Back17 Adaptive Immunity: Specific Defenses of the Host
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Adaptive Immunity: Specific Defenses of the Host
Introduction to Adaptive Immunity
Adaptive immunity is a specialized defense mechanism that targets specific pathogens. Unlike innate immunity, which provides general protection, adaptive immunity develops after exposure to antigens through infection or vaccination. It is characterized by specificity and memory, allowing for a more rapid and effective response upon subsequent exposures to the same pathogen.
Primary response: The initial adaptive immune reaction to a new antigen.
Secondary response: A faster, stronger reaction upon re-exposure to the same antigen, due to immunological memory.
Comparison of Adaptive and Innate Immunity
Innate immunity: Non-specific, immediate defense present from birth (e.g., skin, phagocytes).
Adaptive immunity: Specific, acquired defense that develops after exposure to antigens; involves lymphocytes (B and T cells) and antibodies.
Dual Nature of the Adaptive Immune System
The adaptive immune system consists of two main components: humoral and cellular immunity. Both systems interact and contribute to overall host defense.
Humoral immunity: Mediated by B cells and the antibodies they produce. Effective against extracellular pathogens (e.g., bacteria, toxins, viruses before cell entry).
Cellular immunity (cell-mediated immunity): Mediated by T cells, which recognize and destroy infected or abnormal cells. Effective against intracellular pathogens (e.g., viruses, some bacteria).
B Cells and Humoral Immunity
B cells are lymphocytes that mature in the bone marrow (in birds, the bursa of Fabricius).
They recognize antigens and produce antibodies.
T Cells and Cellular Immunity
T cells mature in the thymus and are found in blood and lymphoid organs after maturation.
T cells have T cell receptors (TCRs) that recognize antigenic peptides presented by antigen-presenting cells (APCs).
Upon activation, T cells secrete cytokines to direct immune responses.
Cytokines: Chemical Messengers of Immune Cells
Cytokines are signaling proteins that mediate and regulate immunity, inflammation, and hematopoiesis. Overproduction can lead to a cytokine storm, causing tissue damage.
Interleukins (ILs): Communication between leukocytes.
Chemokines: Induce migration of leukocytes to infection sites.
Interferons (IFNs): Interfere with viral replication.
Tumor necrosis factor alpha (TNF-α): Involved in inflammation.
Hematopoietic cytokines: Control development of blood cells.
Antigens and Antibodies
Antigens are substances that provoke an immune response, typically by stimulating the production of antibodies. Antibodies interact with specific regions on antigens called epitopes. Haptens are small molecules that become antigenic only when attached to larger carrier molecules.
Epitope: The specific part of an antigen recognized by an antibody.
Hapten: A small molecule that is not immunogenic by itself but can elicit an immune response when attached to a carrier.
Structure and Classes of Antibodies (Immunoglobulins)
Antibodies are Y-shaped proteins composed of two heavy and two light chains, with variable regions that bind antigens and a constant region that determines the antibody class. Each antibody has at least two antigen-binding sites (valence).
Variable (V) region: Binds to the epitope of the antigen.
Constant (Fc) region: Determines the class and effector function of the antibody.
Five classes of immunoglobulins: IgG, IgM, IgA, IgD, IgE.
Summary Table: Immunoglobulin Classes
Class | Structure | Serum % | Main Functions |
|---|---|---|---|
IgG | Monomer | 80% | Crosses placenta, protects fetus, triggers complement, enhances phagocytosis, neutralizes toxins/viruses |
IgM | Pentamer | 6% | First antibody produced, causes agglutination, activates complement |
IgA | Monomer/dimer | 13% | Protects mucosal surfaces, found in secretions (saliva, tears, breast milk) |
IgD | Monomer | 0.02% | On B cells, assists in immune response |
IgE | Monomer | 0.002% | Involved in allergic reactions, defense against parasitic worms |
Humoral Immune Response Process
B cells are activated to produce antibodies through antigen recognition and interaction with T helper cells (for T-dependent antigens) or directly (for T-independent antigens). Activated B cells differentiate into plasma cells (which secrete antibodies) and memory cells (which provide long-term immunity).
