How Your Immune System Works and How to Improve It

Most people think of the immune system as something that keeps them from getting sick. When it works, they feel healthy. When it fails, they catch a cold. And when they miss a few nights of sleep, they seem more likely to get sick.

That picture is not wrong. It is just remarkably incomplete.

Your immune system is constantly measuring you. It monitors tissues, helps manage the microbes that live in and on your body, participates in repair, and determines when a change deserves a response. It also communicates with your nervous system. Some of the most intriguing experiments in immunology now suggest that the brain can retain information about an immune state and help recreate aspects of that state later.

My discussion with immunologist Dr. Max Krummel centered on a crucial shift in perspective: better immunity does not mean more immune activity everywhere, all the time. It means having the appropriate response, in the appropriate tissue, at the appropriate time.

Table of Contents

• Your Immune System Is a Sensory System
• Why Children Get Sick So Often
• Aging Changes Both the Immune System and What It Must Recognize
• Why the Speed of Change Matters
• The Thymus: Where T Cells Develop and Learn Tolerance
• Why Sleep Matters for Immune Function
• Stem Cells, Cord Blood Banking, and the Difference Between Promise and Readiness
• Spatial Biology: Where an Immune Signal Occurs Matters
• Can the Brain Remember an Immune State?
• Cancer Immunotherapy Changed How We Think About Immunity
• Vaccines: Separate the Benefit From Questions About Optimization
• Why Trust Requires More Than Telling People What to Do
• Autoimmunity Is Not One Disease or One Kind of Overactivity
• Why Future Treatments May Require a Sequence, Not a Single Switch
• Why Basic Research and Failure Are Essential
• A Practical Framework for Supporting Immune Health

Your Immune System Is a Sensory System

The traditional model of immunity is a battle between self and non-self. Your own cells belong. An invading virus does not. The immune system distinguishes between the two and attacks the invader.

But consider a tumor. It is not an outside organism. It arose from your own cells. Or consider the bacteria in your gut. They are not genetically you, yet many contribute to your health. A system that simply destroyed everything foreign would not serve you very well.

Krummel describes immunity as a distributed sensory system. Vast numbers of immune cells move through the body, detecting molecular information and responding to what they encounter. T cells, for example, use receptors to recognize particular molecular fragments called peptides, presented to them by other cells.

Those cells are not operating in isolation. They exchange information. One cell may detect tissue damage, another may recognize an unfamiliar molecular signal, and others may help determine whether the situation requires repair, containment, tolerance, or attack.

The immune system therefore does much more than fight infections:

• In the gut, it helps regulate relationships with resident microbes.
• In the brain, immune cells called microglia participate in maintenance and cleanup.
• In the heart, immune cells help manage material released by working heart muscle cells.
• Across tissues, it contributes to repair and helps maintain local function.

The National Institute of Allergy and Infectious Diseases’ immune system overview provides useful background on the cells and tissues involved. The larger conceptual point is that immunity is not a single defense switch. It is an ongoing relationship between the body and its environment.

What HIV Revealed About Immune Function

Krummel entered immunology around the height of the AIDS crisis. HIV targets CD4 T cells, a critical subset of immune cells. As those cells were lost, people developed infections that healthy immune systems ordinarily controlled, along with certain cancers and neurological complications.

That tragedy revealed how much the immune system was doing in the background. Its importance extended well beyond the infections people usually associated with illness.

Understanding those cells required basic work: learning how to keep them alive outside the body, identifying their molecular components, and developing tools to test what activated or inhibited them. Much of today’s therapeutic capability rests on those seemingly narrow questions.

Why Children Get Sick So Often

A young child is encountering a world of microbes for the first time. An adult may already have immune memory of a particular pathogen. A child may not.

That helps explain the familiar pattern of repeated childhood illnesses. Each new exposure presents a learning problem. Once the immune system responds, it can retain information that allows a faster response to later encounters.

Early life also requires restraint. A developing body is changing rapidly, and the immune system must learn to tolerate its own tissues while becoming capable of responding to threats. Infant immunity is therefore not simply a smaller version of adult immunity.

