Human Health and Disease · Lesson 4 of 11
Acquired Immunity: Antibodies, T Cells and Immune Memory
“Specific recognition, antibody architecture, humoral and cellular responses, immune memory and graft rejection.”
• Explain clonal selection and the biological basis of immune memory. • Compare primary and secondary adaptive responses. • Identify the heavy and light chains of an antibody. • Distinguish antibody-mediated and T-cell-mediated defence. • Explain why transplanted tissues can trigger rejection.
Specific recognition and the formation of memory
Adaptive, also called acquired, immunity depends on lymphocytes that possess highly diverse antigen receptors. During an encounter with an infectious agent, particular B or T cells recognise compatible antigenic structures and become activated in a suitable signalling environment. These cells proliferate through clonal expansion, producing many descendants with related specificity. Some descendants become effector cells that fight the current infection, whereas others persist as memory cells. Unlike the broad, immediate action of many innate defences, adaptive responses often require time for receptor-bearing clones to expand.
The first exposure typically produces a primary response that is slower and of lower intensity than a later response to the same antigen. A subsequent exposure can activate pre-existing memory cells, leading to a faster and frequently stronger secondary or anamnestic response. Memory does not make illness impossible: immune protection depends on pathogen variation, time since exposure and host immune competence. Its chief biological advantage is that the immune system does not have to begin every response from a small population of unprimed cells.
How B cells produce antibodies
B cells carry antigen-binding receptors on their surfaces. With suitable activation, many differentiate into plasma cells that secrete large quantities of antibodies, or immunoglobulins. Antibodies are soluble proteins that bind antigenic sites called epitopes. Depending on class and context, they can prevent toxins or viruses attaching to cells, mark microorganisms for engulfment by phagocytes, or help activate complement proteins. An antibody does not need to be a poison to protect the host: binding can block a pathogen's required interaction or recruit other immune components.
A conventional antibody monomer consists of two identical heavy polypeptide chains and two identical light polypeptide chains. Its structure is represented as H₂L₂ and is often depicted as a Y shape. Each arm contains a variable antigen-binding region, creating two related binding sites per monomer. More constant parts of the heavy chains, including the Fc region, influence the antibody class and its interactions with immune cells. Disulfide bonds help stabilise the molecule, and differences in amino-acid sequence explain why antibodies have distinct antigen specificities.
The antibody classes IgM, IgG, IgA and IgE differ in where they act and what immune functions they support. IgM commonly appears early in a primary humoral response, while IgG is plentiful in blood and can cross the placenta. Secretory IgA protects mucosal surfaces and is prominent in early breast milk. IgE participates in some parasite-related responses and in immediate allergic reactions by binding to mast-cell receptors. These are different functional proteins, not four stages that every antibody must pass through.
Cell-mediated immunity and T lymphocytes
T lymphocytes generally recognise antigen-derived peptides presented by cell-surface major histocompatibility complex molecules. Helper T cells send coordinating signals and can support B-cell antibody production, macrophage activation and other defences. Cytotoxic T cells can recognise and destroy infected or otherwise abnormal host cells. This is especially relevant when a pathogen is replicating inside a host cell and cannot be neutralised by an antibody that acts only outside that cell. T cells do not themselves produce secreted immunoglobulin antibodies; antibody secretion belongs to the plasma-cell stage of B-cell development.
Humoral immunity is therefore largely mediated by antibodies in blood and extracellular fluid, whereas cell-mediated immunity, or CMI, depends strongly on T-cell effector functions. The two overlap because helper T cells assist many antibody responses and because antibodies assist phagocytic cells that participate in innate defence. An accurate model of immunity must connect these pathways instead of treating them as sealed compartments.
Why the immune system may reject a transplanted organ
A transplanted organ contains living cells with surface antigenic molecules that may differ from the recipient's tissue markers. Recipient T cells and sometimes antibodies can recognise these differences and damage the graft. Blood-group compatibility and matching relevant human leukocyte antigen types can reduce some risks, but not eliminate all immune recognition. Immunosuppressive medicines may be needed to prevent or treat rejection, and their use increases vulnerability to some infections. The mechanism is a consequence of the same non-self recognition that ordinarily helps protect the body.
| Feature | Humoral immunity | Cell-mediated immunity |
|---|---|---|
| Main effector | Secreted antibodies from B-cell-derived plasma cells | T cells and their recruited partners |
| Main strengths | Neutralising soluble toxins and extracellular pathogens | Recognising and eliminating infected host cells |
| Memory | Memory B cells and long-lived plasma cells | Memory T cells |
| Connection | Often receives helper-T-cell signals | Can support B-cell antibody responses |
Quick Quiz
Quiz
Why is a secondary adaptive immune response often faster?
What is the chain composition of a conventional immunoglobulin monomer?
Which immune cells can become antibody-secreting plasma cells?
Which class is important at mucosal surfaces and in colostrum?
What characterises cell-mediated adaptive immunity?
Why does the immune system sometimes reject a graft?
Practice Problems
- Explain the development of adaptive memory and compare the first and later responses to the same antigen.
- Describe a labelled H₂L₂ antibody and explain how its structure connects recognition to immune action.
- Compare humoral and cell-mediated immunity using a virus before and after it enters host cells.
- Explain the role of matching and immunosuppressive treatment during organ transplantation.
Antigen-presenting cells and other immune signals activate rare lymphocytes carrying receptors that recognise a particular antigen. The selected cells expand clonally and differentiate into effector and memory populations. The first response can take time because few relevant cells are initially available. After the antigen clears, memory B and T lymphocytes can persist, sometimes alongside long-lived plasma cells. A later encounter may therefore elicit faster antibody production and cellular activity, though protection varies with antigenic changes and immune status.
Key Takeaways
• Adaptive immunity is antigen-specific and capable of forming memory. • Clonal expansion produces effector cells and memory lymphocytes. • A secondary response is often faster than a primary response. • A conventional antibody contains two heavy chains and two light chains. • Plasma cells secrete antibodies; T cells coordinate or execute cellular defence. • IgA, IgG, IgM and IgE perform different physiological roles. • Graft rejection results from immune recognition of donor tissue antigens.