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๐Ÿ›ก๏ธ Physiology ยท Immune

Memory tricks for immune physiology

Innate vs adaptive immunity, B and T cells, antibodies, and hypersensitivity.

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๐Ÿ›ก๏ธ Immune Physiology

Memory Tricks

Proven Mnemonics & Acronyms โ€” fast to learn, hard to forget.

Innate vs Adaptive
Innate = Instant ยท Adaptive = Accurate with memory
Non-specific fast first response ยท Specific slow response with immunological memory
Two divisions of immunity โ€” how they differ and how they cooperate
Innate immunity is the immediate, non-specific first line of defense โ€” responds within minutes to hours. Physical barriers (skin, mucus, cilia), phagocytes (neutrophils, macrophages), NK cells, complement, fever, and inflammation. No memory โ€” same response to same pathogen every time. Adaptive immunity is specific and slow (days first exposure, hours on re-exposure). T cells and B cells recognize specific antigens. Has immunological memory โ€” basis of vaccination. Both cooperate: innate activates adaptive (APCs present antigen), adaptive enhances innate (antibodies opsonize for phagocytosis).
Innate cells
Neutrophils (first responders), macrophages (phagocytes + APCs), NK cells, dendritic cells, mast cells, basophils, eosinophils.
Adaptive cells
T lymphocytes (cell-mediated) + B lymphocytes (humoral/antibody). Both need activation.
PRRs
Pattern recognition receptors (TLRs) detect PAMPs โ€” pathogen-associated molecular patterns.
Memory cells
Long-lived T and B memory cells โ€” persist after infection, enable faster secondary response.
Difficulty: Beginner
MHC and Antigen Presentation
MHC I = 8 (CD8 cytotoxic) ยท MHC II = 4 (CD4 helper)
MHC class I presents to CD8+ ยท MHC class II presents to CD4+ T cells
MHC molecules โ€” how antigens are displayed and which T cells respond
MHC (major histocompatibility complex) molecules display peptide fragments on cell surfaces for T cell recognition. MHC class I: expressed on ALL nucleated cells โ€” presents intracellular peptides (from viruses, tumors) to CD8+ cytotoxic T cells โ†’ kill the cell. MHC class II: expressed only on professional APCs (dendritic cells, macrophages, B cells) โ€” presents extracellular peptides (from phagocytosed bacteria) to CD4+ helper T cells โ†’ activate response. Memory trick: MHC I ร— CD8 = 8, MHC II ร— CD4 = 8. Both equal 8 โ€” easy to remember the pairing.
MHC I
All nucleated cells. Intracellular antigens (virus, tumor). โ†’ CD8+ T cells kill.
MHC II
APCs only (DC, macrophage, B cell). Extracellular antigens. โ†’ CD4+ T cells activate.
MHC I ร— CD8 = 8
Memory trick โ€” both products equal 8. Pairs: I with 8, II with 4.
HLA
Human version of MHC. HLA mismatches cause transplant rejection. HLA-B27 โ†’ ankylosing spondylitis.
Difficulty: Intermediate
T Cell Activation
Two signals needed โ€” antigen + costimulation ยท One signal = anergy
Signal 1: TCR binds MHC-peptide ยท Signal 2: CD28 binds B7 (costimulation)
How T cells are activated โ€” the two-signal rule and why it prevents autoimmunity
T cell activation requires two simultaneous signals. Signal 1: T cell receptor (TCR) binds the MHC-peptide complex on an APC โ€” antigen specific. Signal 2 (costimulation): CD28 on T cell binds B7 (CD80/86) on APC โ€” confirms it's a real immune threat. Both signals โ†’ T cell activates โ†’ proliferates โ†’ differentiates into effector cells. Signal 1 alone (without costimulation) โ†’ T cell anergy โ€” the T cell is rendered unresponsive. This two-signal requirement prevents accidental activation against self-antigens (which lack B7 expression). CTLA-4 competes with CD28 for B7 โ€” immune checkpoint โ€” used therapeutically as cancer immunotherapy.
