BIOSCI107 · Biology for Biomedical Science: Cellular Processes and Development
Blood & the Immune System
Topic 5 (exam Section A) covers blood and defence: blood composition, haemoglobin and the coagulation cascade; the innate system and complement (C3b opsonisation, the membrane attack complex); antibodies and V(D)J recombination (the five Ig classes, affinity vs avidity, RAG1/2, clonal selection); and cellular immunity and MHC restriction — MHC class I to CD8 cytotoxic T cells, MHC class II to CD4 helper T cells — plus allergy and hypersensitivity. Examined in the 40% final exam as paper Teleform MCQ, often as applied clinical scenarios.
What this chapter covers
- 01Blood composition: plasma (55%, has fibrinogen) vs serum; formed elements (RBC 45%, buffy coat of WBC + platelets); centrifuged order bottom→top
- 02Haemoglobin loads/unloads O₂ by partial pressure; CO/cyanide displace O₂ (CO → cherry-red blood)
- 03Haematopoiesis from the HSC (CD34⁺ marker) → myeloid and lymphoid lineages
- 04Coagulation cascade: intrinsic + extrinsic pathways converge on Factor X → thrombin → fibrinogen to fibrin (Ca²⁺ essential)
- 05Complement: three pathways converge on C3; C3b opsonises (binds covalently); MAC (C5–C9) lyses; anaphylatoxins C3a/C5a
- 06Innate immunity: barriers, phagocytes (neutrophils most abundant), NK cells, pattern-recognition receptors
- 07Antibodies: Y-shaped 2 heavy + 2 light chains, variable/CDR region binds antigen, Fc defines class; five classes (GAMED); affinity vs avidity; V(D)J recombination (RAG1/2); clonal selection
- 08Cellular immunity: MHC class I → CD8 cytotoxic (intracellular/viral), MHC class II → CD4 helper (extracellular/bacterial); MHC restriction; hypersensitivity types
MHC restriction — matching antigen source to T cell
- +1Cell 1 (viral, intracellular). Peptides from proteins made inside the cell are loaded onto MHC class I, which is expressed on all nucleated cells. This is the pathway for intracellular/viral antigen. [+1]
- +1Cell 1 responder. MHC class I is recognised by the CD8 co-receptor on CD8⁺ cytotoxic T lymphocytes (CTLs). The outcome is killing of the infected cell — granzyme + perforin (and Fas/FasL) trigger apoptosis, eliminating the viral factory. [+1]
- +1Cell 2 (bacterial, extracellular). Phagocytosed extracellular antigen is presented on MHC class II, expressed only on professional antigen-presenting cells (dendritic cells, macrophages, B cells). This is the extracellular/bacterial pathway. [+1]
- +1Cell 2 responder. MHC class II is recognised by the CD4 co-receptor on CD4⁺ helper T lymphocytes, which provide help (cytokines) to activate macrophages, B cells and CTLs rather than killing directly. In every case a T cell only recognises foreign peptide on a self-MHC molecule — MHC restriction. [+1]
Key terms
- Complement / C3b
- A cascade of ~9 innate serum proteins whose three activation pathways (classical, lectin, alternative) converge on C3. C3b binds covalently to a microbial surface = opsonisation, tagging it for phagocytosis; C3a/C5a are anaphylatoxin chemoattractants; C5–C9 assemble the membrane attack complex (MAC) that lyses the target.
- Coagulation cascade
- A proteolytic amplification chain: the intrinsic (contact) and extrinsic (tissue-factor) pathways converge on Factor X → Xa, which helps convert prothrombin to thrombin; thrombin cleaves fibrinogen to fibrin, forming the clot. Ca²⁺ is essential at several steps; plasmin later dissolves the clot.
- Affinity vs avidity
- Affinity is the strength of a single antigen–binding-site interaction; avidity is the combined strength of all the binding sites acting together. A pentameric IgM has low per-site affinity but high avidity from ten binding sites, letting naïve antibody bind before affinity maturation.
