The Immune System: Innate and Adaptive Body Defenses

The Immune System: Innate and Adaptive Body Defenses

Overview of Immunity

The immune system protects the body from disease by recognizing and eliminating pathogens. It is divided into two main branches: the innate (nonspecific) defense system and the adaptive (specific) defense system. These systems work together to provide comprehensive protection.

• Innate defenses: Provide immediate, general protection against pathogens.

• Adaptive defenses: Target specific pathogens and provide long-lasting immunity.

Innate (Nonspecific) Defense System

Surface Barriers

Surface barriers are the body's first line of defense, preventing the entry of pathogens through physical and chemical means.

• Skin: Acts as a mechanical barrier to block pathogen entry.

• Mucous membranes: Trap and eliminate microbes; secrete mucus, acids, and enzymes like lysozyme to inhibit pathogen growth.

Internal Defenses

If pathogens breach surface barriers, internal defenses are activated. These include cellular and chemical mechanisms.

• Phagocytes: Engulf and destroy pathogens. Main types are macrophages (develop from monocytes) and neutrophils (become phagocytic upon infection).

• Natural Killer (NK) cells: Attack cells lacking "self" markers, induce apoptosis in infected or cancerous cells, and secrete chemicals to enhance inflammation.

• Inflammation: Local response to injury or infection, characterized by redness, heat, swelling, and pain.

• Antimicrobial proteins: Interferons and complement proteins that attack microbes or hinder their reproduction.

• Fever: Systemic response that increases body temperature to inhibit pathogen growth and speed up tissue repair.

Antimicrobial Proteins

These proteins play a crucial role in defending against pathogens by interfering with their replication or marking them for destruction.

• Interferons: Released by virus-infected cells to warn neighboring cells and stimulate production of antiviral proteins.

• Complement proteins: A group of about 20 plasma proteins that, when activated, enhance inflammation, promote phagocytosis (opsonization), and cause cell lysis by forming membrane attack complexes (MAC).

Inflammation

Inflammation is triggered by tissue injury or infection and serves to contain damage, remove pathogens, and initiate repair.

• Cardinal signs: Redness, heat, swelling, pain.

• Mechanisms: Release of inflammatory mediators (histamine, cytokines, kinins, prostaglandins, leukotrienes, complement) leads to vasodilation and increased vascular permeability.

Fever

Fever is a systemic response to infection, mediated by pyrogens released from leukocytes and macrophages. Pyrogens reset the hypothalamic thermostat, raising body temperature.

• Benefits: Sequesters iron and zinc (needed by microbes), increases metabolic rate, and accelerates tissue repair.

• Risks: High fever can denature proteins and be life-threatening.

Adaptive (Specific) Defense System

General Properties

The adaptive immune system is characterized by specificity, systemic action, and memory. It consists of two main arms: humoral (antibody-mediated) and cellular (cell-mediated) immunity.

• Specificity: Targets particular antigens.

• Memory: Mounts stronger responses upon re-exposure to the same antigen.

Cells of the Adaptive Immune System

Lymphocytes are the main cells of adaptive immunity. They originate in the red bone marrow and become immunocompetent in primary lymphoid organs (B cells in bone marrow, T cells in thymus).

• B cells: Responsible for humoral immunity; produce antibodies.

• T cells: Responsible for cellular immunity; directly attack infected cells or coordinate immune responses.

• Antigen-presenting cells (APCs): Dendritic cells, macrophages, and B cells that present antigens to T cells.

Development of Self-Tolerance

T cells undergo positive and negative selection in the thymus to ensure they recognize self-MHC but do not react strongly to self-antigens, preventing autoimmunity.

• Positive selection: T cells must recognize self-MHC to survive.

• Negative selection: T cells that bind strongly to self-antigens are eliminated.

Humoral Immunity (Antibody-Mediated)

Mechanism of Humoral Response

Humoral immunity is mediated by B cells, which produce antibodies that circulate in body fluids and target extracellular pathogens.