Signal 1
TCR + CD3 binds MHC-peptide. Antigen-specific. Necessary but not sufficient.
Signal 2
CD28 binds B7 on APC. Costimulatory. Confirms real immune threat.
Anergy
Signal 1 without Signal 2 โ†’ T cell becomes unresponsive. Peripheral tolerance.
CTLA-4
Competes with CD28 for B7 โ†’ dampens T cell response. Cancer immunotherapy blocks CTLA-4 (ipilimumab).
Difficulty: Advanced
T Helper Cell Subsets
Th1 kills intracellular ยท Th2 fights parasites ยท Th17 fights bacteria ยท Treg suppresses
CD4+ T helper subsets โ€” each specializes for a different type of threat
Four CD4+ T helper subsets โ€” what each fights and what cytokines they use
Th1 cells: activated by IL-12. Secrete IFN-ฮณ โ†’ activate macrophages โ†’ kill intracellular bacteria and viruses. Fight tuberculosis, Listeria, Leishmania. Th2 cells: activated by IL-4. Secrete IL-4, IL-5, IL-13 โ†’ activate eosinophils and mast cells โ†’ fight parasites and helminths. Also drive allergic responses. Th17 cells: activated by IL-6 + TGF-ฮฒ. Secrete IL-17 โ†’ recruit neutrophils โ†’ fight extracellular bacteria and fungi. Implicated in autoimmune diseases (psoriasis, IBD). Treg (regulatory T cells): secrete IL-10 and TGF-ฮฒ โ†’ suppress immune responses โ†’ prevent autoimmunity.
Th1
IFN-ฮณ โ†’ macrophage activation โ†’ intracellular bugs (TB, viruses). IL-12 induces.
Th2
IL-4, IL-5, IL-13 โ†’ eosinophils, IgE โ†’ parasites and allergies. IL-4 induces.
Th17
IL-17 โ†’ neutrophil recruitment โ†’ extracellular bacteria + fungi. IL-6 + TGF-ฮฒ induces.
Treg
IL-10, TGF-ฮฒ โ†’ immune suppression. Prevent autoimmunity. FoxP3 transcription factor.
Difficulty: Advanced
B Cell Activation and Antibodies
B โ†’ Plasma cell โ†’ Antibody ยท T-dependent vs T-independent
B cells require T helper help for most antigens ยท Plasma cells are antibody factories
How B cells produce antibodies โ€” T-dependent and T-independent responses
B cells recognize antigen via BCR โ†’ internalize and present on MHC II โ†’ Th2 cell binds โ†’ CD40L on T cell binds CD40 on B cell (critical co-stimulation) โ†’ B cell activated โ†’ proliferates in germinal centers โ†’ somatic hypermutation (affinity maturation) โ†’ class switching โ†’ differentiate into plasma cells (antibody factories) or memory B cells. T-independent antigens (polysaccharides, LPS) activate B cells without T help โ†’ IgM only, no memory. T-dependent antigens (proteins) need T cell help โ†’ class switching to IgG, IgA, IgE โ†’ memory. This is why protein-conjugate vaccines are more effective than pure polysaccharide vaccines.
CD40-CD40L
Critical B-T interaction. CD40L on T cell binds CD40 on B cell โ†’ B cell activates fully.
Germinal centers
Lymph node site where B cells hypermutate and undergo affinity maturation.
Class switching
IgM โ†’ IgG/IgA/IgE. Requires T help + cytokines. Changes function, not specificity.
T-independent
Polysaccharides โ†’ IgM only, no memory. Infants respond poorly (immature T cells).
