Video 2 - Immune System Specific Defenses & Pathogen-Related Disorders

Third‐Line / Specific Defenses

• Represent the branch of immunity that is learned and refined through life experience (previous infections, vaccinations, environmental exposures).
• Called “third-line barriers” because they come into play after physical & innate chemical barriers have been breached.
• Key players:
  • Lymphocytes (B cells & T cells) that display antigen specificity.
  • Require activation by antigen presentation.

Antigen Presentation & MHC

• Antigen-Presenting Cell (APC) steps:
  1. Phagocytosis (e.g., by a neutrophil or macrophage).
  2. Fusion of the phagosome with a lysosome ⇒ digestion by lysozymes.
  3. Small peptide fragments are loaded onto Major Histocompatibility Complex (MHC) proteins.
  4. MHC–peptide complex is expressed on the plasma membrane.
• Purpose: "Show" B & T cells what pathogen bits look like so they can mount a targeted response.
• Genetic diversity of MHC molecules determines how many different pathogen peptides an individual can present.

Evolutionary Significance of MHC Diversity

• Greater allelic diversity = broader pathogen recognition.
• Olfactory mate-choice hypothesis: Females subconsciously prefer the body odor of males with MHC genes most different from their own (experiment with unwashed T-shirts; preference peaks during ovulation).
  • Evolutionary benefit ➜ offspring inherit a highly diverse set of MHC alleles ⇒ more robust immunity.

Lymphocyte Categories

B Cells

• Differentiate into plasma cells that secrete antibodies.
• Aid in activating certain T-cell subsets.

T Cells (Cell-Mediated Immunity)

• T helper (TH) cells
  • Express CD4 receptor.
  • Orchestrate & regulate immune responses (activate B cells, cytotoxic cells, macrophages).
• Cytotoxic T (TC) cells
  • Express CD8 receptor.
  • Directly kill virus-infected or tumor cells.
  • Described as “aggressive killers.”
• Regulatory T (Treg) cells
  • Also CD4⁺.
  • Dampen immune response, restore homeostasis after pathogen clearance.
• Memory T cells
  • Persist long-term; enable rapid secondary responses.

Note on HIV

• HIV uses the CD4 receptor to enter TH & certain TC cells ➜ hides inside immune cells to avoid detection, causing immunodeficiency.

Antibodies & Humoral Immunity

• Antibodies (immunoglobulins, Ig): Y-shaped soluble proteins released into plasma.
  • Constant regions (green/purple in diagram) are invariant.
  • Variable region (yellow) binds the unique antigenic determinant (epitope) of a pathogen.
• Functions
  • Opsonization: "Flag" pathogens for phagocytosis by macrophages/ neutrophils.
  • Neutralization, complement activation, etc. (not outlined in lecture but implicit).
• Major classes (IgG, IgM, IgA, IgE, IgD) briefly referenced (IgE & IgA examples).

Bacterial vs. Viral Infections (Comparison Table)

• Cellular status: Bacteria = living cells; viruses = non-cellular particles.
• Reproduction: Bacteria divide independently (binary fission); viruses require host cell machinery.
• Treatment: Antibiotics disrupt bacterial cell processes (e.g., cell-wall synthesis); ineffective vs viruses.
• Distribution: Bacterial infections often remain localized; viral infections more systemic.
• Beneficial roles: Commensal/ probiotic bacteria exist; no truly beneficial viruses (except engineered vectors).
• Size: Bacteria ≫ viruses.
• Clinical implication: "True or false: antibiotics cure viral infections" ⇒ False.

Clinical Notes: Lymphedema & Elephantiasis

• Edema = swelling; lymphedema = swelling due to failed lymph drainage (lymph fluid, not blood serum).
• Cause: Blockage of lymphatic vessels; may be infectious.
• Elephantiasis (elephantitis)
  • Etiology: Parasitic roundworm blocking lymphatics (esp. groin).
  • Massive enlargement of legs, scrotum, sometimes arms.
  • Painful, function-limiting.

