Immunity
Immunity is the body’s ability to resist or eliminate potentially harmful foreign substances (antigens) and abnormal cells. The PMDC MDCAT 2026 syllabus expects you to distinguish innate (non-specific) from adaptive (specific) defense, understand B-cell and T-cell biology, list antibody classes, and explain vaccination. Expect 2-4 MCQs from this chapter.
Specific Defense Mechanism
Defense in mammals operates at two levels: a fast, generic innate (non-specific) system and a slower, antigen-specific adaptive system. The adaptive system has memory; the innate one does not.
Non-specific (innate) defense — context
The first lines stop or attack any pathogen, regardless of identity:
- Physical barriers: intact skin, mucous membranes, ciliated epithelium of trachea.
- Chemical barriers: stomach HCl, lysozyme in tears and saliva, sebum on skin.
- Phagocytes: neutrophils and macrophages engulf and digest pathogens (phagocytosis).
- Inflammation: mast cells release histamine → vasodilation, increased capillary permeability → redness, heat, swelling, pain.
- Fever: pyrogens reset the hypothalamic set point; higher temperature inhibits microbial growth and accelerates immune responses.
- Natural killer (NK) cells and the complement system attack virus-infected and tumour cells.
Specific (adaptive) defense — the deep dive
Two co-ordinated arms: cell-mediated immunity (T cells, against intracellular pathogens) and humoral immunity (B cells → antibodies, against extracellular pathogens and toxins). Both arms have specificity, diversity, memory and self/non-self recognition.
| Property | Innate (non-specific) | Adaptive (specific) |
|---|---|---|
| Speed | Immediate — minutes to hours | Slow — days for primary response |
| Specificity | Generic — same response to any pathogen | Antigen-specific — tailored to each pathogen |
| Memory | None — same speed each time | Yes — faster & stronger on re-exposure |
| Components | Skin, mucous, HCl, lysozyme, phagocytes, NK cells, complement, inflammation, fever | B cells, T cells, antibodies, lymph nodes, spleen, thymus |
| Recognition | Pattern-based (PAMPs) | Antigen-receptor based (BCR / TCR) |
| Diversity | Limited (~100 receptor types) | ~1011 different antibodies / TCRs |
| Present in | All animals | Vertebrates only |
Mature in the bone marrow. Each B cell carries a unique membrane-bound antibody (B-cell receptor). On encountering its specific antigen (with help from a TH cell) it proliferates and differentiates into:
- Plasma cells — antibody factories that secrete ~2,000 antibody molecules per second.
- Memory B cells — long-lived; provide a faster, larger response on re-exposure.
Mature in the thymus. Recognise antigens only when presented on MHC molecules. Three main subtypes:
- T helper cells (TH, CD4+) — recognise antigen on MHC class II; release cytokines that activate B cells, TC cells and macrophages. Targeted by HIV.
- T cytotoxic cells (TC, CD8+) — recognise antigen on MHC class I; kill virus-infected and tumour cells using perforin and granzymes.
- T memory and T regulatory cells — provide long-term memory and prevent autoimmunity.
Major Histocompatibility Complex molecules display peptide fragments on cell surfaces.
- MHC class I — on every nucleated cell. Presents intracellular (e.g. viral) peptides to TC (CD8) cells.
- MHC class II — only on antigen-presenting cells (macrophages, dendritic cells, B cells). Presents extracellular peptides to TH (CD4) cells.
MHC matching is critical for tissue/organ transplantation.
Y-shaped glycoproteins with two heavy and two light chains. The variable regions form the antigen-binding site (Fab); the constant region (Fc) determines class and effector function.
- IgG
- Most abundant in serum (~75%). Crosses the placenta to give passive immunity to the foetus. Main antibody of the secondary response.
- IgM
- Pentamer with 10 binding sites. First antibody produced in the primary response. Excellent at agglutination and complement activation.
- IgA
- Dimer found in mucous secretions, saliva, tears and breast milk. Protects mucosal surfaces and provides passive immunity to neonates.
- IgD
- Membrane-bound on naive B cells; functions as an antigen receptor.
