Red Light Therapy for Autoimmune Conditions

Autoimmune conditions occur when the immune system mistakenly attacks the body’s own tissues. There are more than 80 recognised autoimmune diseases, affecting an estimated 5–8% of the population, with prevalence rising. Conditions range from organ-specific (Hashimoto’s thyroiditis, type 1 diabetes) to systemic (lupus, rheumatoid arthritis, scleroderma).

The appeal of red light therapy for autoimmune patients is obvious: PBM is known to modulate inflammation and immune cell behaviour. If you could calm an overactive immune system without the side effects of immunosuppressive drugs, that would be transformative. But the relationship between PBM and autoimmunity is more complex than simple “immune modulation,” and the evidence is limited.

This page examines what the science actually shows — and where genuine caution is warranted.

How autoimmunity works

In a healthy immune system, self-tolerance mechanisms prevent immune cells from attacking the body’s own tissues. In autoimmune disease, this tolerance breaks down. The result varies by condition:

Lupus (SLE): Autoantibodies attack multiple organ systems — skin, joints, kidneys, brain, blood cells
Multiple sclerosis (MS): T cells attack the myelin sheath surrounding nerve fibres in the brain and spinal cord
Rheumatoid arthritis: Immune cells attack the synovial membrane lining joints
Scleroderma: Excessive collagen production and vascular damage affecting skin and internal organs
Hashimoto’s thyroiditis: Antibodies destroy thyroid tissue (covered in our thyroid page)
Mast cell activation syndrome (MCAS): Mast cells release excessive mediators causing widespread symptoms
POTS (postural orthostatic tachycardia syndrome): Often autoimmune in origin, affecting autonomic nervous system function

Treatment typically involves immunosuppressants (methotrexate, azathioprine), biologics (adalimumab, rituximab), or corticosteroids — all effective but carrying significant side effect profiles including increased infection risk, liver toxicity, and bone loss.

PBM and the immune system: modulation, not simply suppression

The most important concept to understand about PBM and immunity is that photobiomodulation appears to modulate rather than simply suppress or stimulate the immune system. This is both its promise and its uncertainty.

What the basic science shows

Anti-inflammatory effects: PBM at 630–850nm consistently reduces pro-inflammatory cytokines (TNF-alpha, IL-1beta, IL-6, IL-8) and increases anti-inflammatory mediators (IL-10, TGF-beta) in cell culture and animal models. This is well-established across dozens of studies (Hamblin, 2017).

T cell modulation: PBM has been shown to influence T helper cell differentiation, potentially shifting the Th1/Th2/Th17 balance. In some models, PBM promotes regulatory T cell (Treg) activity — these are the “peacekeeping” cells that prevent autoimmune responses. Increased Treg function could theoretically dampen autoimmune attacks (Choi et al., 2012).

Macrophage polarisation: PBM can shift macrophages from the M1 (pro-inflammatory) to M2 (anti-inflammatory/repair) phenotype. In autoimmune conditions characterised by macrophage-driven inflammation, this shift could be beneficial.

NF-kappaB pathway: PBM modulates nuclear factor kappa-B, a master regulator of inflammatory gene expression. Downregulating NF-kappaB reduces the transcription of multiple inflammatory mediators simultaneously.

The critical caveat: immunostimulation risk

Here is where autoimmune patients must exercise genuine caution. PBM has a biphasic dose-response — the Arndt-Schultz principle. At certain doses and wavelengths, PBM can stimulate immune cell activity rather than calm it.

Some studies show that PBM increases:

Natural killer cell cytotoxicity
Lymphocyte proliferation
Reactive oxygen species production in immune cells
Neutrophil activity

For someone with a normally functioning immune system, these effects might be beneficial (e.g., fighting infection). For someone with an overactive immune system already attacking their own tissues, stimulating immune cells could theoretically worsen their condition.

This is not a theoretical concern to be dismissed. It is a genuine gap in the evidence. We do not have enough clinical data in autoimmune patients to know with certainty that PBM will modulate rather than stimulate their specific immune dysfunction.

Condition-specific evidence

Lupus (systemic lupus erythematosus)

Evidence level: Very limited

There are no RCTs examining PBM for systemic lupus. A handful of case reports and small observational studies exist:

PBM has been used for lupus-related skin lesions (discoid lupus) with some reported improvement in wound healing and inflammation, but these are not controlled studies
The systemic nature of lupus — affecting kidneys, joints, brain, and blood — means that local PBM application would likely only address skin manifestations, not the underlying systemic autoimmunity

Specific concern with lupus: Many lupus patients are photosensitive — UV light and sometimes visible light can trigger disease flares. Red and near-infrared wavelengths (630–850nm) are not UV and should not trigger photosensitivity reactions, but lupus patients should be aware of this distinction and start cautiously. Blue light (400–500nm) is more likely to be problematic for photosensitive patients.

Multiple sclerosis

Evidence level: Very limited, but some interesting preliminary data

MS involves demyelination of nerve fibres in the central nervous system. The blood-brain barrier limits what reaches the brain, making direct PBM treatment of CNS lesions challenging.

Transcranial PBM (applying NIR light to the skull) has been explored for various neurological conditions, and some preliminary evidence suggests NIR photons can penetrate the skull to reach superficial cortical tissue. However, the dose delivered is very low, and MS lesions can occur anywhere in the brain and spinal cord.

