Immunity is the body’s defence system against pathogens. It has two lines — innate (fast, general) and acquired (slow, specific but with memory). CBSE Class 12 and NEET test this in Human Health and Disease.
Core Concepts
Innate immunity
Non-specific, always on. Physical barriers (skin, mucus), chemical barriers (HCl, lysozyme in tears), cellular barriers (neutrophils, macrophages, natural killer cells), cytokines (interferons). Works from birth.
The four barriers of innate immunity:
| Barrier type | Examples | How it works |
|---|---|---|
| Physical | Skin, mucous membranes, cilia in trachea | Block pathogen entry physically |
| Chemical | HCl in stomach, lysozyme in tears/saliva, sebum on skin | Kill or inhibit pathogens chemically |
| Cellular | Neutrophils, macrophages, NK cells | Phagocytose or kill infected cells |
| Cytokine | Interferons, complement proteins | Signal other immune cells, lyse pathogens |
Phagocytosis is the workhorse of innate immunity. Neutrophils and macrophages engulf pathogens, trap them in a phagosome, fuse with lysosomes (forming a phagolysosome), and digest them with enzymes and reactive oxygen species. Macrophages also present fragments of the pathogen on their surface using MHC class II molecules — this bridges innate and acquired immunity.
Inflammation is a hallmark of innate immunity. When tissue is damaged or infected, mast cells release histamine, causing blood vessels to dilate and become more permeable. This brings more blood (redness, warmth) and immune cells to the site. Swelling and pain follow. Inflammation is protective, not pathological — unless it becomes chronic.
Acquired immunity
Specific, with memory. B cells make antibodies against extracellular pathogens. T cells (helper, cytotoxic, regulatory) handle intracellular pathogens. First exposure is slow; memory cells make second exposure fast and strong.
Two arms of acquired immunity:
Humoral immunity (antibody-mediated):
- B cells recognise antigen via their surface immunoglobulin
- Helper T cells provide co-stimulation (through cytokines)
- B cells differentiate into plasma cells (secrete antibodies) and memory B cells
- Antibodies neutralise toxins, opsonise bacteria, activate complement
Cell-mediated immunity (CMI):
- Cytotoxic T cells (CD8) recognise infected cells presenting antigen on MHC class I
- They release perforins (make holes) and granzymes (trigger apoptosis)
- Kills virus-infected cells, cancer cells, and transplanted tissue
- This is why organ rejection is a T cell problem, not a B cell problem
Primary vs secondary immune response:
- Primary: First exposure. Slow (7-10 days). Low antibody titre. Mainly IgM produced.
- Secondary: Subsequent exposure. Fast (1-3 days). High antibody titre. Mainly IgG produced. Memory cells are responsible for this speed.
Antibodies
Y-shaped proteins with a constant region and variable region. Five classes — IgG (most abundant, crosses placenta), IgA (secretions), IgM (first response), IgE (allergy), IgD (B-cell receptor).
Structure of an antibody: Two heavy chains and two light chains linked by disulphide bonds. The variable region at the tips (Fab region) binds antigen — each antibody has a unique variable region. The constant region (Fc region) determines the class and function.
| Antibody | % in serum | Key function | Special feature |
|---|---|---|---|
| IgG | 75% | Long-term protection, opsonisation | Crosses placenta (passive immunity to baby) |
| IgA | 15% | Mucosal defence | Found in saliva, tears, breast milk |
| IgM | 10% | First responder | Pentameric (5 units), very effective at agglutination |
| IgE | 0.05% | Allergy response, anti-parasite | Binds mast cells, triggers histamine release |
| IgD | 0.2% | B cell activation | Found on B cell surface |
Mnemonic for antibody order by serum concentration: GAMED — IgG > IgA > IgM > IgE > IgD. NEET loves asking which antibody is most abundant (IgG) or which crosses the placenta (also IgG).
Active vs passive immunity
Active — body makes its own antibodies from infection or vaccine, lasts long. Passive — antibodies received pre-made from mother to baby or antiserum injection, works fast but short-lived.
| Feature | Active immunity | Passive immunity |
|---|---|---|
| Source | Self-produced antibodies | Pre-formed antibodies from outside |
| Speed of onset | Slow (days to weeks) | Immediate |
| Duration | Long-lasting (years to lifetime) | Short-lived (weeks to months) |
| Memory cells | Yes | No |
| Examples | Vaccination, natural infection | Mother to foetus (IgG), colostrum (IgA), anti-venom |
Types of vaccines:
- Live attenuated: Weakened pathogen (BCG for TB, oral polio, MMR). Strong immunity but risk in immunocompromised.