- IgE
- Binds mast cells and basophils. Mediates allergic reactions and defends against parasitic worms.
| Property | B lymphocytes | T lymphocytes |
|---|---|---|
| Maturation site | Bone marrow | Thymus |
| Receptor | BCR (membrane antibody) | TCR (T-cell receptor) |
| Antigen recognition | Direct (free antigen) | Only when displayed on MHC |
| Arm of immunity | Humoral (antibody-mediated) | Cell-mediated |
| Targets | Extracellular pathogens, toxins | Intracellular (viruses, tumour cells) |
| Effector forms | Plasma cells (secrete antibodies), memory B cells | TH (CD4) helper, TC (CD8) cytotoxic, T regulatory, T memory |
| HIV target | No | Yes — TH (CD4) cells |
| Class | Structure | % of serum Ig | Main role / site | Special feature |
|---|---|---|---|---|
| IgG | Monomer | ~75% (most abundant) | Secondary response; opsonisation | Crosses placenta → passive immunity to foetus |
| IgM | Pentamer (10 binding sites) | ~10% | First antibody in primary response | Strongest activator of complement, agglutination |
| IgA | Dimer | ~15% | Mucous, saliva, tears, breast milk | Passive immunity to neonate via colostrum |
| IgD | Monomer | < 1% | Surface of naïve B cells | Acts as antigen receptor |
| IgE | Monomer | < 0.01% | Bound to mast cells / basophils | Allergy (hay fever, asthma); parasitic worms |
Primary vs secondary response
| Property | Primary response | Secondary response |
|---|---|---|
| Trigger | First exposure to antigen | Re-exposure to the same antigen |
| Lag time | 5–10 days | 1–3 days |
| Peak antibody level | Modest | Far higher (10–100×) |
| Predominant antibody | IgM (early), then IgG | IgG (memory cells switch class) |
| Affinity | Lower | Higher (affinity maturation) |
| Duration | Short-lived | Long-lasting (years) |
| Basis of | First infection / first vaccine dose | Vaccination effectiveness, booster doses |
Vaccination
A vaccine introduces antigen (without causing disease) so the body mounts a primary response and builds memory cells. On real exposure, a swift secondary response prevents illness. Major vaccine types:
- Live attenuated
- Weakened pathogen that still replicates a little. Strong, durable immunity. Examples: BCG (TB), MMR, oral polio. Contraindicated in immunocompromised patients.
- Killed (inactivated)
- Pathogen killed by heat or chemicals. Safer but weaker; needs boosters. Examples: injectable polio (IPV), rabies, hepatitis A.
- Subunit / toxoid / conjugate
- Only a portion (protein, polysaccharide) or detoxified toxin is used. Examples: hepatitis B (subunit), tetanus and diphtheria (toxoids).
- mRNA / viral vector
- Modern platforms (e.g. COVID-19 vaccines) deliver genetic instructions for the antigen.
Immune disorders
- AIDS — HIV destroys CD4 T helper cells → collapse of adaptive immunity.
- Allergies — hypersensitivity mediated by IgE binding to mast cells.
- Autoimmunity — immune attack on self (e.g. type 1 diabetes, rheumatoid arthritis, multiple sclerosis).
- SCID — severe combined immunodeficiency; both B and T cells defective.
Worked MCQs
Five MCQs that capture the high-yield testing patterns for immunity. Read every explanation carefully.
Q1. Which class of antibody is the first to appear in a primary immune response?
IgM is a pentamer with 10 antigen-binding sites and is secreted first by newly activated plasma cells. Class switching to IgG (and others) occurs later in the same response and dominates the secondary response.
Q2. HIV preferentially infects which of the following cells, leading to AIDS?
HIV uses CD4 (and a co-receptor) to enter helper T cells. As CD4 counts collapse, both the cell-mediated and humoral arms of adaptive immunity fail, leaving the host vulnerable to opportunistic infections.
Q3. A mother passes IgG antibodies to her foetus across the placenta. This is an example of:
The antibodies are pre-formed (passive) and transferred without medical intervention (natural). The infant’s own immune system did not make them, so there are no memory cells — protection lasts only weeks to months.
Q4. MHC class I molecules present peptides to which cell type?
MHC class I is expressed on all nucleated cells and presents intracellular (often viral) peptides to CD8 cytotoxic T cells. MHC class II, on antigen-presenting cells, presents to CD4 helper T cells. A handy rule: 8 × 1 = 4 × 2 = 8 (CD8 with class I, CD4 with class II).
Q5. The BCG and oral polio vaccines are examples of which vaccine type?
Both BCG (against tuberculosis) and the Sabin oral polio vaccine use weakened, replicating forms of the pathogen. Live attenuated vaccines provide strong, long-lasting immunity but must be avoided in severely immunocompromised individuals.
Quick Recap
- Innate = fast, generic, no memory; adaptive = slow first time, specific, has memory.
- B cells mature in bone marrow → plasma + memory cells; T cells mature in thymus.
- TH (CD4) help; TC (CD8) kill infected cells.
- MHC I → CD8; MHC II → CD4.
- Antibody classes: IgG (most abundant, crosses placenta), IgM (first, pentamer), IgA (mucous, milk), IgD (B-cell receptor), IgE (allergy + parasites).
- Primary response — slow, IgM dominant; secondary — fast, IgG dominant.
- Vaccines: live attenuated, killed, subunit/toxoid, mRNA.