NAD+ and Autoimmune Disease: What the Research Shows Across Seven Conditions

Key Takeaways

• Autoimmune diseases arise when the immune system attacks the body’s own tissues, leading to chronic inflammation, tissue damage, and often lifelong treatment needs.
• Immune cells are highly energy-dependent, and NAD+ helps power key immune functions, cellular repair, and stress responses that may influence autoimmune activity.
• Disruptions in NAD+ metabolism have been observed across several autoimmune diseases, including immune thrombocytopenia (ITP), inflammatory bowel disease (IBD), multiple sclerosis (MS), psoriasis, rheumatoid arthritis, systemic lupus erythematosus (SLE), and systemic sclerosis.
• NAD+ precursors like NR, NMN, and niacin are being studied in cells, animal models, and early human studies for their potential to restore NAD+ and modulate immune and inflammatory pathways.
• While early findings are promising, NAD+ precursors remain experimental in the context of autoimmune disease, and larger, well-controlled clinical trials are needed before they can be considered established treatments.

Autoimmune diseases encompass more than 100 distinct conditions, collectively affecting hundreds of millions of people around the world.¹ Despite their diversity of symptoms and presentation, these disorders share a common and defining feature: the immune system mistakenly attacks the body’s own tissues.² Currently, treatments typically focus on suppressing immune activity to manage symptoms rather than correcting the underlying dysfunction. Although often effective in the short term, these approaches can come with long-term trade-offs, including significant side effects, increased infection risk, and often diminishing effectiveness over time.

In recent years, researchers have begun to reexamine autoimmune disease through the lens of cellular metabolism, highlighting the role of metabolic pathways in shaping immune cell behavior, resilience, and dysfunction. Within this framework, nicotinamide adenine dinucleotide (NAD+), an essential coenzyme involved in cellular energy production and metabolic signaling, has emerged as a molecule of growing interest in the autoimmune space.

In this article, we’ll explore the current state of the science on NAD+ and autoimmune disease, including how NAD+ biology intersects with immune function, and what existing research suggests across seven specific autoimmune conditions. It’s important to note that much of the available evidence comes from preclinical models, alongside a limited number of early-stage human studies. While these findings are promising, the research is still evolving, and larger, well-controlled clinical trials are needed before definitive conclusions or clinical recommendations can be made.

What Is an Autoimmune Disease? Causes, Mechanisms, and Types

Autoimmune diseases occur when the immune system mistakenly identifies the body’s own cells or tissues as foreign, mounting an attack against them.² Under normal conditions, the immune system is trained to distinguish “self” from “non-self,” using a series of checks and balances to prevent this misdirected response. However, these mechanisms can break down, ultimately leading to autoimmunity. 

That said, autoimmunity exists on a spectrum—some are organ-specific, such as Hashimoto’s thyroiditis, which is localized to the thyroid gland, while others are systemic, such as systemic lupus erythematosus, affecting multiple organs and systems throughout the body.³ But across this spectrum, autoimmune conditions tend to share a common arc: an initial immune response or triggering event becomes dysregulated and persists over time, leading to chronic inflammation and progressive tissue damage. 

How Autoimmune Diseases Develop: From Trigger to Chronic Inflammation

The immune system operates in two primary layers that work together—the innate immune system, which provides rapid and non-specific defense, and the adaptive immune system, which mounts more targeted responses and “remembers” past threats. In a healthy immune system, developing T cells and B cells are screened to eliminate any that would attack the body’s own tissues—but in autoimmunity, that screening process breaks down.² Self-reactive T and B cells survive, become activated, and begin to target the body’s own proteins or organs.² 

Several key immune players are repeatedly implicated in autoimmune disease:⁴ Th17 cells,⁵ which promote inflammation; regulatory T cells,⁶ which normally act as brakes on the immune response; macrophages,⁷ a type of innate immune cell that drives inflammatory responses; and cytokines,⁸ small signaling proteins that coordinate and amplify immune activity.

