The Immune System: Innate & Adaptive Defenses
Barriers, inflammation, antigens, T and B cells, antibodies and immune disorders
By the end of this unit you can…
- ✓Describe the surface barriers and internal innate defenses
- ✓Explain the inflammatory response, fever, interferons and complement
- ✓Describe antigens, antigen presentation (MHC) and the roles of APCs
- ✓Compare humoral (B cell / antibody) and cellular (T cell) immunity
- ✓Describe antibody structure, classes and functions; active vs passive immunity
- ✓Explain immunodeficiencies, autoimmune diseases and hypersensitivities
Key terms
Practice →1Two defense systems
| Innate (nonspecific) | Adaptive (specific) | |
|---|---|---|
| Speed | Immediate, always ready | Takes days on first exposure |
| Specificity | Same response to any pathogen | Targets specific antigens |
| Memory | No | Yes — faster, stronger second response |
| Components | 1st line: skin and mucous membranes. 2nd line: phagocytes, NK cells, inflammation, antimicrobial proteins, fever | 3rd line: lymphocytes (B and T cells) and antibodies |
2Innate defenses
- Surface barriers
- Skin (keratin, acid mantle pH 3–5, sebum, dermcidin) and mucous membranes (sticky mucus, cilia, lysozyme in tears/saliva, HCl in the stomach, acidic vaginal secretions).
- Phagocytes
- Neutrophils (most abundant; first to arrive) and macrophages (from monocytes; most voracious). They engulf microbes into a phagosome, which fuses with a lysosome (phagolysosome) to destroy them. Opsonization — coating pathogens with antibodies or complement — makes them easier to eat.
- Natural killer (NK) cells
- Large granular lymphocytes that kill virus-infected and cancer cells nonspecifically — they recognize cells lacking “self” MHC markers — by inducing apoptosis (using perforins and granzymes).
- Interferons
- Proteins secreted by virus-infected cells that warn neighbors to make antiviral proteins (IFN-α, IFN-β); IFN-γ activates macrophages. Used to treat hepatitis and some cancers.
- Complement
- ~20 plasma proteins that, when activated (classical pathway by antibodies; lectin and alternative pathways by microbes), cause cell lysis (membrane attack complex), opsonization, enhanced inflammation, and clearance of immune complexes.
- Fever
- Systemic response: pyrogens released by leukocytes and macrophages reset the hypothalamic thermostat. Moderate fever makes the liver and spleen sequester iron and zinc (which bacteria need) and speeds repair.
3The inflammatory response
Inflammation is triggered by any tissue injury (trauma, heat, chemicals, infection). It prevents spread of damaging agents, disposes of debris and pathogens, alerts the adaptive system and sets the stage for repair.
| Cardinal sign | Cause |
|---|---|
| Redness | Vasodilation (more blood) |
| Heat | Vasodilation |
| Swelling (edema) | Increased capillary permeability — fluid, proteins leak out |
| Pain | Edema pressure on nerves + bradykinin, prostaglandins |
| (Impaired function) | Sometimes the fifth sign |
- 1Injured cells, mast cells (histamine), and macrophages release inflammatory chemicals; Toll-like receptors on macrophages recognize microbes.
- 2Vasodilation and increased vascular permeability → hyperemia and exudate (fluid with clotting proteins, antibodies, complement). Clotting proteins wall off the area.
- 3Phagocyte mobilization: neutrophils leave the marrow (leukocytosis), stick to vessel walls (margination), squeeze through (diapedesis) and follow chemicals (chemotaxis). Monocytes follow ~12 h later and become macrophages.
- 4Phagocytes destroy pathogens and debris; pus (dead neutrophils, tissue and pathogens) may form; if not cleared, an abscess may be walled off.
4Antigens & the cells of adaptive immunity
Antigens are substances that can mobilize adaptive defenses and provoke an immune response — mostly large, complex molecules (proteins, nucleic acids, some lipids and polysaccharides) not normally in the body. Only specific parts, antigenic determinants (epitopes), bind antibodies or receptors. Haptens are small molecules (penicillin) that become antigenic only when bound to body proteins.