Major histocompatibility complex (MHC): Glycoproteins on cell surfaces that present antigen fragments to T cells.
Class I MHC: Present on all nucleated cells; identify as "self".
Class II MHC: Present on antigen-presenting cells (APCs) such as B cells, macrophages, and dendritic cells.
Clonal Selection and Expansion
Activated B cells undergo clonal expansion, differentiating into plasma cells and memory cells.
Clonal deletion removes self-reactive B cells via apoptosis, preventing autoimmunity.
T-Dependent vs. T-Independent Antigens
T-dependent antigens: Require help from T helper cells to activate B cells; generate strong, long-lasting immunity with memory cell formation.
T-independent antigens: Activate B cells without T cell help; usually polysaccharides; provoke a weaker response, mainly IgM, and do not generate memory cells.
Results of Antigen-Antibody Interaction
When antibodies bind to antigens, they form antigen-antibody complexes that protect the host by tagging foreign molecules for destruction. Key mechanisms include:
Agglutination: Clumping of antigens, enhancing phagocytosis.
Opsonization: Coating of antigens to enhance phagocytosis.
Neutralization: Blocking of pathogen attachment or toxin activity.
Antibody-dependent cell-mediated cytotoxicity (ADCC): Target cell lysis by immune cells.
Activation of the complement system: Leads to cell lysis.
Cellular Immunity Response Process
Cellular immunity is mediated by T cells, which combat intracellular pathogens and abnormal cells. T cells mature in the thymus, undergo selection, and migrate to lymphoid tissues. They recognize antigens presented by MHC molecules on APCs.
CD4+ T cells (T helper cells): Activate other immune cells via cytokine secretion; recognize antigens presented by MHC II.
CD8+ T cells (Cytotoxic T lymphocytes, CTLs): Kill infected or abnormal cells; recognize antigens presented by MHC I.
T regulatory cells (Treg): Suppress immune responses to maintain self-tolerance and prevent autoimmunity.
Antigen-Presenting Cells (APCs)
Dendritic cells: Engulf and present antigens to T cells; found in skin and lymphoid tissues.
Macrophages: Present antigens after activation; migrate to lymph tissues.
B cells: Can also act as APCs.
Effector Functions of T Cells
TH1 cells: Activate macrophages and CTLs, promote phagocytosis.
TH2 cells: Stimulate B cells to produce IgE, activate eosinophils.
TH17 cells: Recruit neutrophils, stimulate antimicrobial protein production.
CTLs: Induce apoptosis in infected or abnormal cells by releasing perforin and granzymes.
Nonspecific Cells and Extracellular Killing
Natural killer (NK) cells: Destroy cells lacking MHC I self-antigens, including virus-infected and tumor cells. They can induce apoptosis or lysis without prior sensitization.
Antibody-dependent cell-mediated cytotoxicity (ADCC): Immune cells recognize and kill antibody-coated target cells, important for defense against large parasites.
Immunological Memory
Immunological memory allows the adaptive immune system to respond more rapidly and effectively to previously encountered antigens. The primary response is slower and less robust, while the secondary (anamnestic) response is faster, stronger, and longer-lasting due to the presence of memory cells.
Antibody titer: The concentration of antibodies in the serum, reflecting the intensity of the humoral response.
Types of Adaptive Immunity
Adaptive immunity can be acquired naturally or artificially, and can be active or passive:
Type | How Acquired | Example |
|---|---|---|
Naturally acquired active | Infection | Recovery from measles |
Naturally acquired passive | Maternal antibodies | Antibodies via placenta or breast milk |
Artificially acquired active | Vaccination | MMR vaccine |
Artificially acquired passive | Injection of antibodies | Gamma globulin injection |