These developmental differences matter for vaccination, but they do not translate into a blanket rule to wait until a particular age. Vaccines have different recommended ages because protection, immune development, and disease risk differ by vaccine. Questions about an individual child’s timing belong with their pediatric clinician.

Learning What to Live With

Immune development is not only about learning what to eliminate. It is also about establishing workable relationships with the microbes that live on our skin and in our digestive tract.

Those organisms bring biological capabilities we do not possess on our own. Gut microbes help process dietary components and modify molecules involved in digestion. The developing immune system must help keep those communities in suitable locations and quantities without treating every organism as an enemy.

That is a much richer task than simply strengthening a defensive barrier. It involves learning when coexistence is beneficial and when an organism’s behavior or location makes it dangerous.

Aging Changes Both the Immune System and What It Must Recognize

At the other end of life, several problems converge. Some immune cells become less functional, the production of new cells changes, and cells maintained over many years can be lost.

But Krummel emphasized another challenge: the body the immune system is monitoring is itself changing.

We begin life with cells that largely share the same inherited genetic information. Over time, cells accumulate different mutations. Some changes disappear when cells die. Others persist in descendants of those cells, creating patches of related cells with their own genetic differences.

The result is a biological mosaic. You are not genetically identical, cell for cell, to the person you were at birth.

That does not mean every mutation is dangerous. Many are inconsequential. But the accumulating diversity raises an interesting recognition problem: how does an immune system identify a dangerous departure from normal when normal is continually changing?

The Submarine Recognition Problem

Krummel used an analogy from an earlier generation of immunologists. Imagine a submarine crew using two reference books. One describes the engine sounds of friendly submarines. The other describes enemy vessels. A sound from the first book means hold fire. A sound from the second means respond.

Now imagine that the friendly fleet gradually develops an enormous variety of engine sounds. The distinction becomes harder to make.

This is a useful way to think about one possible consequence of aging. As the molecular background becomes more varied, a dangerous change may become less conspicuous. Krummel presented this as a conceptual explanation for part of the aging problem, not as a complete, settled account of immune aging.

Cancer risk also rises as mutations accumulate. These two issues can interact: potentially dangerous cells emerge within a body whose immune surveillance has changed and whose definition of normal has become more complicated.

Repair and Cancer Share Some Biological Demands

When you sustain a wound, cells must grow and divide to fill the gap. A cell that grows efficiently can be useful in that setting.

But growth needs limits. Cancer involves more than rapid division, yet inappropriate growth and failure to respect normal tissue controls are central problems. A trait that helps a cell compete during repair can become harmful in another context.

This is one reason the immune system cannot simply eliminate every altered cell or encourage every repair process indefinitely. It must help distinguish useful regeneration from uncontrolled growth.

Why the Speed of Change Matters

Your nervous system adapts to persistent input. Walk into a place with a powerful smell, and it is initially overwhelming. Stay there long enough, and you may barely notice it.

Krummel described visiting Époisses, the French village associated with a particularly pungent cheese. On arrival, the smell was striking. After some time, it faded into the background. The odor had not vanished. His sensory system had adjusted.

Immune cells also interpret signals in context and over time. A virus can produce a rapid increase in unfamiliar molecular material, accompanied by tissue damage. That combination is very different from a molecular feature that has remained within a familiar range for years.

A slowly developing tumor presents a more difficult problem. It may change incrementally, without the sharp rise and immediate damage associated with an acute infection. Krummel’s hypothesis is that this gradual progression can help a tumor become incorporated into what the immune system accepts.

This is not the only mechanism by which tumors evade immunity. It illustrates why the trajectory of a signal can matter as much as its presence.

The Thymus: Where T Cells Develop and Learn Tolerance

The “T” in T cell refers to the thymus, an organ located near the heart. Immune precursor cells originate in the bone marrow and travel to the thymus, where they develop into T cells.

The thymus has two closely connected jobs:

1. Generate a diverse T-cell population capable of recognizing many potential molecular targets.
2. Help select that population so that cells leaving the thymus are not dangerously reactive to the body’s own tissues.

Think of it as both a production facility and an educational environment. Developing T cells encounter representations of the body’s molecular identity. Cells with unsuitable responses are removed or directed into other roles.

