NIH “From Mechanisms To Medicine” Workshop Highlights
Neuroimmune Connections Across Autoimmune & Chronic Diseases
September 23 -24, 2026
Researchers studying autoimmune disease, chronic pain, post-infectious illness, dysautonomia, and other complex chronic conditions are increasingly encountering the same challenge: the biology does not always fit neatly within the boundaries of individual diagnoses or medical specialties.
That was a central theme of the National Institutes of Health (NIH) workshop “From Mechanisms to Medicine: Rethinking the Discovery-to-Care Continuum in Multi-System Disorders,” held September 23–24, 2026, at the Neuroscience Center in North Bethesda, Maryland.
The two-day meeting brought together researchers, clinicians, advocates, and people with lived experience to examine chronic overlapping pain conditions, infection-associated illnesses, and the biological mechanisms that may connect them. Discussions spanned immunology, neuroinflammation, genetics, hormones, infection, pain, and autonomic nervous system dysfunction, with an emphasis on breaking down research silos that can obscure shared biology.
For autoimmune disease research, several discussions were particularly significant. Rather than viewing the immune system separately from the brain, nervous system, hormones, or cardiovascular and gastrointestinal systems, researchers highlighted the complex, bidirectional interactions that can contribute to chronic disease.
Infection, Autoimmunity, And The Transition From Trigger To Chronic Disease
One of the workshop’s most directly relevant sessions examined infection-associated chronic conditions, including Long COVID and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).
The session brought together researchers studying clinical immunology, autoimmune disease, Long COVID, ME/CFS, Lyme disease, and dysautonomia. Nancy Klimas, M.D., described research examining common immune mediators across chronic illnesses that can begin with very different triggers yet produce overlapping symptoms. She emphasized that biological convergence does not necessarily mean that different conditions have the same underlying cause.
That distinction is particularly important when considering autoimmunity. Long COVID, ME/CFS, and other infection-associated chronic conditions should not simply be classified as autoimmune diseases. Instead, researchers are investigating several possible mechanisms that may contribute to different disease subtypes, including persistent immune activation, altered immune regulation, neuroinflammation, autonomic dysfunction, and, in some individuals, autoimmune processes.
The connection between infection and established autoimmune disease was illustrated particularly clearly by Judith James, M.D., Ph.D., whose research focuses on the development and progression of lupus and related rheumatic diseases.
James discussed research on Epstein-Barr virus (EBV) and systemic lupus erythematosus (SLE). Studies have found differences in the immune response to EBV among people with lupus, including antibodies targeting multiple regions of the viral protein EBNA-1. Some of those viral regions resemble targets of lupus autoantibodies, raising the possibility of molecular mimicry, in which an immune response initially directed against a pathogen may cross-react with the body’s own molecules.
This type of research is helping scientists investigate a larger question in autoimmunity: why an infection that is common in the general population might contribute to autoimmune disease only in susceptible individuals.
The Immune System And Nervous System Are Closely Connected
Another major theme was neuroimmunology, the study of interactions between the nervous and immune systems.
Notably, the workshop’s session on “Neuroimmune Dynamics of Chronic Illness” was moderated by Victoria Shanmugam, MBBS, MRCP, FACR, CCD, Director of the NIH Office of Autoimmune Disease Research (OADR). Shanmugam leads NIH-wide efforts to coordinate autoimmune disease research and helped launch the first NIH-wide Strategic Plan for Autoimmune Disease Research.
Researchers presented several ways immune activity may influence pain and neurological symptoms, including communication between immune cells and sensory neurons, inflammatory signaling within the central nervous system, and differences related to sex and hormonal biology.
The session also highlighted new approaches for making these processes more measurable.
Michelle James, Ph.D., of Stanford Medicine is developing PET imaging tools designed to visualize immune cells and mitochondrial function in the body. Her research includes applications in multiple sclerosis (MS) as well as ME/CFS, offering researchers ways to investigate immune activity in locations that are otherwise difficult to study directly.
These approaches could be particularly valuable in diseases where symptoms involve several organ systems or where conventional tests do not fully capture ongoing biological changes.
