Adaptive immunity
Also known as: acquired immunity, specific immunity, adaptive immune system, humoral immunity, cell-mediated immunity, active immunity, passive immunity
The specific, slower-starting arm of immunity mediated by T and B lymphocytes, whose clonally distributed receptors recognise virtually any antigen, which expands selected clones and which remembers each encounter.
Overview
Adaptive immunity has hallmark features: specificity (each lymphocyte carries one receptor for one epitope), enormous diversity (an individual's repertoire contains on the order of 10⁷–10⁸ different receptors, generated by V(D)J recombination, combinatorial chain pairing and junctional diversity), clonal expansion, specialisation of effector responses to the type of microbe, contraction after the threat is removed, memory, and self-tolerance. On first exposure there is a lag of several days while rare specific clones are found and expanded.
It has two arms. Humoral immunity is mediated by antibodies from B cells and plasma cells; it defends against extracellular microbes and toxins and can be transferred to a non-immune individual by serum. Cell-mediated immunity is mediated by T cells: CD4 helper cells activate macrophages and help B cells, and CD8 cytotoxic cells kill infected cells; it defends against intracellular microbes and tumours and can be transferred only by cells. Both are coordinated by helper T cells and depend on innate immunity for antigen presentation and co-stimulation.
Adaptive immunity may be active — produced by the individual after infection (natural) or vaccination (artificial), slow to develop but long-lasting with memory — or passive — preformed antibody received across the placenta or in breast milk (natural) or as an injection of immunoglobulin, antitoxin or monoclonal antibody (artificial), giving immediate but temporary protection (weeks to months) without memory.
Innate vs adaptive at a glance: innate — present from birth, immediate, germline PRRs recognising shared patterns, same response each time; adaptive — develops over days, somatically rearranged receptors recognising specific epitopes, improves with each exposure (memory).
Parts & subdivisions
- B cells, plasma cells and antibodies; extracellular pathogens and toxins.
- CD4 and CD8 T cells; intracellular pathogens, tumours, grafts.
- Antigen selects and expands pre-existing specific clones.
- Faster, stronger secondary responses.
- Active — made by the host (infection, vaccination), slow and lasting. Passive — antibodies received (placenta, breast milk, immunoglobulin), immediate and temporary.
Function
- Eliminate pathogens that evade or overwhelm innate defences.
- Provide long-lasting, specific protection against re-infection.
- Recognise and destroy tumour cells and foreign tissue.
Clinical significance
Immunodeficiency
Primary (inherited: SCID, XLA, CVID, DiGeorge) or secondary (HIV, chemotherapy, corticosteroids and other immunosuppressants, malnutrition, diabetes, extremes of age, splenectomy, protein loss). Antibody defects mainly cause recurrent sinopulmonary bacterial infections; T-cell defects cause viral, fungal and opportunistic infections.
Passive immunisation in practice
Tetanus and rabies immunoglobulin after high-risk wounds or exposures (given with vaccine at a different site), hepatitis B immunoglobulin for babies of infected mothers, varicella-zoster immunoglobulin for susceptible pregnant women, anti-D for RhD-negative mothers, and long-acting monoclonal antibodies against RSV for infants.
Mnemonics
Active vs passive
Active — you make it (slow, lasting, memory). Passive — you take it (fast, short, no memory).
Compiled from standard anatomy and physiology references — see the Lymphatic & Immune System sources. For education only; not medical advice.