Adaptive- Humoral1
Adaptive Defenses
Adaptive Immune (Specific Defense) System
Functions:
Protects against infectious agents and abnormal body cells
Amplifies inflammatory response
Activates complement system
Must be primed by initial exposure to specific foreign substances (priming takes time)
Characteristics:
Specific: Recognizes and targets specific antigens
Systemic: Not restricted to original site of infection
Memory: Produces stronger attacks to previously encountered antigens
Two separate, overlapping arms:
Humoral Immunity: Antibody mediated
Cellular Immunity: Cell mediated
Adaptive Immunity – Two Overlapping Arms
Humoral Immunity (Antibody-Mediated):
Involves:
B lymphocytes (B cells) producing antibodies
Antibodies circulate freely in bodily fluids
Functions:
Bind temporarily to target cells to inactivate them
Mark target cells for destruction by phagocytes or complement
Focus: Extracellular targets
Cell-Mediated Immunity:
Involves:
T lymphocytes (T cells) acting against target cells
Functions:
Directly kill infected cells
Indirectly enhance the inflammatory response via chemical release
Focus: Cellular targets including virus-infected cells, cancer cells, foreign grafts
“Non-Self” Antigens
Definition:
Non-self antigens are substances that mobilize adaptive defenses and provoke an immune response.
Characteristics:
Generally large, complex molecules not normally found in the body (non-self)
Examples: Foreign proteins, polysaccharides, lipids, nucleic acids
Immunogenicity:
Ability to stimulate proliferation of specific lymphocytes
Reactivity:
Ability to react with activated lymphocytes and antibodies released during immunogenic reactions
Antigenic Determinants
Definition:
Only certain parts of an entire antigen, known as antigenic determinants, are immunogenic.
Functions:
Antibodies and lymphocyte receptors bind to these determinants.
Most naturally occurring antigens have numerous antigenic determinants, which:
Mobilize several different lymphocyte populations
Form various kinds of antibodies against them
Self-Antigens: MHC Proteins
Definition:
Proteins on the surface of cells that are not antigenic to self but can provoke an immune response in others, especially in transfusions or grafts.
Example: MHC Glycoproteins
Functions:
Coded by genes in the Major Histocompatibility Complex (MHC), unique to each individual
Include a groove that holds self- or foreign antigens
T lymphocytes can only recognize antigens presented on MHC proteins
Cells of the Adaptive Immune System
Types of Cells:
B Lymphocytes (B cells):
Responsible for humoral immunity
T Lymphocytes (T cells):
Responsible for cellular immunity
Antigen-Presenting Cells (APCs):
Do not respond to specific antigens but play essential auxiliary roles in immunity
Lymphocyte Development, Maturation, and Activation
Five General Steps:
Origin: All lymphocytes originate in red bone marrow
Maturation:
B cells mature in the bone marrow
T cells mature in the thymus
Seeding Secondary Lymphoid Organs and Circulation:
Immunocompetent but naive lymphocytes leave primary organs to seed secondary organs (e.g., lymph nodes, spleen)
Antigen Encounter and Activation:
Activation occurs when antigen receptors bind to antigens
Proliferation and Differentiation:
Activated lymphocytes proliferate and differentiate into effector and memory cells
Maturation of B and T Cells
Education Process:
B cells mature in the bone marrow; T cells in the thymus
Immunocompetence:
Lymphocytes recognize one specific non-self antigen by binding to it
Unique Antigen Receptors:
B or T cells display only one unique type of antigen receptor at maturity
Self-Tolerance:
Lymphocytes are unresponsive to self-antigens and should not bind to them
T Cell Education in the Thymus: Positive and Negative Selection
Positive Selection:
T cells must recognize self-major histocompatibility proteins (self-MHC)
T cells failing to recognize self-MHC undergo apoptosis
Negative Selection:
T cells must not recognize and bind to self-antigens
Self-antigen recognition leads to apoptosis, eliminating self-reactive T cells to prevent autoimmune diseases
Seeding Secondary Lymphoid Organs, Antigen Encounter & Proliferation
Definition of “Naive” Cells:
Immunocompetent B and T cells that have not yet been exposed to foreign antigens
These cells are exported from primary lymphoid organs to increase chances of encountering antigens in secondary lymphoid organs
Clonal Selection:
The first encounter of a naive lymphocyte with its specific antigen selects it for further development
Proliferation:
Activated lymphocytes multiply, forming effector cells that fight infections
A few remain as memory cells, ready for future responses
Overview of B and T Lymphocytes
B Lymphocytes
Type of Immune Response: Humoral
Antibody Secretion: Yes
Primary Targets: Extracellular pathogens (e.g., bacteria, fungi, parasites, some viruses in extracellular fluid)
Site of Origin: Red bone marrow
Site of Maturation: Red bone marrow
Effector Cells: Plasma cells
Memory Cell Formation: Yes
T Lymphocytes
Type of Immune Response: Cellular
Antibody Secretion: No
Primary Targets: Intracellular pathogens (e.g., virus-infected cells) and cancer cells
Site of Origin: Red bone marrow
Site of Maturation: Thymus
Effector Cells: Cytotoxic T cells, Helper T cells, Regulatory T cells
Memory Cell Formation: Yes
Antigen-Presenting Cells (APCs)
Function:
Engulf antigens and present fragments of antigens to T cells for recognition
Major Types:
Dendritic Cells:
Phagocytize pathogens and present antigens to T cells
Most effective antigen presenter known, key link between innate and adaptive immunity
Macrophages:
Widespread in lymphoid organs and connective tissues
Present antigens to activate themselves into phagocytes that secrete bactericidal chemicals
B Lymphocytes:
Present antigens to helper T cells to aid in their activation
Activation and Differentiation of B Cells
Activation:
B cells become activated when antigens bind to their surface receptors, leading to cross-linking
Clonal Selection:
Receptor-mediated endocytosis of the cross-linked antigen-receptor complexes occurs.