The importance of the thymus became clear through experiments by Jacques Miller. Removing the thymus from newborn mice left them profoundly vulnerable to infection, demonstrating that this once poorly understood organ was essential to immune development.

Why the Thymus Attracts Interest in Aging

The thymus is especially active early in life. It then undergoes involution, becoming smaller and producing fewer new T cells with age.

That creates an obvious therapeutic question: could restoring thymic function provide new immune capabilities later in life?

In cancer, for example, a fresh population of T cells might offer opportunities to recognize a tumor that existing cells have failed to control. Researchers are also exploring ways to engineer immune cells outside the body and give them useful recognition capabilities.

But the thymus is not just a bag of T cells. Its epithelial cells form a specialized environment that supports development and selection. Recreating its function means recreating important aspects of that environment, not merely adding a few cells.

Interest in thymus rejuvenation does not establish that commercially offered thymic peptides or self-directed interventions are safe or effective. Krummel was clear that the underlying ideas are interesting while their practical application remains uncertain.

Why Sleep Matters for Immune Function

The association is familiar: after inadequate sleep, people often feel more vulnerable to illness. The mechanistic explanation is less tidy than a single molecule suppressing a single immune cell.

Sleep changes where immune cells are located and what they are doing. Krummel highlighted research showing substantial shifts in immune-cell trafficking, including movement of some cells back toward the bone marrow during the sleep period.

He also described evidence for nighttime tissue-maintenance programs involving immune cells, including neutrophils. The emerging picture is that sleep helps coordinate immune activity with repair.

A useful analogy is cleaning a windshield. It is easier to clear accumulated debris when new material is not continually striking the glass. Similarly, a period of reduced activity may allow the body to get ahead of some maintenance demands.

That is an explanatory framework, not a complete mechanism. Sleep affects many systems simultaneously, including neural activity, metabolism, fluid movement, and immune-cell behavior. Scientists do not yet agree on how much each component explains susceptibility to infection after sleep loss.

The practical implication is straightforward: treat adequate, consistent sleep as foundational support for immunity. There is no established substitute in this discussion that reproduces all the immune functions of sleep.

Stem Cells, Cord Blood Banking, and the Difference Between Promise and Readiness

It is easy to move from an exciting biological principle to a seemingly obvious personal decision: if young cells are valuable, why not store them now for future use?

The answer depends on which cells, which disease, and which treatment.

Cord Blood Is Different From Thymic Tissue

Umbilical cord blood contains blood-forming stem cells. Those cells can be relevant to transplantation because they can give rise to cells of the blood and immune system.

That is a different function from the thymus, which provides a specialized setting in which T cells develop and undergo selection.

In our discussion, Krummel was enthusiastic about the biological potential of stored blood-forming cells, but he did not know the specific evidence for successful use of privately banked material by the same child. That uncertainty matters. It would be too strong to turn the discussion into a claim that storing a child’s cord blood guarantees a cure for future leukemia.

For a practical account of uses and limitations, the FDA’s cord blood banking information is a useful starting point. A storage decision should be based on the actual transplant indication, suitability of the cells, family circumstances, and clinical advice.

Organoids Are Models, Not Automatically Replacement Organs

Another approach begins with an adult cell, such as a skin fibroblast, and reprograms it into an induced pluripotent stem cell. Researchers can then guide those cells toward particular identities or grow collections of cells that resemble aspects of an organ.

These organoids can help study disease and test biological ideas. But an important question is whether the model faithfully reproduces the relevant features of the actual organ.

Stored cells also do not solve a timing problem. A technology might eventually become useful without becoming useful soon enough for a particular person. Biological plausibility, experimental success, and a reliable clinical treatment are different milestones.

Banking thymic tissue adds another concern: obtaining it would require an invasive procedure, while its future usefulness remains unclear. Krummel did not recommend elective thymus removal for storage.

Spatial Biology: Where an Immune Signal Occurs Matters

The immune system is mobile, but not every immune cell is constantly circulating. Some T cells reside in particular tissues and remain there, providing local surveillance and protection.

Other cells travel through blood, tissues, and lymphatic vessels. Lymphatic vessels drain fluid from tissues and connect to lymph nodes, where immune information can be exchanged.

