therapies are intro‑ duced at the moderate stage; however, clinical guidelines offer limited data to guide the selec‑ tion of first‑line systemic agents, especially as oral small molecules, such as DEU, become more widely available and may be favored for reasons including perceived convenience or patient pref‑ erence [20].

  Risankizumab versus Deucravacitinib in Adults With Moderate Plaque Psoriasis: 16-Week Results from the Phase 4 IMMpactful Trial · 2026 · DOI

• This work establishes BAI-NHG as a scientifically well- characterised, QbD-optimised, and SOEM-AI-designed topical platform for targeted immunomodulatory therapy in chronic plaque psoriasis, warranting further investigation through clinical phase evaluation.

  Quality by Design-Assisted Development and SOEM-AI DrivenOptimization of Baicalin-Loaded Thermoresponsive NanocompositeHydrogel for Targeted Immunomodulatory Therapy in ChronicPlaquePsoriasis · 2026 · DOI

• While research activity peaked in 2022, critical gaps persist: M2 macrophages and resolution remain understudied (1. 1% of publications); mechanisms translational research bridging preclinical and clinical domains is sparse (12%); and potential “paradigm lock-in” around IL-17 pathways may obscure alternative therapeutic targets.

  Macrophages in psoriasis: a bibliometric analysis of research trends, knowledge gaps, and future directions (2015–2024) · 2026 · DOI

• Although the level of evidence is limited due to the ethical and practical difficulties in conducting rigorous double‐blinde clinical trials to evaluate the efficacy of focal infection treatment, the treatment recommendations were determined through expert consensus based on extensive clinical experience accumulated in Japan, together with relevant basic research findings.

  Treatment Guidance for Palmoplantar Pustulosis 2022 · 2026 · DOI

• IL-17 and TNF pathways are well established in psoriasis, but the other mechanisms that keep the disease active and link it to systemic comorbidities are not yet fully understood.

  Systems Level Analysis of Gene, Pathway and Phytochemical Associations with Psoriasis · 2026 · DOI

• REFERENCES However, several limitations should be acknowledged. First, the observational design of our study precludes causal inference, and residual confounding may persist despite multivariable adjustment. Second, psoriasis was defined by self-reported physician diagnosis, which may have introduced exposure misclassification. In addition, information on psoriasis severity, disease duration, lesion extent, treatment and changes in psoriasis or CKM status during follow-up was unavailable; therefore, the observed associations should be interpreted as estimates for a heterogeneous psoriasis population rather than severity-specific effects. Third, the study population was derived from U.S. adults 1. Armstrong AW, Mehta MD, Schupp CW, Gondo GC, Bell SJ, Griffiths CEM. Psoriasis prevalence in adults in the United States. JAMA Dermatol 2021; 157: 940–946. https://doi.org/ 10.1001/jamadermatol.2021.2007 2. Armstrong AW, Read C. Pathophysiology, clinical presentation, and treatment of psoriasis: a review. JAMA 2020; 323: 1945– 1960. https://doi.org/10.1001/jama.2020.4006 3. Masson W, Lobo M, Molinero G. Psoriasis and cardiovascular risk: a comprehensive review. Adv Ther 2020; 37: 2017–2033. https://doi.org/10.1007/s12325- 020-01346-6 4. Takeshita J, Grewal S, Langan SM, Mehta NN, Ogdie A, Van Voorhees AS, et al. Psoriasis and comorbid diseases. J Am Acad Dermatol 2017; 76: 377–390. https://doi.org/10.1016/j. jaad.2016.07.064 5. Ndumele CE, Rangaswami J, Chow SL, Neeland IJ, Tuttle KR, Khan SS, et al. Cardiovascular-kidney-metabolic health: a Acta Derm Venereol 2026 9/9 J. Zhou et al presidential advisory from the American Heart Association. Circulation 2023; 148: 1606–1635. https://doi.org/10.1161/ CIR.0000000000001184 6. Vollset SE, Ababneh HS, Abate YH, Abbafati C, Abbasgholizadeh R, Abbasian M, et al. Burden of disease scenarios for 204 countries and territories, 2022–2050: a forecasting analysis for the Global Burden of Disease Study 2021. Lancet 2024; 403: 2204–2256. https://doi.org/10. 1016/S0140-6736(24)00685-8 7. Tsai MK, Kao JTW, Wong CS, Liao CT, Lo WC, Chien KL, et al. Cardiovascular-kidney-metabolic syndrome and all-cause and cardiovascular mortality: a retrospective cohort study. PLoS Med 2025; 22: e1004629. https://doi.org/10.1371/journal. pmed.1004629 8. Ostrominski JW, Arnold SV, Butler J, Fonarow GC, Hirsch JS, Palli SR, et al. Prevalence and overlap of cardiac, renal, and metabolic conditions in US adults, 1999–2020. JAMA Cardiol 2023; 8: 1050–1060. https://doi.org/10.1001/jamacardio. 2023.3241 9. McDonald CJ, Calabresi P. Thromboembolic disorders associated with psoriasis. Arch Dermatol 1973; 107: 918. 10. McDonald CJ, Calabresi P.

