MANILA, July 10 — For communities across Asia, the idea that our bodies can “remember” a germ we fought off years ago is a quiet marvel of everyday life. This week, as researchers continue to build on decades of discovery, the science behind that memory—the adaptive immune system—offers a clear window into how vaccines protect families and why new cancer treatments are reaching more patients. The adaptive immune system is our body’s second, more specialised line of defence.
Unlike the immediate but general response of the innate system, this branch provides specific, long-lasting immunity. It relies on two main types of white blood cells called lymphocytes: B cells and T cells.
B cells mature in the bone marrow and are responsible for producing antibodies—proteins also known as immunoglobulins that bind to antigens, neutralising pathogens or marking them for destruction by other immune cells. There are five classes of antibodies, each with a distinct job. IgG is the most abundant, making up about 75% of serum antibodies in the blood.
IgA is found in mucous membranes, such as those lining the respiratory and digestive tracts. IgM is the first antibody produced when the body encounters a new infection.
IgE is involved in allergic reactions, and the function of IgD remains unclear to scientists. For families across the region, this means that when a child catches a cold, a cascade of these specialised proteins is already at work. T cells, meanwhile, mature in the thymus gland.
They come in two main varieties. Helper T cells, marked by the CD4 protein on their surface, activate B cells and macrophages—essentially directing the immune response. Cytotoxic T cells, marked by CD8, kill infected cells directly.
This division of labour is critical: without helper T cells, the body struggles to mount a full response; without cytotoxic T cells, viruses hiding inside cells can evade detection. The way these cells recognise threats is governed by a system of molecules called the major histocompatibility complex, or MHC.
MHC class I molecules present fragments of intracellular antigens—such as those from a virus replicating inside a cell—to CD8+ cytotoxic T cells. MHC class II molecules present extracellular antigens, like those from bacteria floating in the bloodstream, to CD4+ helper T cells. This elegant handoff ensures that the right T cell gets the right information at the right time.
What this means for ordinary people is the basis of vaccination. Vaccines work by exposing the adaptive immune system to harmless versions of a pathogen—dead or weakened germs, or just a piece of them.
The system responds by producing antibodies and activating T cells. More importantly, it creates memory B cells and memory T cells that persist in the body long after the infection is cleared. Upon re-exposure to the same germ, these memory cells mount a faster, stronger response, often preventing illness altogether.
The adaptive system takes days to respond the first time it meets a new pathogen. That lag is why we feel sick before we get better. But the payoff is immunological memory—a lasting protection that can span decades.
For communities across Asia, where infectious diseases like dengue, tuberculosis, and influenza remain significant burdens, this memory is the difference between a mild case and a severe one. The theoretical framework for all this is the clonal selection theory, proposed by Australian immunologist Frank Macfarlane Burnet in 1957.
Burnet’s idea was simple but profound: each lymphocyte carries a unique receptor for a specific antigen. When that antigen appears, the lymphocyte that recognises it is activated and begins to proliferate, producing a clone of identical cells all targeted at the same invader. This explained how the body could mount a specific response to an almost infinite variety of germs.
Closer to home, the practical applications of this science are accelerating. In 2018, the Nobel Prize in Physiology or Medicine was awarded to James Allison and Tasuku Honjo for their discovery of the structure of the T cell receptor and for pioneering work in cancer immunotherapy.
Allison’s work, in particular, showed how blocking certain checkpoints on T cells could unleash them to attack tumours. This has led to a class of drugs called immune checkpoint inhibitors, now used to treat melanoma, lung cancer, and other malignancies. For families in the Philippines and across Southeast Asia, where cancer care is often a struggle against cost and access, these advances offer a new front in treatment.
Immunotherapy does not work for every patient, but for those whose tumours are recognised by the immune system, it can produce durable remissions where chemotherapy failed. The adaptive immune system is also the reason why organ transplants are so difficult. The same T cells that protect us from infection will attack a donated organ as foreign tissue unless suppressed by drugs.
This balancing act—keeping the immune system strong enough to fight infection but weak enough to accept a transplant—is a daily challenge for thousands of patients in Asia. Looking ahead, researchers are working on ways to harness memory B and T cells more precisely.
One goal is to create “universal” vaccines that protect against many strains of a virus at once, by targeting parts of the pathogen that do not mutate. Another is to engineer T cells in the lab—so-called CAR-T therapy—to recognise and kill cancer cells with greater accuracy. For communities across the region, the message is one of hope grounded in solid science.
The adaptive immune system is not a mysterious force; it is a network of cells and molecules that scientists have spent decades mapping. Every vaccine given in a rural health centre, every immunotherapy infusion in a city hospital, builds on that foundation. Consult your doctor for medical advice.
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