What Happens to a Child’s Immune System in September?

The Science of Seasonal Immunity

 

Your child’s immune system does not work at one fixed setting all year. It is a dynamic network of physical barriers, immune cells, proteins, chemical signals and specialised tissues that constantly adjusts to what the body encounters.

 

Immune activity also varies with time. Research has identified daily and seasonal patterns in immune-cell numbers, inflammatory signalling and immune-related gene activity. September is particularly interesting because these biological rhythms meet a dramatic change in exposure as children return to classrooms, routines shift, daylight shortens and respiratory viruses such as rhinovirus circulate readily.

 

So, what is happening inside the immune system when the autumn term begins? To understand that we need to follow a pathogen from the moment it reaches the body.

 

Your first line of defence: mucosal immunity

 

When we think about immunity, we often picture white blood cells circulating through the bloodstream. But some of our most important immune defences are positioned exactly where pathogens are most likely to enter.

 

For a respiratory virus, the mucosal surfaces of the nose, mouth and airways are among the first points of contact. Far from being passive walls, these surfaces form an active biological defence system.

 

The epithelial cells lining the respiratory tract are covered by mucus, which helps trap particles and microorganisms before they travel deeper into the airways. Tiny hair-like structures called cilia move rhythmically, helping transport mucus and trapped material away from the lungs.

 

The secretions covering these surfaces also contain molecules involved in immune defence, including enzymes, antibodies and antimicrobial proteins such as lactoferrin.

 

Together, these mechanisms form part of mucosal immunity, helping identify, trap and remove potential pathogens at some of the body's most exposed surfaces. September does not suddenly change these defences, but school return dramatically increases how frequently they may be called into action.

 

From first alarm to immune memory: innate and adaptive immunity

 

If a respiratory virus such as rhinovirus gets beyond these initial barriers and begins infecting cells, two interconnected arms of immunity come into play: the innate and adaptive immune systems.

 

Innate immunity provides the rapid first response. Cells lining the respiratory tract contain molecular sensors called pattern-recognition receptors, which recognise characteristic signs of infection, including components of viral genetic material.

 

Once a threat is detected, infected cells release signalling molecules including interferons. These act as a kind of biological warning system, helping neighbouring cells switch on antiviral defences. Other chemical messengers called cytokines coordinate inflammation and help recruit immune cells to the affected tissue.

 

Several types of white blood cell can then participate. Macrophages can engulf pathogens, damaged cells and cellular debris, while natural killer (NK) cells can recognise and destroy certain infected cells. Neutrophils, rapid-response cells involved in innate defence and inflammation, may also be recruited during respiratory infections.

 

Innate immunity acts quickly and does not require the body to have encountered that exact virus before. Part of its job is to contain the infection while the more specialised adaptive immune response develops.

 

One of the bridges between these systems is the dendritic cell. Dendritic cells can capture pieces of a pathogen, known as antigens, and present them to lymphocytes, helping activate a more targeted response.

 

T cells can coordinate other parts of immunity or recognise and destroy infected cells, while B cells can develop into plasma cells that produce antibodies specifically able to recognise particular antigens.

 

Once an infection has been controlled, some B and T cells can remain as memory cells. If the same or a sufficiently similar pathogen appears again, these cells can help produce a faster, more targeted response. This principle of immunological memory is also fundamental to vaccination.

 

However, immune memory does not mean one cold protects a child against every future one. Rhinoviruses alone exist in many different types, alongside influenza viruses, RSV, adenoviruses, seasonal coronaviruses and other respiratory pathogens. Immunity to one does not automatically provide complete protection against another.

 

This helps explain the frustrating autumn pattern during which a child appears to recover from one cold only to develop another shortly afterwards. Their immune system may not have failed to clear the first infection at all. It may simply be responding to a completely different virus.

 

Why an immune response can make children feel ill

 

Interestingly, many of the symptoms we associate with being ill are not caused entirely by the pathogen itself. Some are consequences of the immune system responding to it.

 

Inflammatory signalling helps increase blood flow and recruit immune cells to affected tissues, while increased mucus can help trap and remove pathogens. Immune signals can also communicate with the brain, contributing to tiredness, reduced appetite and the familiar urge to rest when we are unwell.

 

Fever, when it occurs, is also a regulated host response rather than simply the body becoming accidentally hot.

 

This means that feeling ill does not necessarily mean immunity is failing. A streaming nose, tiredness or fever can accompany an immune system actively responding to a threat.

