Every day, the human body is under constant attack from a staggering variety of pathogens — bacteria, viruses, fungi, parasites — yet most of the time we remain healthy. This is because of our immune system — a complex, multilayered defence network that identifies, neutralises, and remembers foreign invaders. Immunity is the ability of the body to resist infection and disease. Understanding how the immune system works — from the immediate, non-specific barriers of innate immunity to the highly targeted responses of adaptive immunity — is fundamental to understanding human health and disease. For NEET, this chapter consistently contributes 4–6 questions every year on types of immunity, antibody structure, vaccines, and immune disorders.
1. Overview of Human Defence System
Human immunity operates at three levels of defence:
| Line of Defence |
Components |
Nature |
| First line |
Skin, mucous membranes, secretions (saliva, tears, mucus, stomach acid) |
Physical and chemical barriers — prevent entry |
| Second line |
Phagocytes, NK cells, inflammation, fever, complement system, interferons |
Non-specific innate immune response — rapid, no memory |
| Third line |
B lymphocytes (antibodies), T lymphocytes (cell-mediated), memory cells |
Specific adaptive immune response — slow first time, has memory |
2. Innate Immunity (Non-Specific Immunity)
Innate immunity is the inborn, non-specific defence that is present from birth and does not require prior exposure to a pathogen. It responds immediately (within minutes to hours) to any foreign substance. Key characteristics:
- Present from birth — no prior sensitisation needed.
- Non-specific — responds to any pathogen, not a particular one.
- No immunological memory — same response on every exposure.
- Rapid response — first and second lines of defence.
Components of Innate Immunity
A. Physical Barriers
| Barrier |
Location |
Mechanism of Protection |
| Skin |
Entire body surface |
Physical barrier; slightly acidic pH; sebum (fatty acids) inhibits bacteria; keratin is impermeable |
| Mucous membranes |
Respiratory, digestive, urogenital tracts |
Trap pathogens in mucus; ciliary action sweeps them out (mucociliary escalator) |
| Saliva & Tears |
Mouth, eyes |
Contain lysozyme — enzyme that digests bacterial cell walls (peptidoglycan) |
| Stomach acid (HCl) |
Stomach |
pH ~2 kills most ingested pathogens |
| Normal flora |
Skin, gut, vagina |
Compete with pathogens for nutrients and space; produce inhibitory substances |
B. Cellular Components of Innate Immunity
| Cell Type |
Origin |
Function |
| Neutrophils |
Bone marrow (myeloid) |
Most abundant WBC; first to arrive at infection site; phagocytose bacteria |
| Macrophages |
Monocytes (bone marrow) |
Phagocytose pathogens, dead cells; present antigens to T cells (antigen presenting cells — APCs) |
| Natural Killer (NK) cells |
Bone marrow (lymphoid) |
Kill virus-infected cells and tumour cells without prior sensitisation; release perforin and granzymes |
| Mast cells |
Bone marrow |
Release histamine and heparin in inflammation and allergy; trigger vasodilation |
| Dendritic cells |
Bone marrow |
Key APCs; bridge innate and adaptive immunity; present antigens to T lymphocytes |
| Eosinophils |
Bone marrow (myeloid) |
Defence against parasitic worms (helminths); involved in allergy |
C. Molecular Components of Innate Immunity
- Complement system: A cascade of ~20 plasma proteins that are activated by pathogens. Functions include lysis of pathogens (membrane attack complex), opsonisation (tagging pathogens for phagocytosis), and triggering inflammation.
- Interferons: Small proteins secreted by virus-infected cells. They signal neighbouring cells to increase antiviral defences — prevent viral replication in uninfected cells. Types: IFN-α, IFN-β (innate), IFN-γ (adaptive).
- Inflammation: A local response to infection or tissue damage characterised by redness, heat, swelling, and pain (cardinal signs). Triggered by histamine, prostaglandins, and cytokines. Brings immune cells to the site of infection.
- Fever: Elevated body temperature triggered by pyrogens (e.g., IL-1, IL-6, TNF). Inhibits bacterial growth, increases metabolic rate, and enhances immune cell activity.
3. Adaptive Immunity (Specific Immunity)
Adaptive immunity (also called acquired or specific immunity) is a highly specific immune response that develops after exposure to a pathogen. Key characteristics:
- Specificity: Each response targets a specific antigen.
- Memory: After first exposure, memory cells are formed — subsequent exposure produces a faster, stronger response (secondary immune response).
- Diversity: Capable of recognising millions of different antigens.
- Self-tolerance: Does not attack the body's own cells (failure leads to autoimmune diseases).
