Innate and Adaptive Defenses: Immunity in Anatomy & Physiology

Innate & Adaptive Defenses

Overview of Immunity

Immunity refers to the body's ability to resist or prevent damage and disease caused by pathogens. The immune system is divided into two major types: innate (non-specific) defenses and adaptive (specific) immunity. These systems work together to protect the body from a wide range of harmful agents.

• Innate Immunity: Present at birth, provides immediate, non-specific defense against pathogens.

• Adaptive Immunity: Develops over time, provides specific responses to particular pathogens and has memory for faster future responses.

Types of Immunity

Innate (Non-Specific) Defenses

Innate defenses are the body's first and second lines of defense, acting quickly and generally against all pathogens. They include mechanical and chemical barriers, as well as cellular responses.

• Surface Barriers:

  • Skin: Multiple layers, continual shedding, difficult for pathogens to penetrate unless damaged.

  • Mucous Membranes: Line the GI, respiratory, urinary, and reproductive tracts; trap pathogens.

• Chemical Barriers:

  • Sebaceous Glands: Sebum contains fatty acids and lactic acid, creating a toxic and acidic environment for bacteria.

  • Lysozyme: Enzyme in perspiration, tears, saliva, and tissue fluids; breaks down bacterial cell walls.

  • Hyaluronic Acid: Found in connective and epithelial tissues; helps protect and repair tissue.

  • Gastric Juice: Contains HCl and enzymes that destroy pathogens.

  • Vaginal Secretions: Acidic pH discourages microbial growth.

  • Other Actions: Urination, vomiting, defecation, and sneezing help expel microbes.

• Internal Defenses:

  • Phagocytes: Neutrophils and macrophages ingest and destroy pathogens.

  • Fever: Elevated body temperature inhibits microbial growth and speeds tissue repair.

  • Natural Killer (NK) Cells: Lymphocytes that kill infected or abnormal cells by inducing apoptosis or cytolysis.

  • Antimicrobial Proteins: Transferrins, interferons, and complement proteins inhibit microbial growth and enhance immune responses.

  • Inflammation: Localized response to tissue damage, characterized by redness, heat, swelling, and pain.

Adaptive (Specific) Immunity

Adaptive immunity is the body's third line of defense, providing targeted responses to specific pathogens and retaining memory for future encounters.

• Humoral Immunity: Mediated by B cells, which produce antibodies that neutralize pathogens in body fluids.

• Cellular Immunity: Mediated by T cells, which directly attack infected or abnormal cells.

Comparison of Innate and Adaptive Immunity

Characteristic	Innate	Adaptive
Specificity	Non-specific	Specific
Presence	Present at birth	Develops over time
Activation	Genetics and maternal immunity	Exposure to microbes
Lines of Defense Utilized	1st: skin/mucous membranes, neutrophils, monocytes 2nd: inflammatory response, fever, antimicrobial proteins, NK cells, basophils, eosinophils	3rd: immune response, lymphocytes (T & B cells)
Memory	No memory	Yes, memory
Response	General/similar to all microbes	Specific to a particular microbe
Response Speed	Fast	Slower than innate
Response Area	Localized	Systemic

Key Terms and Definitions

• Antigen (Ag): Anything foreign (non-self) or perceived as foreign, such as bacteria, viruses, toxins, transplanted or cancer cells. Antigens stimulate the immune response and can generate antibodies.

• Pathogen: A disease-causing antigen.

• Antibody (Ab): A protein produced by plasma cells that binds specifically to its corresponding antigen. Antibodies are also known as immunoglobulins (Igs).

• Resistance: The ability to resist or prevent damage/disease.

• Susceptibility: Vulnerability; less than complete immunity.

Mechanisms of Innate Immunity

Mechanical Barriers

Mechanical barriers physically block the entry of pathogens.

• Epidermis: Multiple layers, continual shedding, difficult for pathogens to penetrate unless damaged.

• Mucous Membranes: Trap pathogens in mucus, found in GI, respiratory, urinary, and reproductive tracts.

Chemical Barriers

Chemical barriers create hostile environments for pathogens.

• Sebum: Contains fatty acids and lactic acid, toxic and acidic to bacteria.

• Lysozyme: Enzyme that breaks down bacterial cell walls.

• Hyaluronic Acid: Protects and repairs tissues.

• Gastric Juice: Destroys pathogens with acid and enzymes.

• Vaginal Secretions: Acidic pH discourages microbial growth.

• Other Actions: Urination, vomiting, defecation, and sneezing expel microbes.

Antimicrobial Proteins

• Transferrins: Bind iron, limiting its availability to microbes and inhibiting their growth.

• Interferons: Produced by infected cells, bind to uninfected cells and inhibit viral replication.

• Complement Proteins: Group of 20+ proteins that enhance immune functions such as inflammation, chemotaxis, opsonization, and cytolysis.

Processes Enhanced by Complement Proteins

• Inflammation: Increased blood flow and permeability at injury site.

• Chemotaxis: Migration of WBCs toward chemical signals.