 

 

September does not weaken immunity: it changes within a seasonal rhythm

 

The immune response we have just described does not operate against a completely static biological background. Several components of human immunity appear to fluctuate across the year.

 

In a large analysis of health data that included 27,478 children, white blood cell counts, neutrophils and C-reactive protein (CRP) showed seasonal variation, with higher levels generally observed during winter and spring than during summer and autumn.

 

CRP is produced by the liver in response to inflammatory signalling and is commonly used as a marker of inflammation, while neutrophils form part of the body's rapid innate immune response. Other research has identified seasonal differences in lymphocyte populations and the activity of genes involved in immune and inflammatory pathways.

 

This does not mean that higher numbers automatically equal “stronger immunity”, nor that autumn represents a period of weak immunity. A neutrophil count tells us something very different from antibody levels, interferon responses or mucosal defence, and different components of immunity can follow different patterns.

 

A better way of interpreting the evidence is that the immune system's baseline state, or immune set point, shifts subtly across the year.

 

Why this happens is likely to involve several interacting influences, including daylight, temperature, sleep, behaviour and pathogen exposure.

 

One particularly interesting connection is the circadian system; the network of biological clocks that helps organise processes throughout the body according to time of day.

 

Immune cells themselves contain molecular clocks. The movement of immune cells between the bloodstream and tissues, production of certain cytokines and activity of inflammatory pathways can all vary across a 24-hour period.

 

Hormones including cortisol and melatonin help communicate information about biological time. Cortisol generally follows a strong daily rhythm, typically rising around the beginning of the active part of the day, while melatonin increases in response to darkness and helps coordinate sleep timing. Both interact with immune processes.

 

September changes some of the environmental signals feeding into this system. Summer can bring later evenings and mornings, while school suddenly reintroduces early wake times and more structured bedtimes just as daylight begins to decrease.

 

Sleep and immunity also communicate in both directions. Immune signals can contribute to sleepiness during infection, while adequate sleep supports the normal regulation of immune-cell activity, inflammatory signalling and adaptive immune responses.

 

None of this means that darker September mornings directly weaken a child's immune system, or that an earlier bedtime will prevent the next classroom cold. The relationship is more nuanced: sleep, circadian rhythms, hormones and immune regulation are interconnected, making adequate and consistent sleep one of the foundations of normal immune function.

 

What changes when school starts?

 

This is why September becomes particularly important. The immune machinery itself has not suddenly changed, but the number of times it is called into action can rise sharply.

 

After the more dispersed social contact of summer, children return to classrooms where prolonged close contact and shared indoor air give respiratory viruses more opportunities to spread. Rhinoviruses, among the major causes of the common cold, are particularly associated with the early-autumn respiratory surge.

 

Each new exposure can put the defences we have already explored into action: mucosal barriers encounter the virus, innate immunity responds and, where necessary, adaptive immunity develops a more targeted response.

 

For children with asthma, this period can be particularly noticeable because respiratory viral infections, including rhinovirus, can trigger inflammation in already sensitive airways and contribute to exacerbations. This association is so well recognised that the increase in asthma problems following school return has sometimes been described as the “September asthma epidemic”.

 

As autumn progresses into winter, the microbial landscape continues to change. Rhinoviruses remain important, while respiratory viruses including RSV and influenza become increasingly relevant. More time indoors and repeated contact at school, clubs and home create further opportunities for transmission.

 

So, school does not switch immunity off. It increases the number and variety of challenges the immune system is being asked to respond to.

 

Why lactoferrin is interesting to immune scientists

 

This brings us back to the body's first line of defence. Lactoferrin is an iron-binding glycoprotein naturally produced by the body and found in human milk, particularly colostrum, as well as saliva, tears and mucosal secretions.

 

Its location is significant. Rather than acting like a conventional vitamin or mineral, lactoferrin naturally forms part of the environment surrounding some of the surfaces where the body and outside world meet.

 

One important aspect of its biology is its ability to bind iron. Iron is essential for human cells, but many microorganisms also depend upon it. The body therefore tightly regulates iron availability, particularly during infection and inflammation. This forms part of a wider defence strategy known as nutritional immunity, in which the availability of nutrients such as iron can influence the relationship between the host and microorganisms.

 

Lactoferrin's biology extends beyond iron binding. Research has investigated its interactions with microorganisms and host cells, as well as its involvement in inflammatory signalling and immune-cell activity.

 

It is therefore often described as immunomodulatory. That distinction matters. Immunomodulation is about interacting with the regulation of an immune response, rather than simply making that response “stronger”.