Autonomic Dysfunction May Be Part Of A Larger Multisystem Picture
The workshop also devoted an entire session to the autonomic nervous system, which regulates involuntary functions including heart rate, blood pressure, digestion, temperature regulation, and other processes necessary for maintaining internal stability.
Rather than treating autonomic dysfunction as an isolated problem, researchers discussed the autonomic nervous system as part of a broader network communicating with the brain, immune system, endocrine system, gastrointestinal tract, and cardiovascular system.
Susan Eshleman, M.D., Ph.D., described work at a multidisciplinary Johns Hopkins clinic treating people with moderate-to-severe dysautonomia and complex combinations of chronic pain and other symptoms. The research initiative is designed to improve diagnosis, monitoring, and treatment by examining these conditions across specialties rather than treating each manifestation independently.
Her presentation also described observations from multidisciplinary clinical work in which autonomic dysfunction, gastrointestinal problems, joint hypermobility, neuropathy, and evidence of immune dysregulation or autoimmunity sometimes appeared together.
These observations do not mean that dysautonomia itself is necessarily autoimmune. Instead, they raise questions about whether immune dysfunction may contribute to autonomic abnormalities in certain subgroups and whether identifying those biological differences could eventually help guide treatment.
The Vagus Nerve Provides A Direct Link Between The Nervous And Immune Systems
Perhaps one of the clearest examples of neuroimmune communication discussed during the workshop involves the vagus nerve.
Kevin Tracey, M.D., of the Feinstein Institutes for Medical Research has studied what is known as the inflammatory reflex, a neural pathway through which the nervous system can regulate immune activity and suppress inflammation.
Research stemming from this work helped lead to vagus nerve stimulation as a therapeutic approach for rheumatoid arthritis, providing a striking example of how manipulating a neural pathway can affect an autoimmune inflammatory process.
The concept challenges the traditional idea that autoimmune inflammation is controlled only through immune-targeting medications. Instead, the nervous system itself may represent another route through which inflammatory activity can be regulated.
Shared Symptoms Do Not Necessarily Mean Shared Disease
At the same time, the workshop repeatedly emphasized the need to distinguish overlapping symptoms from identical disease mechanisms.
Conditions such as fibromyalgia, ME/CFS, Long COVID, endometriosis, dysautonomia, and autoimmune diseases may share features such as fatigue, pain, cognitive problems, or autonomic symptoms without sharing a single cause.
That distinction was reinforced by research presented on fibromyalgia genetics, which pointed more strongly toward nervous-system biology than autoimmune mechanisms.
Similarly, researchers studying infection-associated illnesses cautioned against assuming that biological convergence means every person with similar symptoms follows the same disease pathway.
As one presentation summarized the concept, convergence should be viewed as a starting point for investigation rather than proof of a shared pathogenesis.
For autoimmune research, this may be especially important. Identifying which individuals have autoimmune, inflammatory, neurological, autonomic, metabolic, or overlapping mechanisms could ultimately be more informative than grouping people solely according to symptoms.
Moving Toward Mechanism-Based Medicine
The workshop concluded by looking toward clinical research, translational science, and therapeutic development. Researchers discussed the need for better-defined disease subgroups, biomarkers, longitudinal studies, multidisciplinary care, and research methods capable of connecting biological mechanisms with symptoms and treatment response.
That approach could have important implications for autoimmune disease.
Autoimmune conditions are already highly heterogeneous. Two people with the same diagnosis may experience different organs affected, symptoms, disease trajectories, and responses to treatment. At the same time, one person may develop multiple autoimmune or immune-mediated conditions alongside neurological, autonomic, gastrointestinal, or chronic pain symptoms.
Understanding those connections will require research that crosses the traditional boundaries between immunology, neurology, rheumatology, infectious disease, endocrinology, genetics, and other specialties.
The NIH workshop reflected a growing effort to do exactly that: study complex chronic disease according to the biological systems and mechanisms involved, while recognizing that those mechanisms can intersect across diagnostic categories.
For autoimmune disease research, that broader view may help reveal not only why autoimmunity develops, but also why its effects can extend so widely throughout the body.