• Opsonization: Coating pathogens to enhance phagocytosis.

• Cytolysis: Bursting of pathogens by creating pores in their membranes.

Natural Killer (NK) Cells

NK cells are lymphocytes that provide rapid responses to infected or abnormal cells. They do not require antigen-specific recognition and are part of innate immunity.

• Found in spleen, lymph nodes, red bone marrow, and blood.

• Kill by inducing apoptosis (programmed cell death) or cytolysis (rupture of cell membrane).

Phagocytosis

Major Types of Phagocytes

• Neutrophils: Most common phagocyte, first responders to infection.

• Macrophages (Monocytes): Can be wandering (circulate in blood) or fixed (reside in tissues such as skin, lungs, liver, CNS, spleen, lymph nodes).

Mechanisms (Steps) of Phagocytosis

1. Chemotaxis: WBCs migrate toward chemical signals at the site of invasion or injury.

2. Adherence: Phagocyte attaches to the surface of the antigen, often aided by opsonization.

3. Ingestion: Phagocyte extends pseudopods to surround and enclose the microbe, forming a phagosome.

4. Digestion: Phagosome merges with lysosomes to form a phagolysosome, where enzymes degrade the microbe.

5. Killing: Microbe is destroyed, usually within 10-30 minutes.

Inflammation

Inflammation is a localized response to tissue damage caused by infection or injury. It is characterized by four cardinal signs: redness, heat, swelling, and pain.

• Functions: Dispose of microbes and toxins, prevent spread, and prepare site for tissue repair.

• Stages:

  1. Vasodilation and increased blood flow.

  2. Increased permeability of capillaries, allowing WBCs and proteins to enter tissue.

  3. Phagocytic emigration and tissue repair.

• Histamine: Released by mast cells, basophils, and platelets; causes vasodilation and increased permeability.

Fever

Fever is an elevated body temperature, often in response to infection or inflammation. The hypothalamus resets the body's temperature set point.

• Causes: Infection, inflammation, disease, toxins.

• Effects: Increases effects of interferons, inhibits microbial growth, speeds tissue repair.

• Types: Low-grade, intermediate, high-grade, pyrexia, persistent, sudden onset, constant, chronic, intermittent.

Adaptive (Specific) Immunity

Formation and Maturation of B-cells and T-cells

• T-cells: Formed in red bone marrow (RBM), mature in thymus, become immunocompetent, express CD4 and CD8 surface proteins.

• B-cells: Formed and mature in RBM, differentiate into plasma cells (secrete antibodies) and memory B-cells.

Primary and Secondary Immune Response

• Primary Response: First exposure to antigen, slower and produces low-affinity antibodies.

• Secondary Response: Subsequent exposures, faster and produces high-affinity antibodies due to memory cells.

Types of Adaptive Immune Responses

Cell-Mediated Immunity (CMI)

Directed by T-cells, especially cytotoxic (CD8) and helper (CD4) T-cells. Effective against intracellular pathogens, cancer cells, and transplanted tissues.

• Mechanisms:

  • Antigen recognition and T-cell activation (requires two signals).

  • Proliferation and differentiation into helper, cytotoxic, and memory T-cells.

  • Killing by apoptosis (injecting toxins) or cytolysis (releasing perforin).

Antibody-Mediated Immunity (AMI)

Directed by B-cells, assisted by helper T-cells. Effective against extracellular pathogens and non-cellular antigens (toxins, venoms, allergens).

• Mechanisms:

  • B-cells differentiate into plasma cells (secrete antibodies) and memory B-cells.

  • Antibodies form complexes with antigens, neutralize toxins, immobilize pathogens, activate complement, attract phagocytes, and cause agglutination.

Passive vs. Active Immunity

• Passive Immunity: Receiving antibodies from another source (e.g., maternal antibodies, immune serum).

• Active Immunity: Producing antibodies in response to infection or vaccination.

Major Pathogens and Diseases

Pathogens are biological agents that cause disease by disrupting body processes. Common types include bacteria, viruses, fungi, and protozoa. Infectious diseases are a leading cause of death worldwide.

• Bacteria: Unicellular organisms, can be harmful or beneficial.

• Viruses: Require host cells for replication.

• Fungi: Decompose and absorb organic material, affect skin and internal organs.

• Protozoa: Unicellular animals, often parasitic.

Summary Table: Lines of Defense

Line of Defense	Components	Type
1st Line	Skin, mucous membranes, neutrophils, macrophages	Non-specific (innate)
2nd Line	Inflammatory response, fever, antimicrobial proteins, NK cells, basophils, eosinophils	Non-specific (innate)
3rd Line	T-cells, B-cells	Specific (adaptive)

Key Equations and Concepts

• Antigen-Antibody Complex Formation:

$\text{Ab} + \text{Ag} = \text{Ab-Ag Complex}$

• Complement Activation: Cascade of protein activation leading to enhanced immune responses.

Additional info: Some details have been expanded for clarity and completeness, including mechanisms of phagocytosis, fever types, and immune cell maturation.