top of page

August 15, 2025

How Stress Affects Your Immune System and What It Means for Autoimmune Conditions

The connection between chronic stress and the immune system is now being studied scientifically, especially within a young field of medicine known as psychoneuroimmunology.

Lorem

Many people notice that their symptoms shift or intensify during times of strain. They may tire more quickly, sleep less well, or find themselves more prone to infections or flare-ups. For those living with an autoimmune condition, such phases can feel especially challenging.


The connection between chronic stress and the immune system is now being studied scientifically, particularly within a young field of medicine called psychoneuroimmunology. This area of research looks at how the mind, the nervous system, and the immune response interact — and what that might mean for people living with autoimmune conditions.


In this article you will find an overview of what is currently known about these influences, what is still uncertain, and why it is worthwhile to take your own sources of strain seriously. Not because you are expected to solve everything on your own, but because recognizing these connections can help in coping with illness and finding more stability.


What we know today about stress and the immune system

Stress is part of life. In small doses it can even be helpful, keeping us alert, mobilizing energy, and sharpening focus. But when stress becomes constant, it turns into a burden — not only for the mind and daily life, but also for the body.


Medically, the process can be described quite clearly. When a situation is perceived as stressful, the body’s stress system is activated. The so-called HPA axis (hypothalamus–pituitary–adrenal axis) triggers the release of cortisol, along with adrenaline and other messenger substances. In the short term, this reaction is useful: it puts the body on alert, a protective function shaped by evolution — the classic “saber-tooth tiger” example.


When this activation continues for too long, however, it can affect many bodily processes, including immune defense. Studies show that chronic stress can alter the immune system. Inflammatory processes may intensify, certain immune cells may overreact, or they may lose proper regulation. For people with autoimmune conditions, this imbalance can have noticeable consequences.


This does not mean that stress alone causes illness. But it can influence how active the immune system is, how strongly symptoms are felt, and how the body manages strain.


Psychoneuroimmunology: a young science with growing influence

It may sound abstract, but it is something people can feel in very real ways: our immune system does not work in isolation. It is part of a larger network that includes the nervous system and the hormonal system. This interaction is at the heart of psychoneuroimmunology, a young but increasingly important field of research.


At its core, the field asks: how do psychological burdens influence the immune system? And in the other direction, how does the state of the body shape emotional experience?


A central mechanism here is the HPA axis, the body’s own stress-regulation system. When it is activated — for example by social pressure, overwhelm, or inner tension — cortisol levels in the blood rise. Cortisol has an important function: it provides short-term energy and helps regulate inflammation. Yet if cortisol remains elevated over long periods, the effect can tip into its opposite.


Research shows that ongoing stress can disrupt immune regulation. In medical terms, this is described as a TH1–TH2 shift — a change within the immune response. Such a shift can favor inflammatory processes and weaken the fine balance between defense and regulation in the immune system. For people with autoimmune conditions this is particularly relevant: an immune system that is already overactive or misdirected can come under even greater strain when chronic stress is added.


What happens under chronic stress? A closer look at the immune system

The body tries to protect you — sometimes even at the expense of your health.


Stress is not only a feeling; it changes processes throughout the body. This becomes especially clear when stress continues over long periods. In such cases, experts speak of chronic stress, and this can have lasting effects on the immune system.


One key mechanism is the shift in balance between different immune cells, often called the TH1–TH2 shift.


It involves to so called T-Helper Cells:

  • TH1 cells are mainly responsible for fighting viruses and bacteria and tend to promote inflammation.

  • TH2 cells counteract these reactions, dampening inflammation and supporting more regulating processes, including those seen in allergies.


In a healthy state, these systems are in balance. Under chronic stress, the relationship can shift: inflammatory activity increases while regulating processes weaken. The result is a body that is more prone to inflammation.


At the same time, stress alters hormone regulation. The HPA axis, which normally helps keep stress in check, can adapt in ways that become problematic. In some cases, the body may no longer produce enough cortisol despite ongoing stress. This is referred to as functional hypocortisolism. In addition, immune cells may become less responsive to cortisol, a phenomenon known as glucocorticoid resistance. When this happens, the body’s natural “brakes” on inflammation no longer work as they should.


Much of this is complex, and not all of it is fully understood. But the overall picture is clear: prolonged psychological strain can push the immune system out of balance, especially in people whose immune regulation is already disrupted.