Key Terms
| Term |
Definition |
| Antigen (Ag) |
Any substance (usually protein or polysaccharide) that triggers an immune response and binds to an antibody or T-cell receptor. Foreign antigens = non-self. |
| Antibody (Ab) / Immunoglobulin (Ig) |
Glycoprotein produced by plasma cells (activated B cells) that binds specifically to an antigen. Also called immunoglobulin. |
| Epitope |
The specific region of an antigen that binds to an antibody or T-cell receptor (antigenic determinant). |
| Hapten |
Small molecule that can bind antibody but cannot alone trigger immune response — needs to be attached to a carrier protein. |
| Lymphocyte |
White blood cell responsible for adaptive immunity — B cells (humoral) and T cells (cell-mediated). |
Two Arms of Adaptive Immunity
A. Humoral Immunity (Antibody-Mediated)
Mediated by B lymphocytes — effective against extracellular pathogens (bacteria, viruses in blood/lymph).
- B cells originate and mature in the bone marrow.
- When an antigen is encountered, B cells with matching receptors are activated.
- Activated B cells differentiate into plasma cells (secrete antibodies) and memory B cells.
- Plasma cells produce thousands of antibody molecules per second.
- Antibodies neutralise pathogens by: blocking receptor binding (neutralisation), tagging for phagocytosis (opsonisation), activating complement, and clumping pathogens (agglutination).
B. Cell-Mediated Immunity (CMI)
Mediated by T lymphocytes — effective against intracellular pathogens (viruses inside cells), cancer cells, and transplanted tissue.
- T cells originate in bone marrow but mature in the thymus (T = Thymus-derived).
- Types of T cells:
| T Cell Type |
Surface Marker |
Function |
| Helper T cells (Th) |
CD4+ |
Activate B cells and cytotoxic T cells; secrete cytokines (IL-2, IL-4); coordinate immune response; primary target of HIV |
| Cytotoxic T cells (Tc) |
CD8+ |
Directly kill virus-infected cells and tumour cells by releasing perforin (creates pores) and granzymes (trigger apoptosis) |
| Regulatory T cells (Treg) |
CD4+ CD25+ |
Suppress immune response after infection is cleared; prevent autoimmunity |
| Memory T cells |
CD4+ or CD8+ |
Long-lived; respond rapidly to re-exposure to the same antigen (immunological memory) |
4. Antibody Structure and Classes
An antibody (immunoglobulin) is a Y-shaped glycoprotein consisting of 4 polypeptide chains — two identical heavy (H) chains and two identical light (L) chains — held together by disulphide bonds.
Structure of an Antibody (IgG as model)
- Variable region (V): The tip of each arm — the antigen-binding site. Highly variable in sequence — determines antibody specificity. Each antibody has two antigen-binding sites (bivalent).
- Constant region (C): The Fc (crystallisable fragment) region — determines the antibody class and effector functions (complement activation, binding to phagocytes).
- Fab fragment: Antigen-binding fragment — contains one variable and one constant region from H and L chains.
- Fc fragment: Constant fragment — tail of the Y shape; binds to Fc receptors on immune cells.
- Hinge region: Flexible region between Fab and Fc — allows arm movement for antigen binding.
Five Classes of Immunoglobulins
| Class |
Structure |
Location |
Key Function |
| IgG |
Monomer |
Blood, lymph, tissue fluid |
Most abundant (75–80%); secondary immune response; only Ig to cross placenta (passive immunity to foetus); opsonisation |
| IgA |
Dimer |
Secretions (saliva, tears, colostrum, mucus) |
Protects mucosal surfaces; present in colostrum (first milk — passive immunity to newborn) |
| IgM |
Pentamer (5 monomers) |
Blood, lymph |
First antibody produced in primary response; best at agglutination and complement activation; present on naive B cells |
| IgE |
Monomer |
Bound to mast cells, basophils |
Mediates allergic reactions (Type I hypersensitivity); defence against parasitic worms; triggers histamine release; lowest serum concentration |
| IgD |
Monomer |
Surface of B cells |
B-cell receptor on naive B cells; functions in B-cell activation; least understood; very low serum levels |
5. Primary and Secondary Immune Response
| Feature |
Primary Response (1st exposure) |
Secondary Response (2nd exposure) |
| Lag period |
Long (5–10 days) |
Short (1–3 days) |
| Antibody titre |
Low |
Very high (10–100× higher) |
| Main antibody produced |
IgM (first), then IgG |
Mainly IgG (high affinity) |
| Cells involved |
Naïve B and T cells |
Memory B and T cells |
| Antibody affinity |
Lower |
Higher (affinity maturation) |
| Duration of antibody response |
Shorter |
Longer (sustained) |
| Biological significance |
Initial response — may not prevent disease |
Rapid elimination of pathogen before disease develops — basis of vaccination |
The secondary response is the immunological basis of vaccination — exposure to a weakened or killed pathogen (or its antigens) primes memory cells. On real exposure, the secondary response eliminates the pathogen rapidly.