  Joint Relationship of Cardiovascular-kidney-metabolic Syndrome and Psoriasis with All-cause and Cause-specific Mortality in Adults: A Population-based Analysis · 2026 · DOI

• A major strength of this SLR is the inclusion of a broad range of study designs, encompass‑ ing both RCTs and real‑world evidence, which enhances the generalizability of our findings. The large number of studies with diverse patient populations, including those with LTBI and prior biologic exposure, provides a robust evidence base for evaluating TB risk with IL‑23i treatment. Additionally, inclusion of more recent studies ensures that our conclusions reflect the current state of clinical practice. The quality assessments we performed indi‑ cate that the included RCTs were well designed, with robust randomization procedures, adher‑ ence to intended interventions, complete and reliable outcome data, objective and appropriate outcome measurements, and transparent report‑ ing. Further, the assessed real‑world observation studies were generally well conducted, though some risk of bias may limit interpretation of results because of incomplete adjustment for confounders. Another strength is that this SLR, to the best of our knowledge, is the first to leverage gen‑ erative AI for assistance with title and abstract screening of the reports retrieved by our search. We consider it unlikely that this unduly influ‑ enced the studies that were ultimately included in the review because screening was performed in parallel with a human reviewer, and genera‑ tive AI could not independently exclude records. A quality check of 20% of the screening deci‑ sions was performed by an independent reviewer to validate the AI performance. This innova‑ tive approach may serve as a model for future systematic reviews, potentially improving effi‑ ciency and consistency in the screening process when combined with human oversight. Our study also has notable limitations. First, most studies included in this review only included a subset of enrolled patients with LTBI; therefore, risks for reactivation of LTBI could be underestimated in higher‑risk popula‑ tions. Second, although some information on TB outcomes in patients with LTBI who did not receive TB prophylaxis was identified, the num‑ ber of studies reporting data on this subgroup was limited. Thirdly, long‑term data beyond 5 years of follow‑up remain limited, and ongo‑ ing surveillance is warranted to further charac‑ terize the TB‑related safety profiles of IL‑23is. Fourthly, although AI‑assisted screening was implemented with independent human verifi‑ cation, the possibility of missed or misclassified records due to model limitations cannot be fully excluded, and relevant studies may have been omitted. Finally, this review did not systemati‑ cally include national pharmacovigilance data of patients with PsO or PsA treated with IL‑23is from Asian countries, so underreporting of TB events cannot be excluded. International (Singapore) Pte. Ltd provided funding for the journal’s Rapid Service Fee. Dermatol Ther (Heidelb) Data Availability. All data generated or analyzed during this study are included in this published article/as supplementary information files.

