Immunology Lecture 2

Innate (natural) immunity and Adaptive (acquired) immunity.

What are the two broad divisions of the immune system?

Innate is non-specific with no memory; adaptive is antigen-specific with memory.

How does innate immunity differ from adaptive immunity in specificity and memory?

Normal microbiota and anatomical barriers (skin, mucous membranes, cilia).

What components comprise external defenses of innate immunity?

Low pH, lysozyme, fatty acids in sebum.

Name physiologic barriers that contribute to external defense.

Inflammation, phagocytic/endocytic cells, natural killer (NK) cells, and antigen-presenting cells linking to adaptive immunity.

What are the internal defense mechanisms of innate immunity?

Pathogen-Associated Molecular Patterns (PAMPs).

What do Pattern Recognition Receptors (PRRs) recognize?

External and Internal.

What are the two protection mechanisms of innate immunity?

First line = External barriers; second line = Internal defenses such as inflammation and phagocytosis.

What is the difference between first line and second line of defense?

Outcompete pathogens for nutrients and attachment sites; prevent colonization.

How do normal microbiota protect against pathogens?

Skin, mucous membranes, and cilia.

What are examples of external physical barriers?

Low pH in stomach, lysozyme in tears, fatty acids in sebum.

Name physiologic barriers that protect the body externally.

Mucus traps microbes; cilia move them out of the respiratory tract.

What is the function of the mucociliary escalator?

Lysozyme, IgA, IgG, antimicrobial peptides.

What substances are secreted at epithelial surfaces to defend against microbes?

Lysozyme and immunoglobulins (IgA/IgG).

What protective components are found in tears and other secretions?

Low pH and enzymes inhibit or kill ingested microbes.

What is the antimicrobial role of gastric juice?

Disruption can lead to yeast infections due to loss of normal flora.

What effect can antibiotic treatment have on normal flora?

A non-specific protective response to tissue damage.

How is inflammation defined?

Rubor (redness), Tumor (swelling), Calore (heat), Dolor (pain).

What are the four classic signs of inflammation?

Acute: neutrophils; Chronic: macrophages and lymphocytes.

Which cells dominate acute vs chronic inflammation?

Increased blood flow (vasodilation), increased vascular permeability, influx of phagocytes.

List the main steps in the inflammatory sequence.

Serum proteins produced by the liver that rise rapidly during inflammation.

What are acute phase reactants?

C-reactive protein (CRP) – opsonization and activation of complement.

Name a major acute-phase reactant and its role.

Rises 6-10 hours; peaks around 24-72 hours; declines quickly.

Describe the typical time course of CRP after stimulus.

A cascade of about 25 serum proteins activated to promote lysis, opsonization, and chemotaxis.

What is the complement system?

Direct cytolysis of pathogens, opsonization, and recruitment/chemotaxis of phagocytes.

What are the primary functions of the complement system?

Opsonization via C3b and IgG enables phagocyte receptors to recognize targets.

How do complement and antibodies enhance phagocytosis?

Secreted proteins that act as signaling molecules to regulate inflammation and immune cell activity.

What are cytokines?

Promote inflammation, activate NK cells and macrophages, and mediate antiviral responses (IFNs).

What are some key roles of cytokines in inflammation?

Many cells, including macrophages, T cells, B cells, dendritic cells, and endothelial cells.

Who can produce cytokines?

Chemokines are cytokines that mediate chemotaxis, directing immune cells to infection sites.

What are chemokines and their function?

Migration of immune cells toward chemical attractants.

What is chemotaxis?

Migration of leukocytes across endothelium into tissue.

What is diapedesis?

Serum molecules that coat pathogens to enhance phagocytosis.

What are opsonins?

C3b and IgG.

Name two major opsonins for phagocytes.

Neutrophils, macrophages, dendritic cells, and monocytes.

Which cells perform phagocytosis in innate immunity?

A vesicle containing ingested microbes formed during phagocytosis.

What is a phagosome?

A phagosome fused with a lysosome where digestion occurs.

What is a phagolysosome?

Reactive oxygen species (e.g., H2O2), nitric oxide, and lysozyme.

What substances do phagocytes use to kill ingested microbes?

Lysis of virally infected and tumor cells; provides early defense and activates other responses.

What is the role of natural killer (NK) cells in innate defense?

First line: mechanical/chemical barriers; Second line: inflammation and phagocytosis; Third line: specific immune responses (per the lecture).

What are the three lines of defense described in this material?

Trap pathogens in mucus and move them away via the mucociliary escalator.

What is the function of mucus and cilia on mucous membranes?

Found in tears, saliva, and mucus; hydrolyzes bacterial cell walls.

Where is lysozyme commonly found and what is its role?

Serum amyloid A, fibrinogen, haptoglobin, ceruloplasmin, complement C3, mannose-binding protein, alpha-1 antitrypsin.

Name some acute-phase proteins besides CRP.

Opsonizes pathogens and activates complement.

What does CRP do in the immune response?

Interleukin-6 (IL-6).

Which cytokine stimulates the liver to produce acute-phase proteins?

Prevent viral infections and activate NK cells and macrophages.

What are the roles of interferons?

Phagocytosis, antigen presentation, and cytokine production to stimulate adaptive immunity.

What is the role of macrophages in inflammation?

Activate T cells and link innate immunity to adaptive immunity.

What is the purpose of antigen presentation by dendritic cells and macrophages?

Antigen fragments may be presented to T cells by antigen-presenting cells; residual material may be expelled.

What happens to digested material after phagocytosis?

Cytokines and other mediators raise the hypothalamic set-point, causing fever.

What mediators are involved in fever during inflammation?