Immunity and inflammation: basics for pharmacology
The innate and adaptive immune systems and the mediators of inflammation, as the background needed to understand anti-inflammatory and immune drugs.
Immune and anti-inflammatory drugs act on specific cells, receptors and cytokines. To understand what a TNF inhibitor, a calcineurin inhibitor or a vaccine does, it helps to know the main players: barriers and innate cells that act within minutes, lymphocytes that learn and remember, and the chemical signals that link them.
Innate immunity
Skin and mucosa, stomach acid and normal flora are the first defence. Toll-like receptors and other sensors on macrophages and dendritic cells recognise common microbial patterns and trigger cytokine release. Neutrophils arrive first and engulf bacteria; complement coats microbes (opsonisation), attracts cells and can punch holes in membranes. Natural killer cells destroy cells that have lost their normal surface markers.
Adaptive immunity
- Antigen-presenting cells (dendritic cells above all) carry antigen to lymph nodes
- CD4 helper T cells: Th1 (intracellular microbes), Th2 (parasites, allergy), Th17 (fungi, neutrophil recruitment), regulatory T cells (keep tolerance)
- CD8 cytotoxic T cells: kill virus-infected and tumour cells
- B cells and plasma cells: antibodies (IgM first, then IgG; IgA at mucosa; IgE in allergy)
- Memory cells: faster, stronger responses on second exposure, the basis of vaccination
Inflammatory mediators
Pre-formed mediators (histamine) act in seconds; newly made lipids (prostaglandins, leukotrienes) in minutes; cytokines and chemokines over hours. TNF and IL-1 cause fever, activate endothelium and drive the liver to make acute-phase proteins such as C-reactive protein, with IL-6. Chronic inflammatory diseases such as rheumatoid arthritis, psoriasis and inflammatory bowel disease are kept going by a few dominant cytokines, which is why blocking one of them can work so well.
From biology to drugs
- Corticosteroids: switch off the transcription of many inflammatory genes at once
- NSAIDs: block prostaglandin synthesis
- Biologics: block a single cytokine (TNF, IL-6, IL-17, IL-23) or a cell (B cells)
- Small molecules: block signalling inside the cell (calcineurin, JAK, mTOR)
- Replacement: immunoglobulin for antibody deficiency, growth factors for low neutrophils
Test yourself
Think of the answer, then tap the question to see it.
Which T cell type recognises antigen on MHC class I, and what does it do?
CD8 cytotoxic T cells; they kill cells that present foreign (for example viral) or abnormal peptides.
Which three cytokines are targets of approved biologic drugs?
Any three of: TNF, IL-1, IL-6, IL-17, IL-23, IL-12/23, IL-5, IL-4/13.
Why does a second exposure to an antigen give a faster response?
Memory B and T cells formed after the first exposure respond quickly and strongly; this is the basis of vaccination.
What two signals does a naive T cell need to be activated?
Antigen presented on MHC (signal 1) and a costimulatory signal such as CD28 binding CD80/86 (signal 2).
Example drugs
Connections
Educational content on how drugs work; not a prescribing guide and no substitute for a health professional's advice. No doses are given.
Sources: Immune response: MedlinePlus Medical Encyclopedia (MedlinePlus (U.S. National Library of Medicine), 2026).
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Representative model, for educational purposes only.