Difficulty: Advanced
Complement Pathways
Classical โ†’ Lectin โ†’ Alternative โ†’ all meet at C3 โ†’ MAC
Three activation pathways converge at C3 cleavage โ†’ Membrane Attack Complex
The complement cascade โ€” three pathways, one goal: destroy pathogens
Classical pathway: activated by antibody-antigen complexes (IgG or IgM bound to pathogen) โ†’ C1 โ†’ C4 โ†’ C2 โ†’ C3. Lectin pathway: activated by mannose-binding lectin (MBL) recognizing mannose on bacterial surfaces โ†’ C4 โ†’ C2 โ†’ C3. Alternative pathway: spontaneous low-level C3 hydrolysis + amplification on foreign surfaces (no antibody needed โ€” innate). All three converge at C3 โ†’ C3b (opsonin) + C3a (anaphylatoxin) โ†’ C5 โ†’ C5a (chemotaxis) + C5b โ†’ MAC (C5b-9) โ†’ punches holes in pathogen membrane โ†’ lysis.
Classical
Antibody-antigen โ†’ C1 activation. Links adaptive to innate. C1q binds Fc region.
Alternative
No antibody needed โ€” spontaneous C3 hydrolysis + foreign surface stabilization.
C3b
Key opsonin โ€” coats bacteria for phagocytosis by macrophages/neutrophils (CR1 receptor).
MAC (C5b-9)
Membrane attack complex โ€” inserts into membrane โ†’ osmotic lysis. Kills gram-negative bacteria.
Difficulty: Advanced
Hypersensitivity Reactions
ACID โ€” Anaphylactic ยท Cytotoxic ยท Immune complex ยท Delayed
Type I (IgE) ยท Type II (IgG/M vs cells) ยท Type III (immune complexes) ยท Type IV (T cells)
Four types of hypersensitivity โ€” mechanism, mediator, and classic example
Type I (Anaphylactic): IgE on mast cells + allergen โ†’ degranulation โ†’ histamine โ†’ urticaria, anaphylaxis. Examples: peanut allergy, bee sting, asthma. Type II (Cytotoxic): IgG or IgM binds cells โ†’ complement or NK cell kills โ†’ examples: Goodpasture's syndrome, hemolytic disease of newborn, myasthenia gravis, Graves' disease. Type III (Immune complex): antigen-antibody complexes deposit in tissues โ†’ complement โ†’ inflammation โ†’ examples: serum sickness, SLE, post-streptococcal GN. Type IV (Delayed, T cell-mediated): sensitized T cells โ†’ 48-72 hours โ†’ examples: contact dermatitis, TB skin test, transplant rejection, multiple sclerosis.
Type I
IgE + mast cells โ†’ immediate (minutes). Anaphylaxis treated with epinephrine.
Type II
IgG/M binds cell surface โ†’ complement or ADCC kills. Hemolytic anemia, MG, Graves.
Type III
Immune complexes in vessels/tissues โ†’ complement inflammation. SLE, serum sickness.
Type IV
T cells, no antibody. Delayed 48-72 hrs. PPD test, contact dermatitis, MS, T1DM.
Difficulty: Intermediate
Inflammation Mediators
CHIPS โ€” Cytokines ยท Histamine ยท IL-1/6 ยท Prostaglandins ยท Substance P
Five major categories of inflammatory mediators
The key inflammatory mediators โ€” what each does and how to target them clinically
Histamine: from mast cells and basophils โ†’ vasodilation, increased permeability, itching. Blocked by antihistamines. Prostaglandins: from arachidonic acid via COX โ†’ vasodilation, fever, pain sensitization. Blocked by NSAIDs and aspirin (COX inhibitors). IL-1 and IL-6: from macrophages โ†’ fever (act on hypothalamus), acute phase proteins (CRP, fibrinogen), activate liver. TNF-ฮฑ: from macrophages โ†’ fever, cachexia, endothelial activation. Biologic drugs block TNF (etanercept, infliximab) for RA, IBD. Bradykinin: increased vascular permeability, pain. ACE inhibitors prevent bradykinin breakdown โ†’ cough.
Histamine
Mast cells โ†’ vasodilation, permeability, itch. Blocked by H1 antihistamines.
Prostaglandins
COX pathway โ†’ pain, fever, vasodilation. NSAIDs block COX-1 and COX-2.
