Early psoriasis treatment leads to long-term relapse freedom, study finds

Psoriasis is a serious, incurable systemic disease that causes painful skin lesions and significantly increases the risk of cardiovascular disease, diabetes, and arthritis. It affects about 125 million people worldwide—roughly 2–3% of us—and too often demands lifelong treatment.

New research published in Nature shows that early treatment, within one year of disease onset, can significantly reduce the risk of relapse. Genetic profiling can support clinicians on precise diagnosis and timely treatment. It helps moving from one-size-fits-all care to durable and personalized healthcare.

Timely Intervention Improves Outcome

Psoriasis is a severe, chronic, and systemic disease. It affects over 100 million people globally and currently has no cure, meaning it is a lifelong condition. The primary symptom is painful, inflamed skin lesions that are more than just a surface-level issue. The inflammation is not just skin-deep; it significantly increases the risk of developing other major health conditions like heart disease, diabetes, and arthritis. The visible nature of the disease and its chronic pain often lead to stigmatization, a severely impaired quality of life, and mental health challenges.

"Patients with a short disease duration, who had started treatment within a year of onset, remained relapse-free for a long time," says Curdin Conrad, clinical dermatologist and psoriasis researcher at Lausanne University Hospital in Switzerland.

His research found that biology-guided treatment can unlock longer remissions and even planned withdrawal for some people. One transcriptomic meta-analysis across 44 studies and 975 samples maps a consensus immune signature and highlights fresh metabolic programs. Together, these advances show how genomics can sort patients by mechanism, match them to smarter therapies, and time safe step-downs.

Immune Drivers Signal

“We now have a window of opportunity to modify the disease, where we can treat the patient to get them into remission — then potentially wean them off the therapy completely”, says Conrad.

The meta-analysis combined data from diseased skin, nearby normal-looking skin, and healthy volunteers to create a shared molecular fingerprint of psoriasis. It reconfirmed core immune drivers and added insight into how skin cells manage energy, handle stress, and clear worn-out components. These signals link inflammation with metabolism and repair, sorting look-alike cases into subtypes that respond differently to therapy. They also tie skin biology to future heart and diabetes risk—important for long-term outcomes.

Recent trials now align with that biology. STEPIn—an early intervention, treatment-withdrawal study in people whose disease became severe within 12 months —gives one year of targeted therapy, then pauses to see who stays clear. GUIDE is a dose-spacing program after early control with an antibody that blocks IL-23—an immune signal that drives psoriasis inflammation—testing whether complete responders can halve dosing and ultimately stop.

Clinicians can act on this with simple sampling. A skin or blood RNA panel confirms a psoriasis signature and whether IL-23/IL-17 signals remain active on therapy. Repeat tests show whether that overactive immune pathway is truly turning off. Clinicians can adjust treatment according to the changes in signals.

Genomics Support Durable Control

Adaptive immunity profiling adds a second layer. Relapses often come from “resident” memory T cells that live in the skin, a study published in the Journal of Immunology suggests. When treatment works, these cells drop; before flares, they rise. Immune repertoire sequencing maps the mix of T and B cells (producing antibodies while modulating inflammation) and shows which families are growing or shrinking. That lets teams spot the trouble-making cells in a lesion, track them over time, and catch shifts early—turning a simple “clear/not clear” check into a measurable path back to remission.

BGI Genomics supports this approach with Immune Repertoire Sequencing (IR-SEQ). The service profiles immune-cell receptors (TCR/BCR) using validated PCR/RACE methods. Paired with RNA from the same sample, it links pathways with clonal shifts and outcomes in one view. Researchers use IR-SEQ to select participants, track response, and define molecular remission before adjusting doses.

“If early treatment results in a smaller disease burden, then that could be the way to go”, says  Liv Eidsmo of the Karolinska Institute. She advocates for moving beyond lifelong immune suppression and basing taper decisions on measurable remission biology. That view fits emerging evidence of epigenetic “scars” in skin cells that can fuel relapse—and suggests why timing and a molecular readout matter.

Diagnose mechanism, not just morphology. Treat early, track the molecular response, and taper when the signature is silent and pathogenic clones decline. Re-test if symptoms return. This approach reduces trial-and-error, limits unnecessary drugs, and supports durable control. The science backs it—and the tools exist today.

About BGI Genomics Immune Repertoire Sequencing

BGI Genomics Immune Repertoire Sequencing (IR-SEQ) service enables partners to examine the adaptive immune system with bias-controlled multiplex PCR or 5’ RACE amplification and high-throughput sequencing of T-cell and B-cell receptors.

About BGI Genomics

BGI Genomics, headquartered in Shenzhen, China, is the world's leading integrated solutions provider of precision medicine. Our services cover more than 100 countries and regions, involving more than 2,300 medical institutions. In July 2017, as a subsidiary of BGI Group, BGI Genomics (300676.SZ) was officially listed on the Shenzhen Stock Exchange.