  New Tuberculosis Infection and Reactivation of Tuberculosis in Patients with Psoriasis or Psoriatic Arthritis Receiving IL-23 Inhibitors: A Systematic Literature Review · 2026 · DOI

• in meta-analyses of doi: 10.1136/bmj.d4002 for Ioannidis JP, Terrin N, and interpreting examining randomised controlled trials. BMJ. Jones DR, Lau J, et al. asymmetry (2011) 343:d4002. funnel plot 52. Stroup DF, Berlin JA, Morton SC, Olkin I, Williamson GD, Rennie D, et al. Meta- analysis of observational studies in epidemiology: a proposal for reporting Meta- analysis Of Observational Studies in Epidemiology (MOOSE) group. JAMA. (2000) 283:2008–12. doi: 10.1001/jama.283.15.2008 53. Szentkereszty-Kovács Z, Gáspár K, Szegedi A, Kemény L, Kovács D, Törocsik in psoriasis-from bench to bedside. Int J Mol Sci. (2021) 22:4987. D. Alcohol doi: 10.3390/ijms22094987 54. Taniguchi C, Narisada A, Ohshima Y, Inagaki K, Ito M, Ohashi W, et al. Interactive effects of sex and smoking on palmoplantar pustulosis: Japanese healthcare claim database study. J Invest Dermatol. (2024) 144:1651–3. doi: 10.1016/j.jid.2023.12.013 55. Tevik K, Bergh S, Selbæk G, Johannessen A, Helvik AS, A. systematic review of self- report measures used in epidemiological studies to assess alcohol consumption among older adults. PLoS ONE. (2021) 16:e0261292. doi: 10.1371/journal.pone.0261292 56. Wang L, Liu R, Tang Y, Ma Y, Wang G, Ruan Q, et al. Advances in psoriasis research: decoding immune circuits and developing novel therapies. Int J Mol Sci. (2025) 26:9233. doi: 10.3390/ijms26189233 57. Wang Q, Luo Y, Chen M, Zheng X, Zhu W, Shen M, et al. Comparison of behavioral risk factors and cardiometabolic comorbidities of psoriatic arthritis and psoriasis: a case-control study in Chinese patients. Ther Clin Risk Manag. (2021) 17:397–404. doi: 10.2147/TCRM.S307102 58. Wang X, Lai Y. Keratinocytes in the pathogenesis, phenotypic switch, and relapse of psoriasis. Eur J Immunol. (2024) 54:e2250279. doi: 10.1002/eji.202250279 59. Wei J, Zhu J, Xu H, Zhou D, Elder JT, Tsoi LC, et al. Alcohol consumption and smoking in relation to psoriasis: a Mendelian randomization study. Br J Dermatol. (2022) 187:684–91. doi: 10.1111/bjd.21718 60. Wells GA, Shea B, O’Connell D. The Newcastle-Ottawa Scale (NOS) for Assessing the Quality of Nonrandomised Studies in Meta-Analyses (2026). Available online at: http:// www.ohri.ca/programs/clinical_epidemiology/oxford.asp (Accessed January 28, 2026). 61. Wolk K, Mallbris L, Larsson P, Rosenblad A, Vingård E, Ståhle M. Excessive body weight and smoking associates with a high risk of onset of plaque psoriasis. Acta Derm Venereol. (2009) 89:492–7. doi: 10.2340/00015555-0711 62. Wu S, Cho E, Li WQ, Han J, Qureshi AA. Alcohol incident psoriatic of doi: 10.3899/jrheum.140808 J Rheumatol. in women. arthritis intake and risk (2015) 42:835–40. 63. Xu C, Doi SAR. Dose-Response Meta-Analysis. Meta-Analysis in Medicine and Health Policy. Singapore: Springer (2020). doi: 10.1007/978-981-15-5032-4_13 64. Zhang X, Wang H, Te-Shao H, Yang S, Wang F. Frequent use of tobacco J Dermatol. (2002) 41:659–62. and alcohol doi: 10.1046/j.1365-4362.2002.01595.x in Chinese psoriasis patients.

