Lymphatic & Immune
Systems (3B)
Master the innate and adaptive immune responses, lymphatic structures, and defense mechanisms tested on the MCAT.
MCAT Biological Foundations
The Body's Defense Network
The immune system protects the body from pathogens: bacteria, viruses, fungi, and parasites. It works in concert with the lymphatic system, which circulates lymph, houses immune cells, and filters foreign material. Together they form a multi-layered defense that the MCAT tests across anatomy, cell biology, and biochemistry.
Lymphatic System Structures
Lymph Nodes
Filter lymph fluid; packed with B and T cells that screen for antigens
Spleen
Filters blood; removes old RBCs; reservoir for monocytes and lymphocytes
Thymus
Site of T cell maturation and positive/negative selection; involutes with age
Lymph Circulation Pathway
Two Arms of Immunity
Innate Immune Response
1
Physical barriers: Skin (keratinized epithelium), mucous membranes, cilia, stomach acid, lysozyme in tears/saliva
2
Phagocytic cells: Macrophages, neutrophils, and dendritic cells engulf pathogens via pattern recognition receptors (Toll-like receptors)
3
NK cells: Kill virus-infected and tumor cells by detecting absence of \( \text{MHC I} \) (missing self)
4
Complement system: Cascade of ~30 proteins that opsonize pathogens, form MAC (membrane attack complex), and recruit immune cells
5
Inflammation: Mast cells release histamine causing vasodilation, increased permeability, and leukocyte recruitment
Adaptive Immunity: Two Branches
Humoral Immunity
Mediated by B cells and antibodies. Targets extracellular pathogens (bacteria, toxins) in blood and lymph. B cells differentiate into plasma cells that secrete antibodies.
Cell-Mediated Immunity
Mediated by T cells. Targets intracellular pathogens (viruses, intracellular bacteria). Cytotoxic T cells (\( \text{CD8}^+ \)) kill infected cells. Helper T cells (\( \text{CD4}^+ \)) coordinate both branches.
Antibody Structure
\( \text{MHC I} \) vs \( \text{MHC II} \)
| \( \text{MHC Class I} \) | \( \text{MHC Class II} \) | |
|---|---|---|
| Found on | All nucleated cells | APCs (dendritic cells, macrophages, B cells) |
| Presents | Endogenous antigens (intracellular: viral proteins) | Exogenous antigens (extracellular: bacteria) |
| Recognized by | \( \text{CD8}^+ \) cytotoxic T cells | \( \text{CD4}^+ \) helper T cells |
| Structure | 1 alpha chain + beta-2 microglobulin | 1 alpha chain + 1 beta chain |
| Function | Signal to kill infected/abnormal cells | Activate helpers to coordinate full response |
T Cell Activation Pathway
B Cell Activation & Antibody Classes
B cells are activated when they bind antigen via their B cell receptor (BCR) and receive a co-stimulatory signal from a helper T cell (\( \text{CD4}^+ \)). They then differentiate into plasma cells (antibody factories) and memory B cells.
IgM
First antibody produced; pentamer in blood; strong complement activator
IgG
Most abundant; crosses placenta; long-term immunity; secondary response
IgA
Dimer in secretions (saliva, tears, breast milk, gut); mucosal immunity
IgE
Allergic reactions and parasitic defense; binds mast cells and basophils
How to Trace an Immune Response
1
Identify the pathogen type: Extracellular (bacteria, toxin) → humoral emphasis. Intracellular (virus, intracellular bacteria) → cell-mediated emphasis.
2
First line: innate response. Physical barriers → phagocytes engulf → complement activated → inflammation and fever recruit more cells.
3
Antigen presentation: Dendritic cells (primary APCs) migrate to lymph nodes, present antigen on \( \text{MHC II} \) to helper T cells.
4
Adaptive activation: \( \text{CD4}^+ \) helpers release cytokines → activate B cells (antibody production) and \( \text{CD8}^+ \) cytotoxic T cells (cell killing).
5
Resolution + memory: Pathogen cleared → most effector cells die → memory B and T cells persist for faster secondary response.
Example: Bacterial Skin Infection
A patient gets a cut, and Staphylococcus aureus enters the wound. Trace the immune response.
1
Barrier breached: Skin is broken. Resident macrophages in the dermis detect bacteria via Toll-like receptors (PAMPs).
2
Inflammation: Mast cells release histamine → vasodilation, redness, heat, swelling. Neutrophils recruited first (most abundant WBC).
3
Complement: Activated via alternative pathway → opsonization → MAC pokes holes in bacterial membranes.
4
Adaptive response: Dendritic cells present bacterial peptides on \( \text{MHC II} \) → \( \text{CD4}^+ \) T cells activate B cells → IgM then IgG antibodies produced.
Example: Viral Infection (Influenza)
Influenza virus infects respiratory epithelial cells. How does the immune system respond differently than to bacteria?
1
Innate: Infected cells produce interferons (IFN-alpha, IFN-beta) that warn neighboring cells and activate NK cells.