When the body falls out of balance: emotional strain as a disease amplifier

Not all stress is the same. There is a difference between brief tension — like before a presentation or during exercise — and long-lasting emotional strain that weighs heavily over time. Many people with autoimmune conditions describe how especially difficult life events, such as loss, conflict, prolonged pressure, or ongoing inner tension, were followed by changes in their symptoms. What these experiences have in common is that they were emotionally hard to carry and often remained unresolved.


Research is paying increasing attention to this link. Studies suggest that emotional strain can influence the course of autoimmune conditions, and in some cases may even precede the first onset. Scientists continue to investigate whether traumatic experiences, chronic everyday stress, or unresolved conflicts contribute to disease activity. There is some evidence that ongoing emotional stress, especially when experienced early in life, may be connected to higher disease activity later on.


This does not mean that emotions alone explain the course of an illness. But leaving them out of the picture would miss an important part of the whole. Emotional strain may not be the root cause, yet it can act as an amplifier for processes already active in the body.


What this can mean in concrete terms: a look at MS, lupus and RA

Three conditions, many parallels, but also important differences.


Not all autoimmune conditions respond to stress in the same way. But in some illnesses, the link between emotional strain and physical changes is becoming clearer, at least in early research. These include multiple sclerosis (MS), systemic lupus erythematosus (SLE), and rheumatoid arthritis (RA).


Multiple sclerosis (MS): fewer inflammations through stress management?One study explored whether targeted stress-reduction training could positively influence the course of MS. The findings suggested that participants who learned to cope better with strain developed fewer new inflammatory lesions in the brain over several months, measured with MRI scans. This does not mean that stress causes MS, but it does suggest that stress can shape its course, for example by amplifying inflammation. Recognizing and addressing stress early may therefore be worthwhile, both emotionally and physically.


Lupus (SLE): when emotional events leave traces in the blood

In lupus, some studies have found that emotional strain is linked to measurable changes in the immune system. After stressful experiences such as prolonged inner tension or conflict, shifts in inflammatory markers and autoantibodies were observed in patients’ blood, and these changes can be connected to disease flares.


Rheumatoid arthritis (RA): inflammation and experience sometimes go hand in hand

In rheumatoid arthritis, researchers have repeatedly studied how psychological strain influences inflammatory processes in the body — especially messenger substances like interleukin-6 (IL-6). IL-6 is a cytokine, a chemical signal that promotes inflammation and activates the immune system. When the body remains in a state of constant alert due to stress, IL-6 release can increase even without an immediate physical threat. Studies have shown that people with RA who lived under prolonged stress sometimes had elevated IL-6 levels. At the same time, there is evidence that positive experiences, such as social support and relaxation, may reduce certain markers of inflammation.


Self-regulation and emotional support

Not everything can be changed, but much can be influenced.


Autoimmune conditions cannot be “thought away.” Yet how you live with them — and how your body responds to strain — can be influenced. Emotional support and mindful self-regulation can bring relief, both physically and emotionally.


What does that mean in practice?

  • Breathing exercises or brief moments of mindfulness can help calm the nervous system, especially during demanding phases or in stressful situations. They are not a miracle cure, but often a first step toward more balance.

  • Conversations in a safe space, such as psychologist-guided support groups, offer the chance to put experiences into words without justification or judgment. This can ease inner tension that might otherwise remain hidden in the body.

  • Body awareness, gentle movement, creative expression, or psychoeducation can also be effective in better understanding personal patterns of response and in developing new ways of dealing with strain.


The aim is not to pressure yourself or to gloss over difficulties. It is about gradually building more inner stability, even when circumstances remain challenging. For many, it can be a relief to find ways of working with the body rather than against it — and to discover that not everything has to be carried alone. Step by step, it can restore a sense of influence over one’s own well-being.


Conclusion: When emotional strain becomes physical

Autoimmune conditions are complex. Living with them is complex, too.


What we know today: stress is not a single cause, but it can influence what is already happening in the body. It may amplify processes, disrupt balance, or make an illness feel heavier than it otherwise would. This does not apply in the same way to everyone, and there is no simple formula.


Yet studies, case reports, and the lived experiences of many people suggest: emotional strain does affect the immune system. Taking your own stress seriously can sometimes also mean supporting your physical health.


Why we at ImmuniFriend also talk about emotions

Because no one should have to hold on alone.


Many people with autoimmune conditions experience not only physical symptoms, but also emotional exhaustion, social withdrawal, and the feeling of not being understood. That is why at ImmuniFriend we take a holistic approach: guided by psychology and supported by community.


In our groups you meet people who know what it feels like when a diagnosis changes life. We talk about the burdens without the need for long explanations. And together we look for ways to handle them — in a way that fits you and your everyday life.