Parasitic Helminths: Tapeworms

• Transmission: Ingesting meat containing encysted eggs.
• Anatomy
  • Scolex: Head with hooks/ suckers ("grappling hook") that anchors to intestinal mucosa.
  • Proglottids: Repeating hermaphroditic segments; self-fertilize; distal segments slough off as egg packets in feces.
• Lifecycle example (cat tapeworm)
  • Eggs → flea → cat (via grooming or predation) → adult tapeworm in intestine.
• Nutrition: No digestive tract; absorbs nutrients across thin body wall.

Ectoparasite Infestation: Scabies

• Agent: Microscopic mite that burrows in epidermis.
• Pathogenesis: Mite movement + feces deposit proteins ⇒ host mounts localized immune reaction.
• Symptoms: Intense itching, pimple-like red bumps following serpiginous tracks.
• Transmission: Prolonged skin contact, contaminated bedding, tanning beds (real anecdote).

Protozoan Diseases: Sleeping Sickness & Chagas

• Pathogen genus: Trypanosoma (flagellated protozoa).
• African sleeping sickness: Trypanosoma brucei, vector = tsetse fly.
  • Symptoms: Fever, aches, profound fatigue ("sleepy"), CNS invasion can cause confusion & seizures.
  • Untreated ➜ often fatal.
• Chagas disease: Trypanosoma cruzi, endemic to Central/South America.
• Treatment difficulty: U.S. often lacks antiprotozoal drugs for exotic diseases; sometimes better treated in endemic regions.
• Vector mechanism analogous to mosquitoes: fly injects saliva containing protozoa prior to blood meal.

Immune System Disorders

Insufficient Response

• Example: AIDS from HIV ➜ profound immunodeficiency.
  • Death typically from "opportunistic" infections: influenza, Candida, TB, Pseudomonas, etc.

Inappropriate / Autoimmune Response

• Rheumatoid arthritis (RA): T-cell-dominated attack on joints (cell-mediated).
• Systemic lupus erythematosus (SLE): Antibody-mediated attack on multiple tissues (humoral).

Excessive / Misplaced Response (Hypersensitivity)

• Allergies to pollen, peanuts, shellfish, etc.
  • Body perceives harmless proteins as dangerous; launches disproportionate IgE-mediated response.
  • Not self-targeting but "displaced" (environmental antigens).

Study / Exam Guidance Mentioned by Instructor

• Review quizzes after each module: endocrine, heart, circulation, lymphatic/immune.
• Complete the immune system quiz before progressing.
• These four modules comprise Test #2 content.
• Instructor stresses understanding:
  1. Function of lymph nodes & why they swell.
  2. Differences between B cells & T cells (including origin of their names).

Metaphors & Anecdotes Used

• MHC mate selection ↔ choosing partners by “smell” ⇒ genetic advantage for offspring.
• Scolex compared to a Mission-Impossible grappling hook anchoring to intestine.
• "Tapeworm party in your gut" (humorous way to underscore solitary hermaphroditic reproduction).
• Personal story: Student acquaintance contracted scabies from a tanning bed.
• Military veteran suspected to have contracted Trypanosoma abroad – illustrates treatment hurdles when back in U.S.

Practical / Ethical / Real-World Implications

• Importance of genetic diversity for population-level immunity.
• Potential for behavioral cues (odor) in human mate selection and evolutionary fitness.
• Global health inequities: Drug availability differs between endemic regions and developed nations.
• Public health messaging: Clarify antibiotic misuse (ineffective vs. viruses) to curb resistance.
• Vector control (flies, mosquitoes, fleas) vital for preventing parasitic & protozoan diseases.

Key Terms & Quick Definitions

• APC – cell that processes & presents antigens via MHC.
• MHC – cell-surface protein complex displaying peptide fragments.
• CD4 / CD8 – co-receptors defining T-helper vs. cytotoxic T cells.
• Immunoglobulin (Ig) – antibody molecule; subclasses IgG, IgM, IgA, IgE, IgD.
• Lymphedema – lymphatic swelling; can evolve into elephantiasis if due to parasitic worm.
• Scolex / Proglottid – head & segment of a tapeworm.
• Trypanosoma – genus of protozoa causing sleeping sickness & Chagas.
• Hypersensitivity – exaggerated immune response to non-threatening antigen.

Equations & Numbers (None Explicit)

• No explicit quantitative formulas were provided in the lecture; relationships discussed were qualitative.