  Smoking, alcohol consumption, and psoriasis risk: a systematic review and dose-response meta-analysis of observational studies · 2026 · DOI

• should also be acknowledged. First, substantial between-study heterogeneity remained, particularly in the primary smoking analysis. Although heterogeneity was explored, univariable meta-regression showed that geographic region explained only a limited proportion of the observed variability (Wald χ 2 = 2.01, P = 0.3669; R2 ≈ 10.47%). Additional clinically relevant sources of heterogeneity likely included differences in outcome ascertainment, exposure assessment, and adjustment for major confounders such as body mass index, as well as mutual adjustment for smoking and alcohol exposure. More detailed quantitative exploration of these factors was limited by incomplete and non-uniform reporting across the included studies. Therefore, the pooled estimates should be interpreted as summaries of direction and overall magnitude rather than as precise effect sizes applicable across all study settings. a assumption, HRs Second, although ORs and RRs were considered approximately comparable under are low-incidence conceptually distinct time-to-event measures and may not be fully equivalent to cumulative risk estimates. We therefore performed additional stratified and sensitivity analyses for smoking and a limited alcohol-related supplementary analysis restricted to OR-based studies; however, some cross-measure comparability concerns remain. Accordingly, pooled estimates involving different effect measures should be interpreted with caution despite the supporting sensitivity analyses. Third, smoking and alcohol consumption are closely related index, cardiometabolic to socioeconomic status, body mass status, and psychological or behavioral factors, and residual confounding cannot be excluded despite multivariable adjustment in most included studies. The most plausible direction of residual confounding is overestimation of the observed associations, especially for alcohol, because alcohol consumption frequently co-occurs with smoking and other psoriasis-related risk factors. Given the modest alcohol effect size and attenuation after trim- and-fill adjustment, residual confounding could have a meaningful influence on the alcohol estimate. However, the exact magnitude of this bias could not be quantified because the included studies differed in exposure definitions, adjustment models, and reporting detail. Covariate adjustment patterns are summarized in Supplementary Table 9. Fourth, although the literature search was updated through December 18, 2025, no eligible studies published in 2025 met the inclusion criteria; thus, the quantitative synthesis ultimately reflected the available evidence through 2024. Fifth, we did not systematically search trial registries or other gray literature sources, which may have increased the possibility of publication or reporting bias. Finally, publication bias or small-study effects were suggested in some alcohol-related and residual-risk analyses, indicating that those findings should be interpreted cautiously.

  Smoking, alcohol consumption, and psoriasis risk: a systematic review and dose-response meta-analysis of observational studies · 2026 · DOI

• This analysis was limited by its post hoc nature, as it was not prospectively powered to detect dif- ferences between subgroups with or without obe- sity and should thus be considered exploratory. Subgroup sizes, particularly in the mITT popula- tion, were relatively small, limiting the ability to draw definitive conclusions regarding between- subgroup differences. Therefore, the absence of statistically significant differences between BMI subgroups should not be interpreted as establish- ing equivalence, but rather as indicating that no between-subgroup difference was detected within the available sample size. In addition, the patient subgroups with and without obesity were estab- lished using BMI, which does not capture central adiposity, metabolic syndrome status, or inflam- matory burden and may not adequately distin- guish BMI-defined obesity from metabolically unhealthy obesity [12, 27–32]. Waist circumfer- ence was not collected in the parent trial; conse- quently, this analysis could not address whether central adiposity or metabolic dysfunction modi- fied tildrakizumab response beyond BMI classi- fication alone. Further examination by obesity subcategory (eg, obesity Class I and Class III) or alternative indicators specific to chronic inflam- mation and metabolic dysfunction could reveal subtle impacts on the efficacy or safety of treat- ment for plaque psoriasis of the scalp; analyses by body weight could also clarify the effects of pharmacokinetic differences in larger patients ver- sus those of obesity-related inflammatory burden. CONCLUSIONS This post hoc subgroup analysis demonstrated consistent efficacy of tildrakizumab with no new safety signals identified in patients both with and without obesity concomitant with moderate-to- severe plaque psoriasis affecting the scalp. These findings should be interpreted with caution given the small sample subgroup sizes. Tildrakizumab treatment improved efficacy outcomes compared with placebo in patients both with and without obesity, and there was no statistically significant effect of obesity. Further research in larger popu- lations using more specific indicators of chronic inflammation is needed to confirm whether obe- sity-driven inflammation may have subtler effects on the efficacy of tildrakizumab for the treatment of psoriasis. ACKNOWLEDGEMENTS We thank the participants of the study. Dermatol Ther (Heidelb) Medical Writing/Editorial Assistance. Sta- tistical support was provided by Jing Liu and Ewen Wang, of Edetek, and funded by Sun Pharma. Medical writing and editorial support were provided by Sanna Abbasi, Ph.D., of Red Nucleus, and funded by Sun Pharma. Author Contributions. All named authors meet the International Committee of Medical Journal Editors criteria for authorship for this article, take responsibility for the integrity of the work, and have given their approval for this ver- sion to be published. Howard L. Sofen contrib- uted to conceptualization, investigation, writing (review and editing), and visualization. Ranga Gogineni contributed to conceptualization, methodology, writing (review and editing), and visualization. Tushar Nishandar contributed to conceptualization, methodology, writing (review and editing), and visualization. Jerry Bagel con- tributed to conceptualization, investigation, writing (review and editing), and visualization. Funding. The study and the journal’s Rapid Service Fees were funded by Sun Pharma. Data availability. The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request.

