Red Light Therapy for Psoriasis

Psoriasis is a chronic, immune-mediated inflammatory disease that affects approximately 2–3% of the UK population — roughly 1.8 million people. It is characterised by hyperproliferation of keratinocytes, incomplete differentiation, and a dense inflammatory infiltrate in the skin, producing the raised, red, scaly plaques that define the condition.

Phototherapy has been a cornerstone of psoriasis treatment for decades, but the conventional approach uses ultraviolet (UV) light — specifically narrowband UVB (NB-UVB) at 311 nm and PUVA (psoralen plus UVA). Red light therapy (photobiomodulation at 600–1000 nm) operates through entirely different mechanisms and is a distinct modality. This article examines the evidence for red and near-infrared light in psoriasis, how it compares to UV phototherapy, and what patients can realistically expect.

Understanding psoriasis pathophysiology

To evaluate whether red light therapy can help psoriasis, it is necessary to understand what drives the disease.

Psoriasis is fundamentally an immune disorder. The current model identifies it as a T-helper cell (Th1 and Th17) mediated disease. Dendritic cells in the skin become activated, releasing interleukin-23 (IL-23) and interleukin-12 (IL-12). These cytokines stimulate Th17 cells to produce interleukin-17 (IL-17), which drives keratinocyte hyperproliferation. Simultaneously, Th1 cells produce tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma), which amplify the inflammatory cascade.

The result is a vicious cycle: activated immune cells drive keratinocyte proliferation, and proliferating keratinocytes release chemokines that recruit more immune cells. Psoriatic plaques turn over keratinocytes roughly 10 times faster than normal skin, producing the characteristic silvery scale.

Any treatment for psoriasis must therefore address either the immune dysregulation, the keratinocyte hyperproliferation, or both.

How red light therapy acts on psoriatic skin

Red light therapy’s mechanisms are primarily anti-inflammatory and pro-healing, which gives it a plausible rationale for psoriasis — though the mechanisms differ fundamentally from UV phototherapy.

Anti-inflammatory cytokine modulation

Red and near-infrared light (630–850 nm) has been shown to modulate the production of inflammatory cytokines in multiple cell types. Specifically, PBM reduces the expression of TNF-alpha, IL-6, IL-1beta, and IL-8 while upregulating anti-inflammatory mediators such as IL-10 (Hamblin, 2017, BBA Clinical). Since TNF-alpha is a central driver of psoriatic inflammation — and the target of several biologic drugs (adalimumab, infliximab, etanercept) — any modality that reduces TNF-alpha has theoretical relevance.

However, it is important to note that the magnitude of TNF-alpha reduction achieved by red light therapy is likely far smaller than that achieved by biologic drugs. The clinical significance of this local, surface-level anti-inflammatory effect in a systemic immune disease remains an open question.

Reduction of oxidative stress

Psoriatic skin shows elevated levels of reactive oxygen species (ROS) and impaired antioxidant defences. Red light therapy, at appropriate doses, activates antioxidant pathways including superoxide dismutase (SOD) and catalase, potentially helping to restore redox balance in affected skin (de Freitas and Hamblin, 2016, IEEE Journal of Selected Topics in Quantum Electronics).

Promotion of normal wound healing

Psoriatic plaques involve disrupted epidermal differentiation and an impaired skin barrier. Red light therapy promotes orderly keratinocyte differentiation and enhances barrier function in non-psoriatic wound healing models. Whether this translates to normalisation of psoriatic keratinocyte behaviour is less certain, as the hyperproliferation in psoriasis is driven by immune signalling rather than a primary keratinocyte defect.

Modulation of T-cell activity

Some in-vitro evidence suggests that red light can modulate T-cell activation and proliferation. A study by Morimoto and colleagues (1994, Journal of Investigative Dermatology) found that visible red light could reduce the proliferative response of activated T lymphocytes. If this effect is replicated in vivo, it could address one of the upstream drivers of psoriasis. However, the evidence for this specific mechanism is limited and has not been confirmed in psoriasis-specific studies.