For many people, autoimmune diseases develop gradually—often over years or decades—with autoantibodies and immune dysregulation detectable well before symptoms appear and a diagnosis is made. Over time, early, pre-clinical immune activation can cross a threshold into overt disease, driven by a vicious cycle in which inflammation causes tissue damage, and that damage, in turn, triggers more immune activation. Once autoimmune disease is established, chronic and low-grade inflammation can persist and continually harm tissues—a key distinction from the short-lived, acute inflammatory response that helps the body heal after infections or injuries.⁹

NAD+ and the Immune System: Why Cellular Metabolism May Matter in Autoimmune Disease

Sitting at the intersection of cellular metabolism and immune function, NAD+ has become a growing focus of interest in autoimmune disease.¹⁰ Immune cells require substantial energy to activate, communicate, and carry out tasks such as attacking pathogens, clearing debris, and regulating inflammation, and NAD+ is central to these energetic processes.¹¹

As a vital coenzyme involved in cellular energy production, DNA repair, and stress responses, NAD+ supports immune cell activation, growth, and signaling.¹² This connection underlies the field of immunometabolism, which examines how metabolic pathways inside immune cells shape their behavior and function.¹³ NAD+ is central to this picture because it serves as a substrate for the enzymes involved in inflammation and immune regulation, including CD38¹⁴ and PARPs,¹⁵ which depend on and consume NAD+ as they respond to cellular stress and DNA damage. 

Chronic inflammation can also increase NAD+ consumption, depleting cellular NAD+ pools and altering immune-cell function over time.¹⁰ Disruptions in NAD+ metabolism can therefore contribute to elevated inflammatory signaling, impaired immune regulation, and ongoing tissue damage. Across multiple autoimmune diseases, researchers have observed altered NAD+ metabolism alongside changes in immune cell activity, including in T cells, macrophages, and inflammatory cytokines.¹⁰

NAD+ precursors such as nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN) are compounds currently being investigated for their ability to restore NAD+ levels and potentially modulate these pathways.¹⁰ However, the current research is primarily focused on understanding how NAD+ availability and consumption influence autoimmune disease processes, rather than establishing NAD+ precursors as proven treatments.

NAD+ and Autoimmune Disease: A Review of the Evidence

The strength and scope of the evidence linking NAD+ to autoimmune disease vary considerably across conditions. For some diseases, the evidence is largely confined to mechanistic and preclinical animal studies, whereas for others, early clinical findings are beginning to emerge.  Although the seven autoimmune diseases discussed below affect different organs and systems, many of the studies focus on similar biological themes, including immune cell metabolism, inflammatory signaling, and cellular stress responses. In the following sections, we’ll review the potential NAD+ connection in each condition, along with the available preclinical and, where applicable, clinical evidence. 

Immune Thrombocytopenia (ITP)

Immune thrombocytopenia (ITP) is an autoimmune disorder in which the immune system targets and destroys platelets—the blood cells responsible for clotting—leading to low platelet counts and an increased risk of bruising and bleeding. ITP often presents with easy bruising, petechiae (small red or purple spots on the skin), nosebleeds, gum bleeding, or heavy menstrual bleeding. In severe cases, there is a risk of internal bleeding, including a rare but serious intracranial hemorrhage. 

Recent research suggests that changes in NAD+ metabolism may play a role in ITP, particularly by affecting the macrophages and T cells involved in platelet destruction.¹⁶ In this study, researchers found that excessive activity of CD38—an enzyme that consumes NAD+—caused macrophages to become more inflammatory and more likely to engulf antibody-coated platelets.¹⁶ Blocking CD38 or giving NMN restored NAD+ levels, shifted macrophages toward a less inflammatory state, and reduced platelet loss in preclinical models.

The same study also included a small, early-stage clinical trial in adults with ITP who were dependent on steroids or no longer responding well to them. After taking low-dose oral NMN for two weeks, about one in five participants reached a predefined platelet response, while others experienced meaningful increases in platelet counts over the following weeks. Although these findings are preliminary and need to be confirmed in larger clinical trials, they suggest that targeting NAD+ metabolism—particularly the CD38-NAD+ pathway—may offer a promising new approach for understanding and potentially treating ITP.