6. Active and Passive Immunity
Immunity can also be classified based on whether antibodies are produced by the individual's own immune system or transferred from an external source:
| Feature |
Active Immunity |
Passive Immunity |
| Source of antibodies |
Produced by the individual's own immune system |
Transferred from another individual or source |
| Memory |
Yes — long-lasting memory cells formed |
No — no memory cells formed |
| Onset |
Slow (days to weeks) |
Immediate (protection within hours) |
| Duration |
Long-lasting (years to lifetime) |
Short-lived (weeks to months) |
| Natural example |
Recovery from infection |
IgG crossing placenta (foetus); IgA in colostrum (newborn) |
| Artificial example |
Vaccination (immunisation with antigen) |
Injection of antiserum/immunoglobulin (e.g., anti-tetanus serum, anti-snake venom) |
| Risk of serum sickness |
No |
Yes (if antiserum from another species) |
Types of Active Immunity
- Natural active immunity: Acquired through natural infection and recovery (e.g., immunity after recovering from chickenpox).
- Artificial active immunity: Acquired through vaccination — deliberate exposure to antigens (weakened/killed pathogens or toxoids) that triggers immune response without causing disease.
Types of Passive Immunity
- Natural passive immunity: Transfer of antibodies from mother to offspring — IgG across placenta (during gestation) and IgA via colostrum (first milk).
- Artificial passive immunity: Injection of pre-formed antibodies (antiserum, immunoglobulin preparations) — used for immediate protection (e.g., anti-tetanus serum after injury, anti-rabies immunoglobulin, anti-snake venom).
7. Vaccination and Immunisation
Vaccination is the deliberate administration of an antigen (vaccine) to stimulate the immune system and generate immunological memory, providing protection against future infection. The process of building immunity through vaccination is called immunisation.
Types of Vaccines
| Type |
Description |
Examples |
| Live attenuated |
Weakened (attenuated) live pathogen — most immunogenic; produces strong, long-lasting immunity; risk of reversion to virulence |
BCG (TB), OPV (oral polio), MMR (measles, mumps, rubella), varicella |
| Killed/Inactivated |
Dead pathogen — safer; less immunogenic; may need boosters |
IPV (injectable polio), typhoid (killed), influenza |
| Toxoid |
Inactivated toxin — stimulates antitoxin antibodies |
Tetanus toxoid, Diphtheria toxoid (in DPT vaccine) |
| Subunit/Recombinant |
Specific antigenic component (protein/polysaccharide) of pathogen — safest; lower immunogenicity |
Hepatitis B vaccine (recombinant HBsAg), HPV vaccine |
Important Vaccines (NEET-relevant)
| Disease |
Vaccine |
Type |
| Tuberculosis |
BCG (Bacillus Calmette-Guérin) |
Live attenuated |
| Polio |
OPV (Sabin) / IPV (Salk) |
Live attenuated / Killed |
| Tetanus |
Tetanus toxoid (TT) |
Toxoid |
| Hepatitis B |
HBsAg vaccine |
Recombinant subunit |
| Smallpox (eradicated) |
Vaccinia virus |
Live attenuated (cowpox) |
8. Disorders of the Immune System
| Disorder |
Description |
Examples |
| Allergy / Hypersensitivity |
Exaggerated immune response to harmless antigens (allergens). Type I (immediate) involves IgE and mast cells → histamine release |
Asthma, hay fever, food allergy, anaphylaxis |
| Autoimmune disease |
Immune system attacks self-antigens (failure of self-tolerance) |
Rheumatoid arthritis (joint), Type 1 diabetes (islets), SLE, Multiple sclerosis |
| Immunodeficiency |
Reduced immune function — primary (genetic) or secondary (acquired) |
AIDS (secondary, due to HIV); SCID (primary) |
| Transplant rejection |
CMI attacks transplanted organ (recognises as foreign due to different MHC antigens) |
Organ transplant rejection; managed with immunosuppressants |
Allergy — Mechanism
- Sensitisation: First exposure to allergen → IgE is produced → IgE binds to mast cells.
- Challenge: Second exposure → allergen cross-links IgE on mast cells → mast cells degranulate → release histamine, leukotrienes, prostaglandins.
- Symptoms: Vasodilation, increased vascular permeability, smooth muscle contraction — runny nose, watery eyes, wheezing, urticaria.