Proliferation and Differentiation:
Most effector cells become plasma cells, secreting specific antibodies quickly over four to five days before dying
Memory Cells:
Clone cells that do not become plasma cells become memory cells providing immunological memory
Immunological Memory
Primary Immune Response:
Cell proliferation and differentiation upon first exposure to foreign antigen
Lag period: three to six days
Peak levels of plasma antibodies reached in around 10 days before declining
Secondary Immune Response:
Re-exposure to the same antigen leads to faster, more prolonged, and more effective response
Sensitized memory cells respond within hours
Antibody levels reach peak in two to three days, remaining high for weeks to months
Active Humoral Immunity
Definition:
Occurs when B cells encounter antigens and produce specific antibodies against them
Types of Active Humoral Immunity:
Naturally Acquired:
Response to bacterial or viral infection
Artificially Acquired:
Response to vaccination with dead or attenuated pathogens
Vaccines:
Most consist of dead/attenuated pathogens providing antigenic determinants that are immunogenic and reactive
Examples include smallpox, whooping cough, polio, measles.
Passive Humoral Immunity
Definition:
Immunity gained due to ready-made antibodies introduced into the body
B cells are not challenged by antigens, leading to no immunological memory
Protection ends when antibodies degrade
Types of Passive Humoral Immunity:
Naturally Acquired:
Antibodies delivered from mother to fetus via the placenta or to infant through breastmilk
Artificially Acquired:
Injection of serum, such as gamma globulin
Provides immediate protection that ends as the body degrades the antibodies
Treatments include antivenom for snake bites and tetanus antitoxin.
Antibodies
Definition:
Immunoglobulins (Ig) are gamma globulin proteins in blood produced by plasma cells
Capable of binding specifically with antigens detected by B cells
Classes of Antibodies:
Basic Structure:
T- or Y-shaped monomers composed of four looping polypeptide chains linked by disulfide bonds
Composed of two identical heavy (H) chains and two identical light (L) chains
Have variable (V) regions forming identical antigen-binding sites
Constant (C) regions of the stem determine antibody class (IgM, IgA, IgD, IgG, IgE)
Immunoglobulin Classes Overview
Class | Structure | Function |
---|---|---|
IgM (pentamer) | First secreted during primary response; indicates current infection | Activates complement; clumping of pathogens |
IgA (dimer) | Found in body secretions | Prevents pathogen attachment to epithelial cells |
IgD (monomer) | Found on B cells surface | Serves as B cell antigen receptor |
IgG (monomer) | Most abundant; primary in secondary responses | Protects against circulatory pathogens; crosses placenta |
IgE (monomer) | Levels rise during allergic reactions | Binds to mast cells and basophils, triggering histamine release |
Antibody Targets and Functions
Functions of Antibodies:
Antibodies inactivate and tag antigens; do not directly destroy them
Immune Complex Formation:
Form antigen-antibody complexes
Defensive Mechanisms Used by Antibodies:
Neutralization:
Antibodies block specific sites on viruses or toxins, preventing binding to cells
Promotes phagocytosis of complexes
Agglutination:
Antibodies cross-link with multiple antigens on cells, clumping them (e.g., mismatched blood cells)
Precipitation:
Cross-linking soluble antigens leads to precipitation for phagocytosis
Complement Fixation:
Several antibodies binding to a cellular antigen triggers complement activation, leading to cell lysis and enhanced inflammatory response
Mechanisms of Antibody Action
Diagrammatic representation includes:
Neutralization: Antibodies mask dangerous parts of toxins and viruses
Agglutination: Antibodies bind to cell-bound antigens
Precipitation: Specialization of soluble antigens lead to immune response
Complement Activation: Antibodies trigger significant inflammatory responses, enhancing phagocytosis