Inflammatory Bowel Disease (IBD): Evidence in Ulcerative Colitis and Experimental Colitis

Inflammatory bowel disease (IBD) encompasses Crohn’s disease and ulcerative colitis—two chronic autoimmune conditions where the immune system attacks the digestive tract, leading to ongoing inflammation, abdominal pain, and bloody diarrhea. Ulcerative colitis affects the colon or rectum, while Crohn’s disease can affect any part of the digestive tract.

Researchers have recently begun to connect IBD to changes in NAD+ metabolism, especially in the gut lining and immune cells that drive inflammation. In a 2023 study, NAD+ levels were significantly depleted in the intestinal lining of mice with experimental colitis—a preclinical animal model used to mimic aspects of human IBD—as well as in the colonic epithelium of patients with ulcerative colitis.¹⁷ In the same work, mice treated with NR had reductions in colitis severity and restored mitochondrial function in the gut lining.

These preclinical findings help to motivate early-stage clinical trials of NAD+ precursors in ulcerative colitis. A randomized, double-blind pilot study is currently testing NR in pediatric-onset ulcerative colitis, with the goal of assessing safety, changes in NAD-related pathways, and preliminary effects on disease activity. A similar trial is evaluating NMN in adults with ulcerative colitis to see whether it can improve clinical symptoms, inflammatory biomarkers, and endoscopic or histologic measures of disease. Together, these trials will provide more information about whether restoring NAD+ in intestinal and immune cells can modulate inflammation and mucosal healing.

Multiple Sclerosis

Multiple sclerosis (MS) is a chronic autoimmune disease where the immune system attacks myelin—the protective sheath surrounding nerves in the brain and spinal cord, leading to disrupted communication between the brain and body. MS often presents with episodes of neurological symptoms, including vision changes, numbness or weakness in the limbs, problems with balance and coordination, and, in some people, gradual worsening of mobility and daily functioning over time.

In mouse models of MS, known as experimental autoimmune encephalomyelitis (EAE), boosting NAD+ has shown neuroprotective effects.¹⁸ In one set of studies, giving NAD+ directly reduced immune-cell infiltration into the central nervous system, reduced demyelination, and improved neurological scores, in part by dampening inflammatory pathways and supporting cellular stress responses.¹⁹ In another EAE study, daily NR treatment delayed disease onset, reduced symptom severity, alleviated spinal cord demyelination, and increased markers of neuronal health and neurotrophic factors, suggesting that NR helped create a more protective environment for neurons and myelin.²⁰

These preclinical findings have nudged early clinical work with NAD+ precursors in MS, including one ongoing trial testing NR in people with progressive MS and looking at safety, changes in NAD-related biomarkers, and effects on disability and neurodegeneration. For now, these studies are still exploratory and designed to see whether targeting NAD+ metabolism can complement existing MS therapies, rather than to establish NR as a proven treatment. 

Psoriasis

Psoriasis is a chronic autoimmune skin disease where the immune system causes rapid skin cell turnover, leading to thick, red, or scaly plaques that can itch, burn, or crack. The plaques most commonly occur on the elbows, knees, scalp, and trunk, and many people also experience nail changes, joint symptoms, and reduced quality of life. 

Recent studies have begun to connect psoriasis with altered NAD+ metabolism and T-cell-driven inflammation. Research by Han et al. found that boosting NAD+ with NR in CD4+ T cells from people with psoriasis blunted Th17-related inflammation while enhancing the body’s own antioxidant defenses.²¹ In a recently published study, oral NR supplementation similarly increased NAD+ metabolites and markers of antioxidant and stress response pathways, while reducing Th17 immune responsiveness.²² These findings are early, but they suggest that boosting NAD+ may help rebalance pro-inflammatory T cell activity in psoriasis, although the work remains preliminary until further research is done. 

Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a chronic autoimmune disease where the immune system attacks the joint linings, causing pain, swelling, stiffness, and joint damage or deformity. It most often affects the small joints of the hands, wrists, and feet, and is often accompanied by fatigue and systemic symptoms.