 

Lactoferrin should not be presented as a way of making a child's immune system stronger than normal or as something guaranteed to prevent respiratory infections. Its relevance is more biologically interesting: it naturally sits at the interface between mucosal surfaces, microbes, iron regulation and innate immunity, exactly where many encounters between the body and its environment begin.

 

Supporting immunity is different from “boosting” it

 

Once you appreciate how many moving parts make up immunity, the familiar phrase “boost your child's immune system” starts to become rather inadequate.

 

Which part are we trying to boost: interferons, neutrophils, antibodies, T cells or inflammation?

 

More is not always better; an effective immune system needs appropriate regulation. It must respond strongly enough to control a pathogen while limiting unnecessary damage to healthy tissue and then reducing inflammatory activity once the threat has passed.

 

Supporting immunity is therefore less about pushing immune activity upwards and more about providing the physiological conditions and nutrients required for normal immune function.

 

That includes adequate energy and protein, a varied diet providing essential micronutrients, sufficient sleep, regular physical activity, good hygiene, vaccination where recommended and appropriate management of existing health conditions.

 

Vitamin D is particularly relevant as autumn approaches. In the UK, the NHS recommends that adults and children over four consider taking 10 micrograms of vitamin D each day during autumn and winter, with separate guidance for babies and younger children.

 

This same support-not-boost philosophy sits behind Leapfrog Remedies IMMUNE and DAILY. IMMUNE, suitable from age four, pairs lactoferrin with vitamin C and zinc, while DAILY, for adults and children aged 12 and over, provides a lower everyday amount of lactoferrin alongside vitamins C, D, E and K2 and zinc. Rather than promising to keep every seasonal bug at bay, both formulas combine lactoferrin with nutrients that contribute to normal immune function in a simple daily format.

 

So, what really happens to children's immunity in September?

 

There is no September switch that suddenly makes a child's immune system weaker. Instead, an already dynamic biological system enters a much more demanding environment.

 

Children's mucosal, innate and adaptive defences continue doing what they do throughout the year, but school return dramatically increases the frequency and diversity of the microbes they encounter. At the same time, immune activity exists within wider seasonal and circadian rhythms influenced by factors including daylight, sleep and hormones.

 

That makes September less of an “immune dip” and more of an immune transition: changing seasonal biology meeting a sudden increase in exposure.

 

The immune system has not switched off; it is being asked to switch on - again and again - in a much busier microbial world.

 

 

Reference list

 

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Kowalczyk, P., Kaczyńska, K., Kleczkowska, P., Bukowska-Ośko, I., Kramkowski, K. and Sulejczak, D. (2022). The lactoferrin phenomenon—A miracle molecule. Molecules, 27(9), p.2941. doi:10.3390/molecules27092941.

 

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NHS (2020). Vitamin D - vitamins and minerals. [online] NHS. Available at: https://www.nhs.uk/conditions/vitamins-and-minerals/vitamin-d/ [Accessed 4 Sept. 2026].

 

Paynter, S., Ware, R.S., Sly, P.D., Williams, G. and Weinstein, P. (2015). Seasonal immune modulation in humans: Observed patterns and potential environmental drivers. Journal of Infection, 70(1), pp.1–10. doi:10.1016/j.jinf.2014.09.006.

 

Radmanish, M., Khalfallah, O., Glaichenhaus, N., Forhan, A., Heude, B., Charles, M.-A., Davidovic, L. and Plancoulaine, S. (2022). Sleep duration trajectories associated with levels of specific serum cytokines at age 5: A longitudinal study in preschoolers from the EDEN birth cohort. Brain, Behavior, & Immunity - Health, 21, p.100429. doi:10.1016/j.bbih.2022.100429.

 

Satia, I., Adatia, A., Yaqoob, S., Greene, J.M., O’Byrne, P.M., Killian, K.J. and Johnston, N. (2020). Emergency Department visits and hospitalisations for asthma, COPD and respiratory tract infections: What is the role of respiratory viruses, and return to school in september, january and march? ERJ Open Research, 6(4), pp.00593–2020. doi:10.1183/23120541.00593-2020.

 

 

Scheiermann, C., Kunisaki, Y. and Frenette, P.S. (2013). Circadian control of the immune system. Nature Reviews Immunology, [online] 13(3), pp.190–198. doi:10.1038/nri3386.

 

Szredzka, A., Chwastowicz, A., Pergoł, J. and Matryba, P. (2025). Circadian clocks and adaptive immune function: From mechanisms to therapeutic applications. Frontiers in Immunology, [online] 16. doi:10.3389/fimmu.2025.1697854.

 

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