Both arrangements matter. A healthy immune system needs local expertise and the ability to mobilize help.

Keeping Tissue Alive Is Not the Same as Making It Function Safely

Some transplanted tissues can survive outside their usual location if they receive suitable blood flow, growth signals, and other support. Pancreatic cells placed beneath the kidney capsule are a useful experimental example.

But survival in a new location is only part of the problem. The immune system must also accept the tissue.

In type 1 diabetes, the immune system attacks insulin-producing pancreatic cells. Providing new cells does not automatically remove the immune process that destroyed the original ones.

Engineered cells introduce additional questions. Depending on the method, the molecules used to alter them or the new material they express may change how the immune system recognizes them. A technically improved cell is not necessarily an immunologically tolerated cell.

A Wound Is a Set of Different Neighborhoods

Krummel described wound-healing experiments in which cells at different distances from a wound were doing different jobs. Cells near the opening received one set of instructions. Cells farther back received another.

The wound was not just the visible gap. It was a spatially organized response extending into surrounding tissue.

This has direct implications for peptides, growth factors, and cell therapies. A molecule may be helpful at one location, in one dose, during one stage of repair, while being ineffective or harmful elsewhere.

A biological effect is not a treatment protocol. To build a treatment, researchers must determine where, when, how much, and for whom.

Can the Brain Remember an Immune State?

One of the most fascinating areas we discussed concerns the insular cortex, a brain region involved in representing internal bodily states.

Krummel described experiments in mice in which researchers induced intestinal inflammation and identified neurons active during that experience. After the animals recovered, researchers artificially reactivated those neurons.

Aspects of the earlier immune response reappeared in the gut, including changes in the accumulation of immune cells.

That is remarkable. It suggests that neural activity associated with a previous inflammatory state can help organize a later immune response.

But the boundary of the finding is equally important: artificially reactivating selected neurons in a mouse is not the same as demonstrating that a person can recall a memory and reliably treat an immune disease.

What This Might Mean for Meditation, Stress, and Memory

The experiments open interesting questions. Could brain states associated with calm influence inflammatory activity? Could a familiar smell or comforting experience bring back not only an emotional state, but aspects of the bodily state that accompanied it?

Krummel wondered whether some effects of meditation might involve this kind of brain-to-body communication. We also discussed the possibility that sensory cues could become associated with healthier states.

These are hypotheses, not established immune-training protocols. There is no basis here for prescribing a particular memory exercise or scent as a way to prevent infection.

The distinction between chronic and acute stress also matters. Chronic stress and a brief, acute stress response do not have identical immune effects. It is too simplistic to label every stress response immunosuppressive.

And immune cells are not interpreting the wording of affirmations. If a thought influences immunity, the plausible route involves the physiological brain and body state associated with that thought.

This should never become a way to blame people for illness. A person’s infection or autoimmune condition is not evidence that they failed to think positively.

Cancer Immunotherapy Changed How We Think About Immunity

Krummel’s early research helped establish that blocking an inhibitory signal on T cells could enhance their activity. In tumor experiments, that approach produced dramatic responses.

The important shift was that the immune system could be therapeutically retuned. T cells that had not controlled a tumor could, under different signaling conditions, attack it.

This work helped lay the foundation for immune checkpoint blockade. The National Cancer Institute’s immunotherapy guide explains the major treatment approaches and how they differ.

These treatments can produce durable responses in some patients, but they do not work for everyone. More immune activity can also worsen autoimmune disease, reinforcing the point that immune activation is not universally beneficial.

Cancer Vaccines and Engineered T Cells

Therapeutic cancer vaccines aim to direct immune responses toward molecular features of a tumor. They use the immune system’s learning machinery, but their purpose differs from that of routine vaccines used to prevent infectious disease.

Engineered T-cell therapies offer another route. Researchers can modify cells to recognize selected targets and return them to a patient.

It is important not to generalize the difficulties across every cancer. CAR T-cell therapies have established uses in certain blood cancers, while extending their success to many solid tumors remains a major challenge. Cells must reach the tumor, survive, remain functional, and overcome a local environment that may suppress them.