Fitzgerald et al. (2013) published a small pilot study examining near-infrared light therapy in MS patients, reporting improvements in fatigue and quality of life measures. However, this was uncontrolled and could reflect placebo response.

The anti-inflammatory effects of PBM could theoretically reduce the neuroinflammation that drives MS relapses, but this remains speculative.

Scleroderma

Evidence level: Very limited

Scleroderma involves excessive collagen deposition and vascular damage, leading to skin thickening and internal organ fibrosis. PBM’s effects on collagen are complex:

PBM typically increases collagen synthesis — this is beneficial for wound healing but potentially problematic for a condition characterised by excessive collagen production
Some evidence suggests PBM can promote collagen remodelling (breaking down and reorganising collagen) rather than simply adding more, but this is not well established in scleroderma

For Raynaud’s phenomenon (common in scleroderma), PBM’s vasodilatory effects (via nitric oxide release) could theoretically improve blood flow to affected digits. Small studies have shown improved microcirculation with PBM in Raynaud’s patients, but larger trials are needed.

MCAS (mast cell activation syndrome)

Evidence level: Essentially none

MCAS involves inappropriate mast cell degranulation, releasing histamine and other mediators causing widespread symptoms. There is virtually no published research on PBM for MCAS.

Theoretical concern: PBM has been shown to influence mast cell degranulation in some in vitro studies, with effects varying by dose and wavelength. Some studies show PBM can stabilise mast cells (reducing degranulation), whilst others show increased histamine release. For MCAS patients, this uncertainty is problematic.

Practical advice for MCAS patients: If you choose to try PBM, start with very low doses and short sessions. Monitor for symptom flares (flushing, hives, GI symptoms, tachycardia) that could indicate mast cell activation. Discontinue if symptoms worsen.

POTS (postural orthostatic tachycardia syndrome)

Evidence level: None

No published research examines PBM for POTS. The condition involves autonomic dysfunction, often with autoimmune and inflammatory components.

PBM’s effects on the autonomic nervous system are poorly characterised. Some evidence suggests PBM can modulate vagal tone and heart rate variability, but this is from healthy volunteer studies, not POTS patients.

Rheumatoid arthritis

Evidence level: Moderate (better than most autoimmune conditions)

RA is actually one of the better-studied autoimmune conditions for PBM, with several small RCTs showing improvements in joint pain, morning stiffness, and grip strength. This is covered in more detail on our arthritis page. The evidence here, whilst not definitive, is more substantial than for other autoimmune conditions.

A cautious protocol for autoimmune patients

If you have an autoimmune condition and wish to try PBM, the following approach prioritises safety:

Start low and slow

Begin with 50% of standard PBM doses — approximately 5–10 J/cm² rather than the typical 20–40 J/cm²
Use short sessions (2–3 minutes) initially
Increase gradually over 2–3 weeks if well tolerated

Wavelength selection

660nm and 810–850nm are the most commonly used and studied
Avoid blue light (400–500nm) if you have lupus or other photosensitive autoimmune conditions
NIR (810–850nm) may be preferred for deeper tissue effects with less surface photosensitivity risk

Monitor carefully

Track your symptoms daily when starting PBM
Monitor disease-specific markers if possible (e.g., inflammatory markers, antibody levels at your next blood test)
Stop immediately if you experience a disease flare

Treatment area

For joint-specific conditions (RA): Apply directly to affected joints
For systemic conditions (lupus, MS): There is no established protocol. Some practitioners target large vascular areas (inner wrists, neck) for systemic effects, but this is not evidence-based
Avoid applying PBM directly to areas of active disease if there is any concern about stimulating local immune activity

What to avoid

Do not reduce or stop immunosuppressive medications based on PBM use
Do not use PBM during an active disease flare without medical guidance
Do not treat areas of active lupus skin lesions without rheumatologist approval
Do not assume that because PBM is “natural” it cannot affect your autoimmune condition — it interacts with the same immune pathways your medications target

The honest assessment

The theoretical basis for PBM in autoimmune conditions is sound — PBM modulates inflammation and immune cell behaviour through well-characterised mechanisms. But “modulates” can mean either up or down, and the direction may depend on dose, wavelength, timing, and the specific immunological profile of the individual patient.

The clinical evidence is inadequate for any autoimmune condition except possibly rheumatoid arthritis, where small trials show some benefit. For lupus, MS, scleroderma, MCAS, and POTS, we are working from biological plausibility and animal data, not human trial results.

The greatest concern is paradoxical immune stimulation — the possibility that PBM, intended to calm an overactive immune system, instead activates it further. This risk is theoretical but cannot be excluded with current evidence.

The bottom line

Red light therapy is not a treatment for autoimmune disease. It may, for some patients, offer modest symptomatic relief — reduced pain, improved circulation, better wound healing in affected tissues. But it should never replace medical management, and it must be approached with genuine caution.

If you have an autoimmune condition and wish to try PBM:

Discuss it with your rheumatologist, neurologist, or immunologist
Start with very low doses
Monitor closely for flares
Do not stop your medications
Accept that the evidence is limited and the outcome uncertain

The immune system is not a simple dial you can turn down with light. It is an extraordinarily complex network, and our understanding of how PBM interacts with autoimmune dysregulation is still in its early stages.