- Killed/inactivated: Dead pathogen (rabies, injectable polio). Safer but weaker response, needs boosters.
- Subunit/recombinant: Only specific proteins (Hepatitis B surface antigen). Very safe, targeted.
- Toxoid: Inactivated toxin (tetanus, diphtheria). Generates anti-toxin antibodies.
- mRNA: Genetic instructions for antigen (COVID-19 vaccines). Newest platform.
Autoimmunity and allergies
Autoimmune disease — immune system attacks self (rheumatoid arthritis, lupus). Allergy — immune system overreacts to harmless antigen (pollen, dust). Both are failures of immune regulation.
Allergy mechanism:
- First exposure to allergen (pollen, dust mite) → sensitisation
- IgE antibodies produced and bind to mast cells (in tissues) and basophils (in blood)
- Second exposure → allergen cross-links IgE on mast cells
- Mast cells degranulate → release histamine, leukotrienes, prostaglandins
- Symptoms: sneezing, itching, swelling, bronchospasm (asthma)
Antihistamines like cetirizine block histamine receptors, reducing allergy symptoms. Severe allergies (anaphylaxis) require adrenaline injection (EpiPen).
Immunodeficiency
AIDS (Acquired Immunodeficiency Syndrome):
- Caused by HIV (Human Immunodeficiency Virus), a retrovirus
- HIV infects CD4 helper T cells using gp120 protein
- Reverse transcriptase converts viral RNA to DNA, which integrates into host genome
- Progressive loss of CD4 cells → immune system collapses
- Normal CD4 count: 800-1200 cells/L. AIDS diagnosed below 200 cells/L
- Opportunistic infections (Pneumocystis, Toxoplasma, Mycobacterium) become fatal
- Diagnosed by ELISA (screening) and Western blot (confirmatory)
Worked Examples
The first dose triggers a primary response with memory cells. The booster triggers a faster, stronger secondary response, cementing long-term immunity. Tetanus boosters every 10 years follow this logic.
HIV infects CD4 helper T cells. Without them, B cells cannot make effective antibodies and cytotoxic T cells cannot be properly activated. The whole acquired system collapses.
IgG antibodies from the mother cross the placenta during pregnancy. These protect the newborn for the first few months. Colostrum (first milk) provides IgA, which protects the gut. This immunity fades over 3-6 months as the baby’s own immune system matures.
Every cell in your body displays MHC class I molecules on its surface (like an ID card). Transplanted tissue has different MHC molecules. Cytotoxic T cells recognise these as foreign and attack. Immunosuppressive drugs like cyclosporine block T cell activation to prevent rejection.
Solved Problems (Exam Style)
Problem 1 (NEET 2020 pattern): Which antibody is found in colostrum? (a) IgG (b) IgA (c) IgM (d) IgE
Colostrum is the first milk after delivery. It is a secretion, and the antibody class found in secretions (saliva, tears, breast milk, mucus) is IgA. Answer: (b)
IgG is the most abundant in serum and crosses the placenta, but IgA is the one in external secretions.
Problem 2 (NEET pattern): Which cells are affected by HIV?
HIV specifically targets CD4 helper T cells (also called T cells). It uses the CD4 receptor (along with co-receptors CCR5 or CXCR4) to enter the cell. Macrophages also have CD4 and can be infected, serving as reservoirs. Answer: Helper T cells (CD4)
Problem 3 (CBSE Board): Differentiate between active and passive immunity with one example each.
Active immunity: The body produces its own antibodies after exposure to antigen. Takes time but lasts long. Memory cells formed. Example: vaccination with DPT (diphtheria, pertussis, tetanus).
Passive immunity: Pre-formed antibodies are received from an external source. Works immediately but short-lived. No memory cells. Example: anti-tetanus serum (ATS) injection after a deep wound.
Common Mistakes
Confusing IgG and IgM. IgM is first responder; IgG is the most abundant and the one that gives long-term protection.