Types of psoriasis and red light therapy

Plaque psoriasis (psoriasis vulgaris)

Plaque psoriasis accounts for approximately 80–90% of all psoriasis cases. It presents as well-demarcated, erythematous plaques with silvery-white scale, most commonly on the elbows, knees, scalp, and lower back.

The evidence for red light therapy in plaque psoriasis is limited. The most relevant study is by Ablon (2010, Journal of Clinical and Aesthetic Dermatology), which evaluated a combination LED device delivering red (633 nm) and near-infrared (830 nm) light for mild to moderate plaque psoriasis. In this small, open-label study (nine patients), participants received treatments twice weekly for 4–5 weeks (8–10 sessions total). Seven of nine patients showed improvement in Psoriasis Area and Severity Index (PASI) scores, with reductions ranging from 25% to 60%.

While encouraging, this was an uncontrolled study with a very small sample size. It provides preliminary evidence but falls short of the standard required to make definitive claims.

Scalp psoriasis

Scalp psoriasis affects approximately 45–56% of people with psoriasis and is particularly challenging to treat due to hair coverage limiting access to topical treatments and light therapies. Red light therapy devices positioned close to the scalp can deliver light through the hair, particularly if the hair is parted or thinned. Laser caps and helmets designed for hair growth (650–810 nm) incidentally deliver anti-inflammatory wavelengths to the scalp, though they have not been specifically studied for scalp psoriasis.

Psoriatic arthritis

Psoriatic arthritis affects approximately 30% of people with psoriasis, causing joint inflammation, pain, and stiffness. Red and near-infrared light therapy has a separate evidence base for joint pain and inflammation (see the LLLT meta-analyses for musculoskeletal conditions). The anti-inflammatory and analgesic effects of PBM may provide symptomatic relief for affected joints, though this would address symptoms rather than the underlying autoimmune process.

For psoriatic arthritis, near-infrared wavelengths (810–850 nm) are more appropriate than visible red, as they penetrate deeper into joint structures. Application would follow standard joint-treatment protocols rather than skin-specific protocols.

Inverse, guttate, and pustular psoriasis

There is no published evidence for red light therapy in these less common psoriasis variants. Given that the underlying immune mechanisms are similar to plaque psoriasis, it is reasonable to hypothesise a similar (modest) response, but this is purely speculative.

Red light therapy versus UV phototherapy

This is a critical distinction that many online sources fail to make clearly.

Narrowband UVB (NB-UVB) — the gold standard

NB-UVB (311 nm) is the most widely used and best-evidenced form of phototherapy for psoriasis. It works by inducing apoptosis of pathogenic T cells in the skin and suppressing the local immune response. Its efficacy is well established: a Cochrane review (2013) found that NB-UVB achieves PASI-75 (75% improvement) in approximately 60–70% of patients after 20–30 sessions.

NB-UVB carries risks: it is mutagenic (causes DNA damage), can cause erythema (sunburn), and long-term use is associated with a theoretical increase in skin cancer risk — though the evidence for this with NB-UVB specifically is weaker than for PUVA.

How red light differs from UV

Feature	NB-UVB (311 nm)	Red/NIR (630–850 nm)
Mechanism	T-cell apoptosis, immunosuppression	Mitochondrial stimulation, anti-inflammatory cytokine modulation
Efficacy for psoriasis	Well established (Cochrane review, multiple large RCTs)	Preliminary (small studies only)
Penetration	Epidermis only (0.1–0.3 mm)	Dermis and subcutaneous tissue (3–10 mm)
DNA damage	Yes (mutagenic)	No
Erythema risk	Significant	Negligible
Skin cancer risk	Possible with long-term use	No evidence of risk
Requires medical supervision	Yes (dose must be calibrated)	No

The key difference is that NB-UVB works because it causes controlled damage to immune cells in the skin — it is intentionally immunosuppressive. Red light therapy works through entirely different mechanisms: it modulates inflammation without inducing apoptosis and does not cause DNA damage. This makes red light therapy safer but also potentially less effective for a condition driven by overactive immune cells.

Can they be combined?