Research suggests that RA may be linked to NAD+, with studies finding that people with RA have lower plasma NAD+ levels and an increased expression of genes involved with NAD+ consumption.²³ In an external whole-blood dataset, the same team also observed upregulation of NAD-consuming pathways and downregulation of NAD-synthesizing pathways, highlighting the idea that NAD+ balance is shifted more towards depletion in RA. Notably, lower NAD+ levels were inversely associated with markers of inflammation and clinical disease activity, suggesting that greater NAD+ depletion correlated with more active or severe RA. Although it doesn’t prove causation, this study points to altered NAD+ metabolism as a potential contributor to RA’s inflammatory cascades.

Systemic Lupus Erythematosus (SLE)

Systemic lupus erythematosus (SLE) is an autoimmune disease where the immune system attacks multiple organs and tissues throughout the body—including potentially the skin, joints, kidneys, blood cells, and nervous system—leading to widespread inflammation and tissue damage. People with SLE can experience a wide range of symptoms, including fatigue, joint pain, swelling, rashes, fevers, mouth sores, chest pain, and, in some cases, serious complications involving the kidneys, heart, lungs, or brain. 

Studies linking NAD+ to lupus have found that raising NAD+ with NR in white blood cells called monocytes can help “dial down” overactive immune signals tied to type I interferons, a key driver of lupus-related inflammation.²⁴ In cells taken from people with SLE, NR similarly reduced interferon production, suggesting that boosting NAD+ may calm some of the immune overactivation seen in lupus. These early findings helped to encourage a double-blind, placebo-controlled trial testing NR in people with lupus to see if raising NAD+ can reduce this interferon-driven inflammation in the real world. While this work is still in early stages, it points to NAD+ as a possible way to fine-tune dysregulated immune responses in SLE, rather than an established treatment option today.

Systemic Sclerosis

Systemic sclerosis (also called scleroderma) is a rare autoimmune disease in which the immune system drives excessive scarring and tightening of the skin, as well as, in some cases, the lungs, heart, or digestive tract. People with systemic sclerosis often notice skin thickening or hardening on the hands and face, color changes in the fingers with cold (known as Raynaud’s phenomenon), joint pain or stiffness, and sometimes digestive or breathing problems.

Preclinical research suggests that NAD+ is involved in the fibrotic processes that characterize systemic sclerosis. One study found that the NAD-consuming enzyme CD38 was elevated in the skin of people with systemic sclerosis, as well as in mouse models of scleroderma, and that this increase was linked to lower NAD+ levels and more scarring.²⁵ When they blocked CD38 or boosted NAD+ with NR in mice, NAD+ levels rose, and fibrosis in the skin and lungs was reduced. This research suggests that maintaining NAD+ may help limit excessive tissue scarring, though this evidence is still limited to animal models. 

Conclusion: NAD+ Therapy for Autoimmune Diseases: What the Research Says and What Comes Next

Autoimmune diseases are increasingly being studied through the lens of immunometabolism, which examines how cellular metabolism influences immune function, inflammation, and tissue damage. Within this framework, NAD+ has emerged as a molecule of interest because it connects energy metabolism and cellular stress responses to immune regulation. NAD+ supports immune cell activity, mitochondrial function, DNA repair, redox balance, and stress-response signaling. When NAD+ levels decline or NAD-consuming pathways become overactive, these processes may shift toward chronic inflammation, impaired immune regulation, and increased tissue injury.

Evidence of disrupted NAD+ metabolism has been reported across several autoimmune diseases, including immune thrombocytopenia, inflammatory bowel disease, multiple sclerosis, psoriasis, rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis. Findings include increased activity of NAD-consuming enzymes, reduced NAD+ levels in affected tissues, and altered expression of genes involved in NAD+ production and recycling, suggesting that NAD+ imbalance may contribute to autoimmune disease in at least some patients.

A growing body of research is exploring NAD+ precursors, such as NR, NMN, and niacin, as tools to restore or support NAD+ levels in autoimmune disease models and human studies. Studies in cells, animals, and humans have reported effects on immune function, inflammatory markers, and disease-related outcomes. However, the strength of evidence varies considerably by disease: some conditions are supported mainly by mechanistic or preclinical work, while others have only limited human data. For now, NAD+ precursors should be viewed as experimental approaches rather than established treatments, pending larger, well-controlled clinical trials.

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