Self-antigens — MHC proteins: every cell carries major histocompatibility complex glycoproteins that display peptides. MHC class I is on all nucleated cells (displays peptides from inside the cell — e.g. viral proteins); MHC class II is only on antigen-presenting cells (displays peptides from engulfed antigens).
| Cell | Where it matures / role |
|---|---|
| B lymphocytes | Mature in bone marrow → humoral immunity (antibodies) |
| T lymphocytes | Mature in the thymus → cellular immunity. Must pass positive selection (recognize self-MHC) and negative selection (not react strongly to self-antigens) — about 98% die |
| Antigen-presenting cells (APCs) | Dendritic cells, macrophages and B cells — engulf antigens and present fragments on MHC II to T cells |
5Humoral immunity (B cells)
- 1A naive B cell's receptors bind a matching antigen.
- 2With help from a helper T cell (cytokines), it is activated and proliferates into a clone.
- 3Most clone members become plasma cells, which secrete ~2000 antibodies per second for 4–5 days, then die.
- 4Some become long-lived memory B cells, ready for future exposure.
Primary response: 3–6 day lag, peak at ~10 days, then decline. Secondary response: faster (hours to days), stronger, longer-lasting — thanks to memory cells. This is the basis of immunological memory and vaccination.
| Immunity | Active (you make antibodies; memory) | Passive (antibodies given; no memory, short-lived) |
|---|---|---|
| Naturally acquired | Infection | Antibodies from mother via placenta (IgG) or breast milk (IgA) |
| Artificially acquired | Vaccine | Injection of antibodies — antivenom, antitoxin, gamma globulin |
Antibodies (immunoglobulins, Ig): Y-shaped proteins of four chains — two identical heavy and two identical light chains joined by disulfide bonds. Variable regions at the arm tips form the antigen-binding sites; constant regions (stem / Fc region) determine the class and what the antibody does.
| Class | Key facts |
|---|---|
| IgG | Most abundant (~75–85%); main antibody of the secondary response; the only one that crosses the placenta; fixes complement |
| IgA | In secretions (saliva, tears, mucus, breast milk) — protects mucosal surfaces |
| IgM | Pentamer; first released in the primary response; potent agglutinator; fixes complement (anti-A/anti-B blood antibodies) |
| IgE | Binds mast cells and basophils → triggers allergies; also fights parasitic worms |
| IgD | B cell receptor on naive B cells |
Antibodies don't destroy antigens themselves; they inactivate and tag them (PLAN): Precipitation, Lysis (complement fixation — the most important), Agglutination, Neutralization (blocking toxins/viruses). Antibody-coated antigens are also easier for phagocytes to engulf.
6Cellular immunity (T cells)
| T cell | Marker | Recognizes | Job |
|---|---|---|---|
| Helper T (T_H) | CD4 | Antigen on MHC II (APCs) | Central regulators: secrete cytokines (interleukins) that activate B cells, cytotoxic T cells and macrophages. Without them there is virtually no adaptive response |
| Cytotoxic T (T_C) | CD8 | Antigen on MHC I (any infected cell) | Directly kill virus-infected cells, cancer cells and foreign graft cells — release perforins and granzymes |
| Regulatory T (T_reg) | CD4 | — | Dampen the immune response; prevent autoimmunity |
| Memory T cells | — | — | Rapid response on re-exposure |
T cell activation needs a double recognition (antigen binding + MHC) and co-stimulation signals from the APC. Without co-stimulation, the T cell becomes tolerant (anergy).
7Immune disorders
| Disorder type | Examples |
|---|---|
| Immunodeficiency | SCID (severe combined — lacks functional B and T cells; “bubble boy”); AIDS — HIV infects and destroys helper T (CD4) cells → collapse of immunity, opportunistic infections, Kaposi sarcoma |
| Autoimmune disease | Immune system attacks self: multiple sclerosis (myelin), type 1 diabetes (β cells), rheumatoid arthritis (joints), Graves' disease (TSH receptors), systemic lupus erythematosus, myasthenia gravis (ACh receptors), glomerulonephritis |
| Hypersensitivity | Mechanism | Example |
|---|---|---|
| Type I — immediate (allergy) | IgE on mast cells/basophils → histamine release within seconds–minutes | Hay fever, asthma, hives; anaphylactic shock (treated with epinephrine) |
| Type II — antibody-mediated (cytotoxic) | IgG/IgM bind antigens on cells → complement lysis | Mismatched blood transfusion |
| Type III — immune complex | Antigen–antibody complexes deposit in tissues → inflammation | Lupus, some glomerulonephritis |
| Type IV — delayed (cell-mediated) | T cells and macrophages; takes 1–3 days | Poison ivy contact dermatitis, TB skin test |