Saying innate immunity has memory. It does not.
Thinking vaccines contain live dangerous pathogens. Most contain weakened, killed or subunit forms.
Writing that antibodies directly kill pathogens. Antibodies do not kill — they mark pathogens for destruction (opsonisation), neutralise toxins, or activate complement. The actual killing is done by phagocytes, NK cells, or the complement system.
Confusing MHC class I and class II. MHC-I is on ALL nucleated cells (presents intracellular antigens to CD8 T cells). MHC-II is only on antigen-presenting cells like macrophages and dendritic cells (presents extracellular antigens to CD4 T cells).
Exam Weightage and Revision
This topic is a repeat performer in board papers and entrance exams. NEET typically asks one to two questions on the core mechanisms, CBSE boards give three to six marks, and state PMT papers often include a diagram-based long answer. The PYQs cluster around a small set of facts — lock those and you clear the topic.
NEET 2023 asked about the antibody found in colostrum. NEET 2022 tested HIV target cells. NEET 2021 had a question on primary vs secondary immune response. CBSE boards regularly ask five-mark questions on types of immunity or the structure of antibodies. This is a guaranteed scoring area.
When a question gives a scenario, identify the core mechanism first, then match it to the concepts above. Most wrong answers come from reading the scenario too quickly.
Learn the five antibody classes with one function each. NEET asks one question on antibodies almost every year.
Practice Questions
Q1. What is the role of interferons in immunity?
Interferons are cytokines released by virus-infected cells. They do not directly kill viruses. Instead, they warn neighbouring uninfected cells, which then produce antiviral proteins that inhibit viral replication. Interferons are part of innate immunity — they act non-specifically against many viruses.
Q2. Why is a person who has recovered from chickenpox unlikely to get it again?
During the first infection, the acquired immune system produced memory B cells and memory T cells specific to the varicella-zoster virus. On subsequent exposure, these memory cells mount a rapid, strong secondary response that eliminates the virus before symptoms appear.
Q3. Name the diagnostic tests for HIV.
ELISA (Enzyme-Linked Immunosorbent Assay) is the screening test — it detects antibodies against HIV in blood. If positive, Western blot is the confirmatory test — it is more specific and detects antibodies against specific HIV proteins. PCR (polymerase chain reaction) can also detect viral RNA directly.
Q4. Why do allergic reactions get worse with each exposure?
The first exposure sensitises the immune system — IgE antibodies are produced and bind to mast cells. On second and subsequent exposures, the allergen immediately cross-links IgE already sitting on mast cells, causing rapid degranulation. More IgE is produced with each exposure, so mast cells become more heavily armed and the response gets stronger.
Q5. What is the difference between humoral and cell-mediated immunity?
Humoral immunity involves B cells producing antibodies that circulate in blood and body fluids. It targets extracellular pathogens (bacteria, toxins). Cell-mediated immunity involves T cells (mainly cytotoxic CD8 T cells) directly killing infected or abnormal cells. It targets intracellular pathogens (viruses, intracellular bacteria) and cancer cells.
FAQs
What is herd immunity? When a large percentage of a population is immune (through vaccination or previous infection), the pathogen cannot spread easily because it runs out of susceptible hosts. This indirectly protects unvaccinated individuals (babies, immunocompromised people). The threshold varies by disease — measles needs about 95% immunity due to its high transmissibility.
Can you be immune to something without vaccination? Yes. Natural infection also produces acquired immunity with memory cells. However, vaccination achieves immunity without the risk of disease complications. Some innate immunity is also present from birth.
Why do we need a new flu vaccine every year? The influenza virus undergoes antigenic drift (small mutations in surface proteins) every season. Memory cells from last year’s infection or vaccine do not recognise the slightly changed virus. Occasionally, antigenic shift (major reassortment of viral genes) creates entirely new strains, which can cause pandemics.
What is autoimmunity? The immune system normally distinguishes self from non-self through a process called self-tolerance. When this breaks down, immune cells attack the body’s own tissues. Examples include Type 1 diabetes (T cells destroy pancreatic beta cells), rheumatoid arthritis (attacks joint lining), and lupus (attacks multiple organs).
Immunity is pattern matching at the molecular level. Antigens are the key, antibodies are the lock, and memory cells are the spare key drawer.