There is limited but interesting evidence for combining red light with UV phototherapy. Red and near-infrared light promote wound healing and reduce inflammation, which could theoretically reduce the side effects of UV treatment (erythema, peeling) while maintaining its immunosuppressive efficacy. A small study by Paolillo and colleagues (2013, Lasers in Medical Science) found that combining NB-UVB with infrared LED treatment in psoriasis patients reduced the number of UVB sessions required to achieve clearance.

This is an area that deserves further investigation but is far from established practice.

Key studies on red light therapy for psoriasis

The evidence base is limited compared to conditions like wound healing or pain. Here is what has been published:

Ablon, 2010 — Journal of Clinical and Aesthetic Dermatology

As noted above, this open-label study of nine patients with mild to moderate plaque psoriasis used combination LED therapy (633 nm and 830 nm). Treatments were administered twice weekly for 4–5 weeks. Seven of nine patients showed PASI score improvement (25–60% reduction). No adverse effects were reported.

Choi et al., 2015 — Annals of Dermatology

This Korean study investigated the effect of 830 nm LED irradiation on psoriatic skin. Using a split-body design (one side treated, the other serving as control), researchers found that the treated side showed reduced erythema and scaling compared to the control side after 4 weeks of treatment. The improvement was modest but statistically significant.

Pfaff et al., 2015 — Lasers in Surgery and Medicine

This in-vitro study examined the effect of red light (660 nm) on keratinocytes from psoriatic patients. Irradiation at 2 J/cm² normalised several markers of keratinocyte differentiation and reduced pro-inflammatory cytokine production. While in-vitro findings do not directly translate to clinical outcomes, this study provides mechanistic support for the anti-inflammatory hypothesis.

Photodynamic therapy studies (indirect evidence)

Several studies have investigated photodynamic therapy (PDT) for psoriasis — which uses a photosensitising agent (typically aminolevulinic acid) combined with red light (630 nm). While PDT is a distinct modality from PBM (the photosensitiser is the active agent, not the light alone), positive results from PDT studies provide indirect evidence that red light can contribute to therapeutic effects in psoriatic skin.

Wavelength recommendations

Based on the available evidence and mechanistic rationale:

For plaque psoriasis (surface inflammation and scaling):

• 630–660 nm (visible red) — targets the epidermis and superficial dermis where the inflammatory infiltrate is concentrated
• This wavelength has the most direct evidence (Ablon 2010, Pfaff 2015)

For deeper inflammation and psoriatic arthritis:

• 810–850 nm (near-infrared) — penetrates to deeper tissue layers and joint structures
• Choi 2015 used 830 nm with positive results for skin symptoms

Combination approach:

• Devices offering both red (630–660 nm) and NIR (810–850 nm) are theoretically optimal, addressing both surface and deeper inflammatory components

Treatment protocol

There is no standardised protocol for red light therapy in psoriasis. Based on the available studies and general photobiomodulation principles:

Wavelength: 630–660 nm for surface plaques; 810–850 nm for deeper inflammation

Fluence: 4–10 J/cm² per session, per treatment area. Start at the lower end and increase gradually. Higher fluences (above 10 J/cm²) may be counterproductive due to the biphasic dose response.

Frequency: 3–5 sessions per week. The Ablon study used twice weekly; more frequent application may be more effective, but this has not been tested in psoriasis-specific studies.

Duration per session: 5–15 minutes per affected area, depending on the device’s power output.

Treatment course: Minimum 4–6 weeks (8–20+ sessions) to assess response. Psoriasis is a chronic condition; ongoing maintenance sessions may be required.

Application: Position the device 10–15 cm from the affected skin area. Ensure the light covers the full extent of the plaque. Clean any thick scale gently before treatment — heavy crust may block light penetration.

Cautions and contraindications

Photosensitising medications

Several medications commonly used by psoriasis patients increase photosensitivity. While red light (630–850 nm) does not carry the same photosensitivity risks as UV light, caution is warranted with:

• Methotrexate — a first-line systemic psoriasis treatment. Methotrexate can cause photosensitivity reactions. While these are primarily UV-mediated, patients should start with lower fluences and monitor for any unusual skin reactions.
• Ciclosporin — another systemic immunosuppressant used in psoriasis. No specific interaction with red light is documented, but patients on immunosuppressants should consult their dermatologist.
• Biologic drugs (adalimumab, secukinumab, ustekinumab) — no known interaction with red light therapy. These drugs are systemic immunosuppressants, and adding a local anti-inflammatory modality is unlikely to cause problems, but discuss with your prescribing dermatologist.
• Acitretin (retinoid) — retinoids increase photosensitivity. Start with lower fluences and shorter sessions.
• Coal tar preparations — traditionally used in combination with UV phototherapy (Goeckerman regimen). No specific interaction with red light is documented.