  Efficacy and Safety of Tildrakizumab for Treatment of Moderate-to-Severe Scalp Psoriasis in Patients with Obesity Over 52 Weeks · 2026 · DOI

• Refractory Psoriasis continues to represent a challenging therapeutic condition with significant impact on quality of life and limited response to conventional systemic therapies. The present study demonstrated that treatment with Deucravacitinib produced marked clinical improvement in disease severity, symptom control, and dermatology-related quality of life, with an acceptable safety profile over the study period. These findings support its role as an effective oral targeted therapy for difficultto-treat psoriasis. Further large-scale, are long-term multicenter, warranted to confirm sustained efficacy, safety, and real-world applicability.

  Tolerability and Efficacy of Deucravacitinib in the Treatment of Refractory Psoriasis · 2026 · DOI

• An active comparator trial design with two different formulations meant that all patients knew they received active treatment, and they were not blinded; this could have caused perception bias, potentially influencing the response to PROs. Post hoc analyses have inherent limitations related to their post hoc nature. The majority of patients in the trial had moderate disease at baseline, i.e., the mild subgroup and especially the severe subgroup were relatively Dermatol Ther (Heidelb) small, which may limit the generalizability of the results in these subgroups. requirements for authorship as per the ICMJE recommendations have been met.

  Rapid Onset of Action and Quality-of-Life Improvements in Chinese Patients with Plaque Psoriasis Treated with Calcipotriol plus Betamethasone Dipropionate Aerosol Foam in a Randomized Phase 3 Trial · 2026 · DOI

• Biological Refinement of the IL-23/IL-17 Axis Future psoriasis therapies will emphasize integrative and precision strategies that balance efficacy, safety, and personalization. While blockade of the IL-23/IL-17 axis provides www.biomolther.org s e s a e s d i c i t a i r o s p r o f i s x a 7 1 - L I / 3 2 - L I e h t g n i t e g r a t s c i t u e p a r e h t l e b a t c e n i - n o N j. 2 e l b a T Han et al. IL-23/IL-17-Targeted Therapies in Psoriasis Biomol Ther 34(3), 519-529 (2026) s e s a e s d i c i t a i r o s p r o f i s e p a r e h t d e t e g r a t l e b a t c e n i - n o n j r e h t O.

  Current and Emerging Therapies Targeting the IL-23/IL-17 Axis in Psoriasis. · 2026 · DOI

• Seasonal and periodic variations in air pollution and environmental exposures complicate interpretation of short-term associations with psoriasis severity; longitudinal studies examining cumulative year-round environmental exposure patterns and their temporal relationships with disease flares and healthcare utilization are needed.

  Environmental and Neighborhood Determinants of Psoriasis: A Systematic Review of Pollution, Built Environment, and Socioeconomic Vulnerability on Psoriasis · 2026 · DOI

• Social determinant studies predominantly used cross-sectional designs that preclude causal inference; longitudinal designs with temporality assessment are needed to establish whether lower insurance status, income, and educational attainment causally influence psoriasis severity or whether psoriasis-related healthcare costs and disability reverse-causally affect socioeconomic status.

  Environmental and Neighborhood Determinants of Psoriasis: A Systematic Review of Pollution, Built Environment, and Socioeconomic Vulnerability on Psoriasis · 2026 · DOI

• The contradictory findings on green space exposure (some studies show higher psoriasis incidence with green space exposure while others show protective effects) have not been reconciled; mechanistic studies investigating how neighborhood-level built environment characteristics and green space interact with environmental pollution and socioeconomic status to influence psoriasis are needed.