- V(D)J recombination
- The gene-rearrangement process (using RAG1 + RAG2 recombinases, only in B and T cells) that assembles Variable, Diversity and Joining segments into a unique antigen-receptor gene. Imprecise joining at the V-D-J junction generates the hypervariable CDR3 and most receptor diversity.
- MHC class I vs class II
- MHC class I (on all nucleated cells) presents intracellular/viral peptides to CD8⁺ cytotoxic T cells; MHC class II (only on professional antigen-presenting cells) presents extracellular/bacterial peptides to CD4⁺ helper T cells. Highly polymorphic at the peptide-binding cleft, which complicates transplant matching.
- Type I vs Type IV hypersensitivity
- Type I (immediate) allergy is IgE- and mast-cell-mediated — anti-allergen IgE on mast cells triggers histamine release within minutes (hay fever). Type IV (delayed) is T-cell-mediated and peaks at 2–3 days (the Mantoux/tuberculin skin-test welt).
Blood & the Immune System FAQ
How do I keep MHC class I and II straight?
Use two hooks. First the numbers: MHC I pairs with CD8 (I × 8) and MHC II pairs with CD4 (II × 4), and each product is 8. Second the antigen source: class I presents peptides made INSIDE the cell (viral) and sits on every nucleated cell, talking to CD8⁺ cytotoxic T cells that kill; class II presents peptides taken in from OUTSIDE (bacterial), sits only on professional antigen-presenting cells, and talks to CD4⁺ helper T cells that coordinate. And remember MHC restriction: a T cell only sees foreign peptide when it is displayed on self-MHC.
What do the five antibody classes do (GAMED)?
IgG is the most abundant in blood, crosses the placenta, neutralises toxins and activates complement (the affinity-matured workhorse). IgA is a dimer in secretions and breast milk (mucosal defence). IgM is the default naïve B-cell receptor and a blood pentamer with ten binding sites — high avidity, best complement activator. IgE is least abundant, fights parasites and drives Type I allergy via high-affinity receptors on mast cells. IgD is a B-cell receptor involved in B-cell differentiation.
Someone is found unconscious with bright pink venous blood — what is the immune/blood clue?
That is the carbon-monoxide poisoning pattern the exam reuses. CO (like cyanide) displaces O₂ from haemoglobin, but it also holds haemoglobin in a bright cherry-red, oxygen-like colour even in the veins where blood should be dark — so the venous blood looks pink despite tissue hypoxia. It is a haemoglobin/oxygen-transport clue, tying back to how partial pressure normally loads and unloads O₂.
Can AI help me with blood and immunity in BIOSCI 107?
Yes, for study. Sia can drill the MHC I/II–CD8/CD4 pairings, the antibody classes, the coagulation convergence on Factor X, and complement's C3b/MAC roles. Use it to prepare for the final exam — it does not sit the exam for you, and the exam is an AI-free lane under the course's academic-integrity policy. Confirm the rules on Canvas.
Exam move
This topic is large but pattern-rich, so build linked tables rather than reading passively. For innate defence, tie complement (three pathways → C3; C3b opsonises, MAC lyses, C3a/C5a recruit) to phagocytosis and the coagulation cascade (both pathways → Factor X → thrombin → fibrin, Ca²⁺ needed). For adaptive defence, make one antibody table (the five GAMED classes with their jobs, plus affinity vs avidity) and one cellular-immunity table (MHC I → CD8 → intracellular/viral → kill; MHC II → CD4 → extracellular/bacterial → help), memorised via the rule of eights. Learn V(D)J recombination as the source of diversity (RAG1/2, imprecise joining → CDR3) and clonal selection as how the right clone is chosen and matured. Rehearse the applied clinical items (CO poisoning, Mantoux = Type IV, monoclonal-antibody specificity). This is exam material (Topic 5, Section A); confirm the exam date and Teleform format on Canvas.
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