Vaccines: Separate the Benefit From Questions About Optimization

Vaccination can train immune recognition without requiring a person to endure the full consequences of the disease. That benefit is easy to underestimate when the diseases themselves have become unfamiliar.

Smallpox was devastating. Measles can cause severe complications, including brain inflammation. The fact that many people have not personally encountered these outcomes does not make the risks imaginary.

Krummel was clear that he vaccinated his children and regarded the protective benefit as compelling.

At the same time, our conversation explored questions people ask about timing, combinations, side effects, and communication. Those questions should be handled respectfully and answered with evidence rather than treated as a statement of political identity.

What a Question About Timing Does and Does Not Establish

It is reasonable to ask why a vaccine is recommended at a particular age, what is known about giving vaccines together, and whether an individual medical circumstance changes the recommendation.

But asking whether a regimen could be optimized is not evidence that the existing regimen is unsafe. Nor does the fact that another schedule might generate an immune response establish that delaying protection provides a net benefit.

Krummel described postponing one vaccination when his child was unwell. That personal decision is not a general recommendation to delay childhood vaccines. Discuss individual circumstances with the child’s clinician rather than constructing a schedule from anecdotes.

Completion also matters. A schedule that becomes complicated enough to cause missed doses can reduce protection, even if the original intention was to make vaccination more manageable.

Inflammation, Neurodevelopment, and the Limits of Animal Models

We also discussed experiments in which immune activation during pregnancy is used to study changes in brain development and behavior in offspring. These models help researchers investigate how immune signals can influence the nervous system.

They do not establish that childhood vaccines cause autism. An experimentally induced immune challenge during pregnancy, a postnatal vaccination, and a human developmental diagnosis are not interchangeable events.

For clarity, the evidence reviewed by the CDC does not support a causal link between vaccines and autism. The broader scientific observation that inflammation can influence brain biology should not be used to imply that this specific causal claim has been demonstrated.

A family’s experience deserves careful attention. Establishing causation still requires more than the fact that one event occurred before another.

Why Trust Requires More Than Telling People What to Do

Scientific expertise does not remove the need for explanation. People want to understand what a recommendation is trying to prevent, how strong the evidence is, what the uncertainties are, and whether financial incentives influence the choices presented to them.

Krummel raised a useful example from cancer treatment: predicting who will respond to an expensive drug can be enormously valuable to patients, but the commercial incentive to develop such a test may not align neatly with that value.

That does not mean the people working in pharmaceutical companies are indifferent to health. Many are deeply committed to treating disease. It means an institution’s incentives and a patient’s interests are not automatically identical.

The same care applies to interpreting anecdotes. If someone takes a supplement and feels better, the improvement may be real. It does not, by itself, reveal whether the supplement caused it, which ingredient mattered, or whether another person should expect the same result.

Good communication makes room for both realities: people’s experiences matter, and causal claims require appropriately designed evidence.

The early pandemic illustrated how difficult communication becomes when decisions must be made with limited information. Guidance can change as evidence develops. Explaining that uncertainty is more useful than pretending it never existed.

Autoimmunity Is Not One Disease or One Kind of Overactivity

Autoimmune disease involves immune responses directed against the body’s own components. But the phrase covers many different mechanisms.

Some susceptibility is genetic. Krummel described how defects in signals that normally restrain B cells can contribute to the production of autoantibodies. B cells are the cells that produce antibodies, and their activity requires regulation just as T-cell activity does.

Other conditions involve different combinations of immune cells, tissue responses, and environmental triggers.

It is also important not to group every chronic inflammatory condition under the same label. Asthma is heterogeneous and is not simply synonymous with autoimmunity. Persistent fatigue likewise does not establish an autoimmune diagnosis.

The Same Symptom Can Arise From Different Immune Programs

Two people with asthma may both have difficulty breathing while having different underlying inflammatory patterns. Some forms involve prominent eosinophils; others involve different cells and triggers.

That helps explain why one treatment can work well for one person and poorly for another.

Inflammatory bowel disease presents a similar challenge. Drugs that block inflammatory signals, such as TNF, can be highly effective for some patients. Others do not respond, or respond initially and later lose benefit.

The clinical task then becomes finding another treatment without always having a clear prediction of which one will work.