IL-1, IL-6, TNF-ฮฑ
Macrophage cytokines โ†’ fever, acute phase response. Biologic targets in RA/IBD.
Bradykinin
Vasodilation + pain. ACE inhibitors prevent degradation โ†’ bradykinin-mediated cough.
Difficulty: Intermediate
Immunodeficiency Overview
B cell defects = bacterial ยท T cell defects = viral + fungal ยท Combined = everything
Type of pathogen predicts which immune compartment is defective
How to identify immunodeficiency type from the infections โ€” the key clinical pattern
The type of recurrent infection predicts the immune defect. B cell (antibody) deficiencies: recurrent encapsulated bacterial infections (Strep pneumo, H. flu, Neisseria) โ€” no antibodies to opsonize. Starts after 6 months (maternal IgG wanes). Examples: XLA (Bruton's โ€” no BTK โ†’ no B cells), CVID, IgA deficiency. T cell deficiencies: recurrent viral, fungal, intracellular infections โ€” CMV, PCP, Candida, Cryptococcus. DiGeorge syndrome (no thymus โ†’ no T cells). Combined (SCID): everything โ€” no T or B cells. Treat with bone marrow transplant. Phagocyte defects: catalase-positive organisms (Staph, Aspergillus) โ€” chronic granulomatous disease.
B cell defects
Encapsulated bacteria. After 6 months. XLA (Bruton's), CVID, IgA deficiency.
T cell defects
Viruses, fungi, intracellular. DiGeorge (no thymus). HIV destroys CD4+ T cells.
SCID
No T or B cells. ADA deficiency most common. BMT is curative. "Bubble boy" disease.
CGD
Chronic granulomatous disease โ€” NADPH oxidase defect โ†’ no respiratory burst โ†’ catalase+ bugs.
Difficulty: Intermediate
Innate vs Adaptive Immunity
Innate = Instant ยท Adaptive = Aims precisely
๐Ÿ“Œ Immune Overview
Innate immunity is fast and nonspecific; adaptive is slow but targeted and has memory
Innate (first line): physical barriers + neutrophils, macrophages, NK cells, complement โ€” responds in minutes-hours, no memory. Adaptive (second line): T and B lymphocytes โ€” antigen-specific, takes days-weeks, creates immunological memory. Both work together.
IInnate = Immediate, nonspecific
AAdaptive = Antigen-specific + memory
T Cell Types
CHAT โ€” Cytotoxic ยท Helper ยท And ยท T-regulatory
๐Ÿ“Œ Cellular Immunity
Three major T cell subtypes and their distinct roles in immune defense
CD8+ Cytotoxic T cells: kill infected/tumor cells directly via perforin/granzyme. CD4+ Helper T cells: activate B cells and cytotoxic T cells via cytokines (Th1 โ†’ cellular, Th2 โ†’ humoral). T-regulatory cells: suppress immune response and prevent autoimmunity.
CCytotoxic T (CD8+) โ€” kill cells
HHelper T (CD4+) โ€” activate others
AAnd they all require MHC presentation
TT-regulatory โ€” suppress overreaction
Antibody Classes
GAMED โ€” IgG ยท IgA ยท IgM ยท IgE ยท IgD
๐Ÿ“Œ Humoral Immunity
Five immunoglobulin classes and their primary roles
IgG: most abundant, crosses placenta (maternal immunity). IgA: in secretions (saliva, breast milk, gut). IgM: first responder, pentamer, best complement activator. IgE: allergy and parasites (triggers mast cells). IgD: B cell surface receptor, function unclear.
GIgG โ€” most abundant, crosses placenta
AIgA โ€” secretions (gut, saliva)
MIgM โ€” first responder, pentamer
EIgE โ€” allergy + parasites
DIgD โ€” B cell surface receptor
Complement System
MAC Attack โ€” Membrane Attack Complex kills pathogens
๐Ÿ“Œ Innate Immunity
Complement cascades through three pathways to punch holes in pathogen membranes
Three activation pathways (classical, lectin, alternative) all converge at C3 cleavage โ†’ C3b opsonizes pathogens โ†’ C5-C9 form MAC (membrane attack complex) โ†’ pore in membrane โ†’ cell lysis. Also promotes inflammation and recruits phagocytes.