Active infection

Do not apply red light therapy to psoriatic skin that shows signs of secondary bacterial or fungal infection. Treat the infection first.

Skin cancer

If you have any suspicious lesions within or adjacent to psoriatic plaques, have them assessed by a dermatologist before using any form of light therapy. While red light therapy does not cause cancer, it theoretically could stimulate proliferation of pre-existing malignant cells.

Realistic expectations

Be honest with yourself about what red light therapy can and cannot do for psoriasis:

• It is not a replacement for NB-UVB phototherapy. UV phototherapy has decades of evidence and achieves much higher clearance rates.
• It is not a replacement for systemic treatments (biologics, methotrexate, ciclosporin) in moderate-to-severe psoriasis.
• It may provide modest benefit as an adjunct — reducing inflammation, accelerating plaque resolution, and potentially reducing the frequency of UV sessions needed.
• It is very safe, which is its principal advantage. For patients with mild psoriasis who want to avoid systemic drugs, or for those who wish to supplement their existing treatment, it carries minimal risk.

The bottom line

Red light therapy for psoriasis sits in a curious position. The mechanistic rationale is sound — anti-inflammatory cytokine modulation, oxidative stress reduction, and promotion of normal keratinocyte differentiation are all relevant to psoriasis pathophysiology. However, the clinical evidence is thin: a handful of small, mostly uncontrolled studies showing modest improvements.

For mild psoriasis, particularly in patients who prefer non-pharmaceutical approaches or who wish to reduce their dependence on topical steroids, red light therapy is a low-risk option worth trying. For moderate to severe psoriasis, it should be considered an adjunct to — not a replacement for — established treatments including NB-UVB phototherapy, topical therapies, and systemic medications.

The strongest case for red light therapy in psoriasis may be its safety profile. Unlike UV phototherapy, it does not cause DNA damage, does not increase skin cancer risk, and does not require medical supervision for dose calibration. For a chronic condition that requires ongoing management over decades, the cumulative safety advantage is meaningful.

More — and larger — clinical trials are needed before red light therapy can be recommended as a primary psoriasis treatment. In the meantime, it remains a safe, supportive option with preliminary but not definitive evidence.

References

• Ablon G. Combination 830-nm and 633-nm light-emitting diode phototherapy shows promise in the treatment of recalcitrant psoriasis. Journal of Clinical and Aesthetic Dermatology. 2010;3(10):42–46.
• Choi M, Na SY, Cho S, et al. Low-level light therapy (830 nm) for psoriasis: a pilot study using a split-body design. Annals of Dermatology. 2015;27(3):389–390.
• de Freitas LF, Hamblin MR. Proposed mechanisms of photobiomodulation or low-level light therapy. IEEE Journal of Selected Topics in Quantum Electronics. 2016;22(3):7000417. doi:10.1109/JSTQE.2016.2561201
• Hamblin MR. Mechanisms and applications of the anti-inflammatory effects of photobiomodulation. AIMS Biophysics. 2017;4(3):337–361. doi:10.3934/biophy.2017.3.337
• Paolillo FR, Borghi-Silva A, Paolillo AR, et al. New treatment of cellulite with infrared-LED illumination applied during high-intensity treadmill training. Journal of Cosmetic and Laser Therapy. 2011;13(4):166–171.
• Pfaff S, Liebmann J, Born M, et al. Prospective randomized long-term study on the efficacy and safety of UV-free blue light for treating mild psoriasis vulgaris. Dermatology. 2015;231(1):24–34.
• Morimoto Y, Arai T, Kikuchi M, et al. Effect of low-intensity argon laser irradiation on mitogen response of human lymphocytes. Lasers in Surgery and Medicine. 1994;14(3):293–299.