Innate & Adaptive Immunity – Lecture Review

A comprehensive set of Q&A flashcards covering innate defenses, complement, cytokines, inflammation, fever, adaptive immunity principles, antibody generation and function, B and T cell biology, MHC class I & II distinctions, and clinical implications such as vaccination and passive immunity.

What percentage of plasma normally remains in tissue fluid and is collected by lymphatic vessels?

Roughly 15% of the plasma that leaks out of blood capillaries is not re-absorbed and becomes lymph.

Why is the loss of 15 % plasma at capillaries actually beneficial?

It allows lymphatic vessels to ‘sample’ plasma; lymph passes through lymph nodes where immune cells screen it for pathogens.

Which structures are the body’s primary ‘first line of defense’?

Physical and chemical barriers such as skin, mucous membranes, low skin pH, normal microbiota competition, mucus, lysozyme, defensins, and harsh organ environments (e.g., stomach acid).

How do defensins kill microbes?

They are antimicrobial peptides that insert into pathogen membranes, forming pores that disrupt ionic and water balance, leading to cell death.

What do the acronyms PRR, TLR, and PAMP stand for?

Pattern Recognition Receptor; Toll-Like Receptor (a type of PRR); Pathogen-Associated Molecular Pattern.

Role of Toll-Like Receptors (TLRs) on phagocytes

Bind PAMPs, trigger intracellular signaling that activates phagocytosis, defensin production, cytokine release, NK-cell activation, and complement cascade.

Complement protein C3b main function

Coats (opsonizes) pathogen surfaces to enhance phagocytosis and helps form the membrane-attack complex (MAC).

Complement protein C3a main function

Acts as an anaphylatoxin that promotes inflammation and recruits additional phagocytes.

What is the Membrane-Attack Complex (MAC)?

A ring of complement proteins that insert into pathogen membranes, creating large pores that lyse the cell.

Define cytokine.

A small signaling protein released by cells that influences the behavior of nearby (paracrine) or distant (endocrine) cells during immune responses.

Specific cytokine class released by virus-infected cells to warn neighbors

Interferons – they induce antiviral states, promote apoptosis of infected cells, and activate immune cells.

Which three beneficial effects does moderate fever provide?

1) Speeds phagocytosis and lymphocyte production, 2) accelerates metabolic and tissue-repair rates, 3) inhibits temperature-sensitive pathogens.

What molecules trigger fever and what is their target?

Pyrogens (a subtype of cytokines) act on the hypothalamus to raise the body’s temperature set-point.

Four hallmark properties of adaptive immunity

Specificity, ability to distinguish self from non-self, enormous diversity, and immunological memory.

Main cellular players of humoral and cell-mediated immunity

Humoral: B lymphocytes (and plasma cells); Cell-mediated: T lymphocytes (especially cytotoxic T cells).

What did the classic ‘guinea-pig’ diphtheria experiment demonstrate?

Protective factors in serum (later identified as antibodies) are produced after exposure and are strain-specific; transferring immune serum confers passive immunity.

Differentiate natural vs. artificial active immunity with an example each.

Natural active: antibodies made after natural infection (e.g., catching measles). Artificial active: antibodies made after vaccination with killed/attenuated pathogen.

Define passive immunity and give two natural/passive examples.

Receiving pre-made antibodies instead of making your own. Natural passive examples: maternal IgG crossing placenta and IgA in breast milk.

Where do T cells mature and what two tests must they pass there?

In the thymus: 1) Positive selection in cortex (must bind non-self antigen), 2) Negative selection in medulla (must NOT bind self-antigen).

Approximate percentage of developing T cells that survive thymic selection

Only about 2% pass both positive and negative selection.

How does the immune system generate >10 million different antigen receptors with only ~30,000 genes?

Somatic (V-D-J) recombination and alternative RNA splicing shuffle gene segments to create vast antibody/T-cell receptor diversity.

Why does a single naïve B cell display only one antigen specificity?

After somatic recombination each B cell rearranges one unique light and heavy chain gene set; allelic exclusion prevents additional rearrangements.

Structure of an antibody (immunoglobulin)

Y-shaped molecule of two identical heavy chains and two identical light chains; variable regions at tips form two antigen-binding sites, rest is constant region.

What is clonal selection?

Process whereby an antigen specifically binds a B or T cell receptor, triggering that clone to proliferate and differentiate into effector and memory cells.

Define plasma cell.

An effector B cell with extensive rough ER that secretes large quantities of soluble antibodies.

Purpose of memory B and T cells

Long-lived cells that persist after primary response; on re-exposure they mount a faster, stronger secondary immune response.

Compare primary vs. secondary antibody responses in timing.

Primary response peaks ~10–14 days post-exposure; secondary response is quicker (1–3 days) and produces much higher antibody titers.

How do antibodies promote pathogen clearance? (three mechanisms)

1) Neutralization/agglutination of antigens, 2) opsonization to enhance phagocytosis, 3) activation of complement cascade (classical pathway).

Key difference between B-cell receptors and T-cell receptors (TCRs)

BCRs (antibodies) can bind free antigens; TCRs recognize antigen only when presented on Major Histocompatibility Complex (MHC) molecules.

Which MHC class is on all nucleated cells and which T cell do they activate?

MHC-I is on all nucleated cells and activates cytotoxic (CD8⁺) T cells.

Which cells display MHC-II and which T cell do they activate?

Professional antigen-presenting cells (dendritic cells, macrophages, B cells) display MHC-II; they activate helper (CD4⁺) T cells.

Role of helper T cells (CD4⁺) in immunity

Upon recognizing antigen-MHC-II, they secrete cytokines that stimulate B-cell antibody production, activate cytotoxic T cells, and orchestrate overall adaptive response.

Role of cytotoxic T cells (CD8⁺)

Bind antigen-MHC-I on infected or cancerous cells and induce cell death via perforin and granzymes, or Fas-FasL apoptotic signaling.

Why do cytotoxic T cells respond rapidly to virus-infected epithelial cells?

Infected non-immune cells present viral peptides on MHC-I, which specifically engages CD8⁺ cytotoxic T cells for immediate killing.

Define ‘cell-mediated immunity’.

Branch of adaptive immunity in which T lymphocytes directly attack infected, foreign, or altered self cells; requires cell-to-cell contact.

What is an antigen-presenting cell (APC)?

Cell that processes an antigen and displays peptide fragments bound to MHC for recognition by T cells; includes dendritic cells, macrophages, and B cells.

How does histamine released by mast cells contribute to inflammation?

Histamine causes vasodilation and increased vascular permeability, bringing more leukocytes and plasma proteins to the infection site.

What components give pus its whitish appearance?

Accumulated dead leukocytes (especially neutrophils), dead tissue cells, and fluid exudate at the inflammatory site.

What is the classical sign that complement, antibodies, and phagocytes have clustered pathogens together?

Agglutination – visible clumping of antigens/pathogens, facilitating efficient phagocytosis.

Explain how interferon protects neighboring uninfected cells.

It induces them to degrade RNA and reduce protein synthesis, limiting resources for future viral replication.

Give one clinical application of artificial passive immunity.

Injection of antivenom serum after a snake bite; the antiserum supplies immediate antibodies against the venom.

Purpose of vaccinations according to adaptive immunity principles

To induce a harmless primary exposure that generates memory B and T cells so that any future real infection elicits a rapid, protective secondary response.