• Antigen challenge: First encounter between a naive B cell and its specific antigen, usually in lymphoid tissue.

• Clonal selection: Activated B cell proliferates into plasma cells (antibody-secreting) and memory B cells.

• Primary response: Initial antibody production is slow and limited.

• Secondary response: Memory B cells enable a faster, stronger response upon re-exposure to the same antigen.

Types of Humoral Immunity

Type	How Acquired	Example
Active, Naturally Acquired	Infection; contact with pathogen	Chickenpox
Active, Artificially Acquired	Vaccine (dead or attenuated pathogens)	Flu shot
Passive, Naturally Acquired	Antibodies pass from mother to fetus via placenta or to infant in milk	Maternal IgG
Passive, Artificially Acquired	Injection of immune serum (gamma globulin)	Rabies immunoglobulin

Antibodies (Immunoglobulins)

Antibodies are proteins produced by plasma cells that specifically bind antigens. Each antibody consists of two heavy and two light chains, with variable regions forming antigen-binding sites.

• Classes: IgM, IgA, IgD, IgG, IgE—each with distinct roles and properties.

Classes of Antibodies

Class	Structure	Main Function
IgM	Pentamer	First antibody released; potent agglutinating agent; activates complement
IgA	Monomer/dimer	In mucus and secretions; prevents pathogen entry
IgD	Monomer	B cell receptor
IgG	Monomer	Main antibody in plasma; crosses placenta; secondary response
IgE	Monomer	Active in allergies and parasitic infections; triggers histamine release

Actions of Antibodies

Antibodies inactivate and tag antigens for destruction by forming antigen-antibody complexes. Main mechanisms include:

• Neutralization: Block pathogen binding sites.

• Agglutination: Clump cell-bound antigens.

• Precipitation: Clump soluble antigens.

• Complement fixation: Trigger complement cascade leading to cell lysis.

Cellular Immunity (Cell-Mediated)

Antigen-Presenting Cells (APCs)

APCs engulf antigens and present fragments on their surface to T cells. Major types include dendritic cells, macrophages, and B cells.

T Cells and Their Functions

• CD4 cells: Become helper T cells (TH) or regulatory T cells (TREG).

• CD8 cells: Become cytotoxic T cells (TC) that kill infected or abnormal cells.

• Memory T cells: Provide rapid response upon re-exposure to antigen.

T Cell Activation

T cells are activated when their receptors bind to antigen-MHC complexes on APCs. CD4 cells recognize antigens on class II MHC, while CD8 cells recognize antigens on class I MHC.

Actions of Helper T Cells

Helper T cells coordinate the immune response by activating B cells, other T cells, and macrophages. Without them, the adaptive immune response is severely impaired.

Actions of Cytotoxic T Cells

Cytotoxic T cells directly attack and kill infected or abnormal cells by releasing perforin and granzymes, which induce apoptosis in the target cell.

Actions of Regulatory T Cells

Regulatory T cells suppress immune responses to prevent autoimmunity and maintain tolerance to self-antigens.

Clinical Aspects and Homeostatic Imbalances

Organ Transplants and Rejection

• Types: Autografts, isografts, allografts, xenografts.

• Prevention: Immunosuppressive therapy is required to prevent rejection but increases risk of infection and other side effects.

Immunodeficiencies

Conditions where immune function is impaired. Example: Acquired Immune Deficiency Syndrome (AIDS), caused by HIV, which destroys helper T cells and cripples adaptive immunity.

Autoimmune Diseases

Immune system attacks self-tissues due to loss of self-tolerance. Examples include multiple sclerosis, type I diabetes mellitus, and rheumatoid arthritis.

Hypersensitivities (Allergies)

Exaggerated immune responses to harmless antigens (allergens). Acute (type I) hypersensitivities can cause anaphylactic shock, which is life-threatening.

Additional info: This guide covers the essential concepts of the immune system as outlined in Chapter 21, including both innate and adaptive defenses, the cells and molecules involved, and clinical implications of immune dysfunction.