2
NK cells: Detect loss of \( \text{MHC I} \) on infected cells ("missing self") → induce apoptosis via perforin and granzymes.
3
MHC I presentation: Infected cells display viral peptides on \( \text{MHC I} \) → \( \text{CD8}^+ \) cytotoxic T cells recognize and kill them.
4
Humoral backup: Antibodies (especially IgA in mucosa) neutralize free viral particles, preventing reinfection.
Example: Vaccination & Memory
A patient receives a flu vaccine (inactivated viral antigens). What happens immunologically?
Common Mistakes
✕ Confusing \( \text{MHC I} \) and \( \text{MHC II} \)
\( \text{MHC I} \) is on all nucleated cells (not just immune cells). \( \text{MHC II} \) is only on APCs. Mixing them up changes which T cell responds.
✕ Thinking B cells are only humoral
B cells also function as APCs: they can present antigen on \( \text{MHC II} \) to helper T cells. They are not just antibody producers.
✕ Forgetting co-stimulation
TCR binding alone is not enough. Without co-stimulatory signals (\( \text{B7/CD28} \)), T cells become anergic (tolerant), not activated.
Immune Cell Summary
| Cell Type | Branch | Key Function |
|---|---|---|
| Neutrophils | Innate | First responders; phagocytosis; most abundant WBC |
| Macrophages | Innate + APC | Phagocytosis; antigen presentation on \( \text{MHC II} \) |
| Dendritic Cells | Innate + APC | Best APCs; bridge innate and adaptive immunity |
| NK Cells | Innate | Kill cells lacking \( \text{MHC I} \); perforin/granzymes |
| Helper T (\( \text{CD4}^+ \)) | Adaptive | Coordinate response; activate B cells and \( \text{CD8}^+ \) cells |
| Cytotoxic T (\( \text{CD8}^+ \)) | Adaptive | Kill infected/abnormal cells displaying \( \text{MHC I} \) |
| B Cells / Plasma | Adaptive | Produce antibodies; also serve as APCs |
Active vs Passive Immunity
Active Immunity
Body produces its own antibodies and memory cells. Triggered by natural infection or vaccination. Long-lasting (years to lifetime). Takes days-weeks to develop.
Passive Immunity
Pre-formed antibodies transferred from another source. Examples: maternal IgG across placenta, IgA in breast milk, or antiserum injection. Temporary (weeks to months). Immediate protection.
Immune Disorders
Autoimmunity
Immune system attacks self-tissue. Failed self-tolerance. Examples: Type 1 diabetes (attacks beta cells), lupus, rheumatoid arthritis
Hypersensitivity
Exaggerated immune response. Type I (IgE-mediated, allergies). Type IV (delayed, T cell-mediated, e.g. contact dermatitis)
Immunodeficiency
Weakened immune system. Primary (genetic, e.g. SCID) or acquired (e.g. HIV destroys \( \text{CD4}^+ \) T cells → AIDS)
Question 1 of 5
A dendritic cell engulfs a bacterium and presents bacterial peptides to activate other immune cells. On which molecule are these peptides most likely displayed?
Dendritic cells are professional APCs that present exogenous (extracellular) antigens on \( \text{MHC Class II} \), which is recognized by \( \text{CD4}^+ \) helper T cells. \( \text{MHC I} \) presents endogenous (intracellular) antigens.
Question 2 of 5
A patient with HIV has a severely reduced \( \text{CD4}^+ \) T cell count. Which of the following immune functions would be most directly impaired?
\( \text{CD4}^+ \) helper T cells coordinate the adaptive immune response by activating both B cells (for antibody production) and \( \text{CD8}^+ \) cytotoxic T cells. Losing them cripples the entire adaptive response. Neutrophils, NK cells, and complement are part of innate immunity and function independently of \( \text{CD4}^+ \) cells.
Question 3 of 5
Which antibody class is most abundant in blood, provides long-term immunity, and is the only class that can cross the placenta?
IgG is the most abundant serum antibody, dominates the secondary immune response, provides long-lasting protection, and is the only class that crosses the placenta to give the fetus passive immunity. IgM is the first produced but does not cross the placenta. IgA is found in secretions. IgE mediates allergic responses.
Question 4 of 5
A virus-infected cell displays viral peptides on its surface. Which immune cell would directly kill this infected cell?
\( \text{CD8}^+ \) cytotoxic T cells recognize viral peptides presented on \( \text{MHC Class I} \) and directly kill the infected cell using perforin (pore-forming protein) and granzymes (serine proteases that trigger apoptosis). \( \text{CD4}^+ \) helpers coordinate but do not directly kill. Plasma B cells secrete antibodies. Macrophages phagocytose but are not the primary killers of virus-infected cells.
Question 5 of 5
A newborn receives antibodies through breast milk. This is an example of:
Natural passive immunity occurs when pre-formed antibodies are transferred naturally: maternal IgG across the placenta and IgA in breast milk. The baby's immune system did not produce these antibodies, so no memory is formed (passive). It occurs through a natural biological process, not injection (natural, not artificial). Artificial passive = antiserum injection. Active = body produces its own antibodies.