Immunology · Adaptive immunity
What antibodies do: effector functions !
- Process
Antibodies do not kill germs by themselves: they block them, tag them for eating, call in complement and killer cells, and guard the mucosa.
Updated 2026-11-01
What it is
An antibody binds antigen with its Fab arms and recruits the rest of the immune system with its Fc tail. Its main effects are neutralisation of microbes and toxins, opsonisation for phagocytosis, activation of complement, antibody-dependent cellular cytotoxicity (ADCC) and protection of mucosal surfaces by secretory IgA. The isotype (IgM, IgG subclasses, IgA, IgE) decides which of these functions an antibody performs well, which is why class switching matters.
Key facts
- Fab = antigen binding (specificity); Fc = effector functions (what happens next).
- IgM is a pentamer: the first antibody made and the best activator of complement, but a poor opsonin by itself.
- IgG is the only isotype that crosses the placenta and the main opsonin.
- IgA is the most abundant antibody made in the body, mostly secreted on mucosa.
- Neutralisation needs no other cell or protein: it is why antitoxins and many vaccines work.
Effector functions and the isotypes that perform them
| Function | How it works | Main isotypes | Example |
|---|---|---|---|
| Neutralisation | Fab covers the site a microbe or toxin uses to bind cells | IgG, IgA (also IgM) | Antitoxin against tetanus and diphtheria; vaccine antibodies against polio or measles virus |
| Opsonisation and phagocytosis | Fc binds Fcγ receptors on neutrophils and macrophages | IgG (IgG1, IgG3) | Clearance of encapsulated bacteria such as pneumococcus |
| Complement activation | C1q binds Fc of two or more bound antibodies; classical pathway gives C3b and the membrane attack complex | IgM (most efficient), IgG | Lysis of Neisseria; transfusion reactions by anti-A and anti-B IgM |
| ADCC | NK cells bind IgG-coated cells through FcγRIII (CD16) and kill them; eosinophils do it with IgE on helminths | IgG; IgE for eosinophils | Tumour cell killing by therapeutic monoclonal antibodies; defence against worms |
| Mucosal immunity | Dimeric IgA is carried across the epithelium by the poly-Ig receptor and released with the secretory component | Secretory IgA | Protection of gut and airways; IgA in breast milk |
| Neonatal immunity and long half-life | FcRn carries IgG across the placenta and rescues it from breakdown | IgG | Protection of the newborn in the first months; long life of IgG drugs |
| Mast cell sensitisation | IgE binds FcεRI on mast cells and basophils; antigen cross-links it and triggers degranulation | IgE | Type I hypersensitivity and anaphylaxis; helminths |
Clinical notes
- Antibody deficiency (agammaglobulinaemia, common variable immunodeficiency): sinopulmonary infections by encapsulated bacteria and enteroviruses.
- Selective IgA deficiency: often silent; possible anaphylaxis to blood products containing IgA in patients with anti-IgA.
- Maternal IgG crossing the placenta can protect the newborn (vaccines in pregnancy) or harm it (haemolytic disease, neonatal Graves disease).
- Many therapeutic monoclonal antibodies against tumour cells act through ADCC and complement.
Test yourself
Think of the answer, then tap the question to see it.
Which antibody isotype activates the classical complement pathway most efficiently?
IgM, because its pentamer offers several Fc regions for C1q at once.
Which receptor lets NK cells kill antibody-coated cells?
FcγRIII (CD16), which binds the Fc of IgG: ADCC.
How does dimeric IgA reach the lumen of the gut?
The poly-Ig receptor carries it across epithelial cells; part of the receptor stays bound as the secretory component.
Which receptor explains both the placental transfer and the long half-life of IgG?
The neonatal Fc receptor (FcRn).
What is neutralisation?
Antibody binding that blocks the part of a microbe or toxin that attaches to host cells, preventing infection or toxicity.
Related
- Antibody structure and isotypes (IgG, IgA, IgM, IgE, IgD)
- Complement: three pathways, MAC, regulators
- B-cell activation, class switching and affinity maturation
- Phagocytosis and the respiratory burst
- Natural killer cell
- Monoclonal antibodies and biologics: naming and targets
- Passive immunization: immunoglobulins and antitoxins
- B-cell (antibody) deficiencies: XLA, CVID, IgA deficiency, hyper-IgM
Related conditions
Microorganisms
Educational content on the immune system; not a treatment or individual vaccination guide and no substitute for a health professional's advice. No doses are given.
Sources: 21.4 The Adaptive Immune Response: B-lymphocytes and Antibodies (OpenStax (Anatomy and Physiology 2e), 2022); 18.4 B Lymphocytes and Humoral Immunity (OpenStax (Microbiology), 2016); 21.5 The Immune Response against Pathogens (OpenStax (Anatomy and Physiology 2e), 2022).
Spotted a mistake?We are always improving for the community. Tell us what is wrong and our team will review it.Report a mistake
Representative model, for educational purposes only.