MMembrane Attack Complex
AAll 3 pathways converge at C3
CC5-9 form the pore โ†’ cell lysis
🎓 Common Exam Questions
Q: What is the MHC and how do MHC I and MHC II differ in function?
A: MHC (Major Histocompatibility Complex) proteins present antigens to T cells. MHC I: expressed on ALL nucleated cells. Presents endogenous (intracellular) antigens โ€” viral proteins, tumor antigens. Recognized by CD8+ cytotoxic T cells โ†’ kill the cell. MHC II: expressed only on professional antigen-presenting cells (dendritic cells, macrophages, B cells). Presents exogenous antigens. Recognized by CD4+ helper T cells โ†’ activate immune response. Memory trick: CD8 recognizes MHC I (8 รท 2 = 4... no โ€” "1 ร— 8 = 8" and "2 ร— 4 = 8" โ€” both equal 8). Or: "CD8 kills; CD4 helps."
Q: How does a B cell become a plasma cell and produce antibodies?
A: Naive B cell encounters antigen โ†’ binds via B cell receptor (surface IgM/IgD) โ†’ internalizes antigen โ†’ presents on MHC II โ†’ CD4+ helper T cell binds โ†’ T cell releases cytokines (IL-4, IL-5, IL-21) โ†’ B cell proliferates (clonal expansion) โ†’ differentiates into plasma cells (antibody factories) and memory B cells. Plasma cells secrete antibodies. Class switching (IgM โ†’ IgG, IgA, IgE) driven by cytokines from T helper cells. Memory B cells respond faster on re-exposure (secondary immune response).
Q: What are the four steps of the inflammatory response?
A: Cardinal signs: Rubor (redness), Calor (heat), Tumor (swelling), Dolor (pain) โ€” add Functio laesa (loss of function). Steps: (1) Vasodilation: histamine + prostaglandins โ†’ arteriolar dilation โ†’ redness + heat. (2) Increased permeability: gaps in endothelium โ†’ protein-rich fluid leaks โ†’ swelling. (3) Leukocyte recruitment: selectins (rolling) โ†’ integrins (adhesion) โ†’ diapedesis โ†’ chemokines guide to site. (4) Resolution: anti-inflammatory mediators (lipoxins, IL-10, TGF-ฮฒ) โ†’ repair. NSAIDs block COX โ†’ reduce prostaglandins โ†’ reduce fever, pain, swelling.
Q: What is the difference between primary and secondary immune responses?
A: Primary response: first exposure to antigen. Lag period of 5โ€“10 days before antibodies appear (naive B cells must be activated, proliferate, differentiate). IgM produced first, then class switching to IgG. Peak antibody levels lower. Memory B and T cells formed. Secondary response: re-exposure to same antigen. Memory cells respond within 1โ€“3 days. Higher peak antibody levels. Predominantly IgG (already class-switched). More durable response. This is the basis of vaccination โ€” prime with antigen โ†’ memory cells โ†’ fast protective response on real exposure.
Q: How does the complement system work and what are its three outcomes?
A: Three activation pathways (classical: antibody-antigen complex; lectin: mannose-binding lectin on pathogen; alternative: spontaneous C3 hydrolysis on pathogen surface) โ†’ all converge at C3 convertase โ†’ cleaves C3 โ†’ C3a + C3b. Three outcomes: (1) Opsonization: C3b coats pathogen โ†’ phagocytes have C3b receptors โ†’ easier ingestion. (2) Inflammation: C3a and C5a are anaphylatoxins โ†’ mast cell degranulation โ†’ vasodilation + recruitment of neutrophils. (3) Lysis: C5b-C9 = Membrane Attack Complex (MAC) โ†’ pore in membrane โ†’ osmotic lysis. Especially effective against Neisseria โ€” C5-C9 deficiency โ†’ recurrent Neisseria infections.