  Environmental and Neighborhood Determinants of Psoriasis: A Systematic Review of Pollution, Built Environment, and Socioeconomic Vulnerability on Psoriasis · 2026 · DOI

• Heterogeneity in exposure definitions across studies (varying metrics for pollution exposure, social vulnerability indices, and neighborhood deprivation) precludes direct comparison of results; standardized exposure definitions and measurement protocols for environmental air pollutants and socioeconomic vulnerability scales should be established to enable meta-analytic comparisons.

  Environmental and Neighborhood Determinants of Psoriasis: A Systematic Review of Pollution, Built Environment, and Socioeconomic Vulnerability on Psoriasis · 2026 · DOI

Most-cited papers in Psoriasis: Treatment and Pathogenesis

• Pathophysiology, Clinical Presentation, and Treatment of Psoriasis · JAMA · 2020 · 2,120 citations
• Risk of Myocardial Infarction in Patients With Psoriasis · JAMA · 2006 · 1,502 citations
• Psychological stress, distress and disability in patients with psoriasis: Consensus and variation in the contribution of illness perceptions, coping and alexithymia · British Journal of Clinical Psychology · 2002 · 162 citations
• JAK Inhibitors for Treatment of Psoriasis: Focus on Selective TYK2 Inhibitors · Drugs · 2020 · 146 citations
• IL-23 past, present, and future: a roadmap to advancing IL-23 science and therapy · Frontiers in Immunology · 2024 · 120 citations
• Association between systemic immune inflammation index, systemic inflammation response index and adult psoriasis: evidence from NHANES · Frontiers in Immunology · 2024 · 109 citations
• Guselkumab in patients with moderately to severely active ulcerative colitis (QUASAR): phase 3 double-blind, randomised, placebo-controlled induction and maintenance studies · The Lancet · 2024 · 86 citations
• Metabolic coordination between skin epithelium and type 17 immunity sustains chronic skin inflammation · Immunity · 2024 · 83 citations
• Spesolimab: First Approval · Drugs · 2022 · 79 citations
• Inflammatory memory in psoriasis: From remission to recurrence · Journal of Allergy and Clinical Immunology · 2024 · 73 citations

Most recent work

• Environmental and Neighborhood Determinants of Psoriasis: A Systematic Review of Pollution, Built Environment, and Socioeconomic Vulnerability on Psoriasis · Dermatology and Therapy · 2026
• Biological Therapy Leads to a Reduction in Systemic Inflammation but Leaves Serum Uric Acid Unmodified in Moderate-to-Severe Plaque Psoriasis: A Prospective Longitudinal Cohort Study · Journal of Clinical Medicine · 2026
• Epidermal Growth Factor Receptor Pathway Is a Potential Biological Mechanism in Inflammatory Bowel Disease‐Induced Psoriasis · Journal of Gastroenterology and Hepatology · 2026
• A spatial transit–retention axis reveals adaptive immune organisation in psoriatic disease · Molecular and Cellular Biochemistry · 2026
• Unveiling Key Biomarkers of Cardiovascular Risk in Psoriasis Through Explainable Artificial Intelligence · Biology · 2026
• Phytopharmacological Approaches in Psoriasis: Mechanistic Insights and Emerging Therapeutic Potential · Current Journal of Applied Science and Technology · 2026
• Molecular mechanisms underlying psoriasis and depression: an integrated analysis using mendelian randomization, transcriptomics, and single-cell sequencing · Frontiers in Molecular Medicine · 2026
• Macrophages in psoriasis: a bibliometric analysis of research trends, knowledge gaps, and future directions (2015–2024) · Frontiers in Medicine · 2026
• Upadacitinib is effective in treating psoriasis combined with lichen planus: a case report · Frontiers in Medicine · 2026
• Role of the STAT3 Signaling Pathway in Cell Proliferation and Inflammation in Psoriasis and Approaches for Targeted Therapies: A Review · Medical Science Monitor · 2026

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