- Anaphylaxis: Severe systemic allergic reaction — life-threatening; treated with epinephrine (adrenaline).
- Substances used to diagnose allergies: antihistamines block histamine receptors; corticosteroids suppress immune response.
Practice Questions (NEET Level)
Q1: Which immunoglobulin is produced first during a primary immune response?
A) IgG
B) IgA
C) IgM
D) IgE
Answer: C) IgM.
Explanation: IgM is the first antibody produced during a primary immune response due to its rapid synthesis and pentameric structure. It is highly effective at complement activation and agglutination.
As the immune response matures, class switching occurs and IgG becomes the dominant antibody (especially in the secondary response). IgM also serves as the primary antigen receptor on naïve B cells.
Q2: A newborn baby has immunity against many diseases that its mother had previously suffered from. This is an example of:
A) Natural active immunity
B) Artificial active immunity
C) Natural passive immunity
D) Artificial passive immunity
Answer: C) Natural passive immunity.
Explanation: The baby receives IgG antibodies directly from the mother through the placenta during gestation—this is natural passive immunity.
Additionally, IgA is received through colostrum (first milk). This process is natural (not involving deliberate medical intervention) and passive (the baby does not produce these antibodies itself). The immunity is short-lived (weeks to months) and no immunological memory is formed in the baby.
Q3: Which of the following cells are primarily targeted by HIV, leading to AIDS?
A) Cytotoxic T cells (CD8+)
B) B lymphocytes
C) Helper T cells (CD4+)
D) Natural Killer cells
Answer: C) Helper T cells (CD4+).
Explanation: HIV (Human Immunodeficiency Virus) specifically infects cells expressing the CD4 surface receptor, which are primarily Helper T cells (Th/CD4+ cells).
These cells are critical coordinators of the entire immune response—they activate B cells (humoral immunity) and cytotoxic T cells (cell-mediated immunity). The progressive destruction of CD4+ T cells leads to severe immunodeficiency (AIDS — Acquired Immunodeficiency Syndrome), making the individual highly susceptible to opportunistic infections.
Q4: Which immunoglobulin is associated with allergic reactions and is present in the lowest concentration in serum?
A) IgG
B) IgM
C) IgA
D) IgE
Answer: D) IgE.
Explanation: IgE is the immunoglobulin primarily responsible for Type I hypersensitivity (immediate allergic reactions). It binds to Fc receptors on mast cells and basophils.
When an allergen cross-links IgE molecules on mast cells, histamine and other inflammatory mediators are rapidly released, causing allergy symptoms. IgE is present in the lowest concentration in serum compared to all other immunoglobulin classes.
Q5: A person is bitten by a venomous snake and is immediately given anti-snake venom. This is an example of:
A) Natural active immunity
B) Artificial active immunity
C) Natural passive immunity
D) Artificial passive immunity
Answer: D) Artificial passive immunity.
Explanation: Anti-snake venom is a preparation of pre-formed antibodies (antiserum) produced in horses that have been immunized against snake venom. These antibodies are then purified and injected into the patient.
This is artificial (a deliberate medical intervention) and passive (the patient receives ready-made antibodies rather than producing their own). It provides critical, immediate protection in emergency situations, but it is short-lived and provides no long-term memory.
Q6: The secondary immune response differs from the primary immune response in that it:
A) Involves IgM as the predominant antibody
B) Has a longer lag period
C) Produces a higher antibody titre more rapidly due to memory cells
D) Involves only innate immune components
Answer: C) Produces a higher antibody titre more rapidly due to memory cells.
Explanation: The secondary (anamnestic) immune response is much faster (a 1–3 day lag vs. 5–10 days for primary), produces a significantly higher antibody titre (10–100× higher), and predominantly produces IgG rather than IgM.
This happens because memory B and T cells formed during the primary response persist in the body for years. Upon re-exposure to the same antigen, these memory cells rapidly proliferate and differentiate into plasma cells. This mechanism forms the entire immunological basis of vaccination.
Q7: Colostrum, the first milk produced by a mother, confers passive immunity to the newborn. Which immunoglobulin is primarily responsible?
A) IgG
B) IgM
C) IgA
D) IgD
Answer: C) IgA.
Explanation: Colostrum is rich in secretory IgA (sIgA), which is the predominant immunoglobulin found in all mucous secretions (including saliva, tears, breast milk, and intestinal secretions).
The IgA in colostrum coats the gut mucosa of the newborn, providing crucial protection against pathogens entering through the digestive tract. Note: IgG is transferred via the placenta during gestation (prenatal passive immunity), while IgA is transferred via colostrum (postnatal passive immunity).