Krummel’s research approach is to map these different tissue configurations, which he calls archetypes. The goal is to identify what the immune system is actually doing, rather than treating every diagnosis as one uniform process.

Why Potentially Harmful Immune Traits Persist

A biological trait can carry a cost in one environment and a benefit in another. The classic example is the protection against severe malaria associated with sickle cell trait, despite the serious consequences of sickle cell disease.

Krummel used a bacterial culture analogy. In one nutrient environment, certain bacteria grow rapidly while others lag. Change the nutrient source, and some of the former laggards may become the successful population.

Diversity provides options when conditions change.

That is a useful evolutionary framework, but it does not establish that a person with psoriasis or another autoimmune condition is generally better protected from infection. Individual immune advantages and disadvantages are more specific than that.

Why Future Treatments May Require a Sequence, Not a Single Switch

Biological systems are resilient. They tolerate variations in activity, nutrition, temperature, and countless other inputs without collapsing.

That resilience is useful in health. In chronic disease, it can also help maintain an undesirable state.

A tumor, for example, may recruit aspects of tissue repair that support its survival. Simply increasing immune activity may not be enough. A treatment might first need to dismantle a protective environment, then improve recognition, and then enable effective killing.

Krummel’s broader proposal is that some diseases may require a coordinated sequence of interventions, rather than one permanently effective molecular push.

The right intervention could fail if given at the wrong stage. A useful signal could be ineffective before another part of the system has changed. This returns us to the importance of dose, timing, location, and context.

What Computational Tools Can Contribute

Researchers can now examine gene expression in individual cells and use spatial information to investigate how those cells are organized within tissue.

Machine learning can help identify relationships in those data and prioritize possible experiments. It can suggest which interactions might matter or which patients share a biological pattern.

But a predicted relationship is not a demonstrated treatment effect. An experiment still has to test whether changing that interaction produces the intended result.

Large language models can help work with existing knowledge, but discovery also requires learning things that are not yet established. Computational power can improve the search. It does not eliminate the need to interrogate biology directly.

Why Basic Research and Failure Are Essential

Many major advances began with questions that did not initially look like treatment development.

• CRISPR emerged from research into microbial defense systems.
• GLP-1 drug development benefited from insights involving an unusual animal, the Gila monster.
• Checkpoint immunotherapy grew from asking what particular signaling molecules did to T cells.

The common thread is curiosity about how the world works.

Research does not provide a fixed return for effort. Five hours can produce no useful answer. Another five hours, after years of groundwork, can produce an insight that changes a field.

That is why a well-designed experiment is not merely one that supports an exciting idea. It is one capable of showing that the idea is wrong. Krummel called attention to the value of these decisive tests: they prevent researchers from building indefinitely on an attractive but mistaken explanation.

Scientific communication should make that process visible. It should include the uncertainty, failed attempts, and practical limits, not just the breakthrough announcement.

It should also recognize that trust has a history. Scientific jargon can exclude people, and past abuses can shape how communities interpret present recommendations. Being technically correct does not excuse failing to communicate in a human way.

A Practical Framework for Supporting Immune Health

The most useful lesson is not to search for a universal immune booster. It is to support the conditions under which an extraordinarily complex regulatory system can do its work.

1. Prioritize sleep. Sleep coordinates immune-cell movement and maintenance processes that are not fully reproduced by simply resting while awake.
2. Seek appropriate protection from disease. Discuss vaccination and individual medical circumstances with a qualified clinician.
3. Distinguish established treatments from experimental possibilities. Thymus rejuvenation, tissue engineering, and many peptide applications remain at very different stages of development.
4. Ask about context. A useful treatment needs the right target, dose, timing, location, and patient.
5. Respect brain-body interactions without overstating them. Neural control of immune activity is an exciting research area, not proof that thoughts can replace medical care.
6. Look for evidence beyond testimonials. A compelling personal story can generate a hypothesis, but it cannot determine safety or effectiveness on its own.

The aim is not maximal immune aggression. An immune system that attacks indiscriminately can injure the very body it is meant to protect.

The aim is appropriate immunity: enough responsiveness to control danger, enough restraint to preserve healthy tissue, and enough flexibility to maintain a body that is continually changing.