Connection can create a sense of safety. Not because everything suddenly gets better, but because you no longer have to feel alone with it.


If you would like to take a first step

If you feel you are carrying too much on your own, our group counselling may be a good place to begin. You are welcome to learn more without any obligation. We look forward to meeting you if you decide to join.


Disclaimer

The contents of this article are for general information about the current state of research. They are not a substitute for medical diagnosis or treatment. For any health concerns, please always consult qualified medical professionals.

Quellen

Assaf, A. M., Al-Abbassi, R., & Al-Binni, M. (2017). Academic stress-induced changes in Th1- and Th2-cytokine response. Saudi Pharmaceutical Journal25(8), 1237–1247. https://doi.org/10.1016/j.jsps.2017.09.009


Ayano, M., & Horiuchi, T. (2023). Complement as a biomarker for systemic lupus erythematosus. Biomolecules13(2), 367. https://doi.org/10.3390/biom13020367


Cohen, S., Janicki-Deverts, D., Doyle, W. J., Miller, G. E., Frank, E., Rabin, B. S., & Turner, R. B. (2012). Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk. Proceedings of the National Academy of Sciences109(16), 5995–5999. https://doi.org/10.1073/pnas.1118355109


Cohen, S., Janicki-Deverts, D., & Miller, G. E. (2007). Psychological stress and disease. JAMA298(14), 1685. https://doi.org/10.1001/jama.298.14.1685


Davis, M. C., Zautra, A. J., Younger, J., Motivala, S. J., Attrep, J., & Irwin, M. R. (2007). Chronic stress and regulation of cellular markers of inflammation in rheumatoid arthritis: Implications for fatigue. Brain Behavior and Immunity22(1), 24–32. https://doi.org/10.1016/j.bbi.2007.06.013


Dhabhar, F. S. (2014). Effects of stress on immune function: the good, the bad, and the beautiful. Immunologic Research58(2–3), 193–210. https://doi.org/10.1007/s12026-014-8517-0


Hannemann, J., Ott, M., Singer, M., Zimmermann, U., & Schubert, C. (2016). Selbstzerstörung bei Stress? Deutsche Heilpraktiker-Zeitschrift11(01), 30–34. https://doi.org/10.1055/s-0036-1579564


Kiecolt-Glaser, J. K., McGuire, L., Robles, T. F., & Glaser, R. (2002). Psychoneuroimmunology: Psychological influences on immune function and health. Journal of Consulting and Clinical Psychology70(3), 537–547. https://doi.org/10.1037/0022-006x.70.3.537


Miller, G. E., Chen, E., & Zhou, E. S. (2007). If it goes up, must it come down? Chronic stress and the hypothalamic-pituitary-adrenocortical axis in humans. Psychological Bulletin133(1), 25–45. https://doi.org/10.1037/0033-2909.133.1.25


McCray, C. J., & Agarwal, S. K. (2010). Stress and autoimmunity. Immunology and Allergy Clinics of North America31(1), 1–18. https://doi.org/10.1016/j.iac.2010.09.004


Mohr, D. C., Lovera, J., Brown, T., Cohen, B., Neylan, T., Henry, R., Siddique, J., Jin, L., Daikh, D., & Pelletier, D. (2012). A randomized trial of stress management for the prevention of new brain lesions in MS. Neurology79(5), 412–419. https://doi.org/10.1212/wnl.0b013e3182616ff9


Pawlak, C. R., Witte, T., Heiken, H., Hundt, M., Schubert, J., Wiese, B., Bischoff-Renken, A., Gerber, K., Licht, B., Goebel, M. U., Heijnen, C. J., Schmidt, R. E., & Schedlowski, M. (2003). Flares in Patients with Systemic Lupus erythematosus Are Associated with Daily Psychological Stress. Psychotherapy and Psychosomatics72(3), 159–165. https://doi.org/10.1159/000069735


Peralta-Ramírez, M. I., Jiménez-Alonso, J., Godoy-García, J. F., & Pérez-García, M. (2004). The effects of daily stress and stressful life events on the clinical symptomatology of patients with lupus erythematosus. Psychosomatic Medicine66(5), 788–794. https://doi.org/10.1097/01.psy.0000133327.41044.94


Zhang, C. (2020). Flare‑up of cytokines in rheumatoid arthritis and their role in triggering depression: Shared common function and their possible applications in treatment (Review). Biomedical Reports14(1). https://doi.org/10.3892/br.2020.1392

bottom of page