Immunology Flashcards
1
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Branch of biomedical science concerned with antigenic challenge and the recognition of self from nonself; biological, serological, and physicochemical aspects of immune system
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Immunology
2
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Recognizes, reacts with, and eliminates antigens (foreign/non self substances)
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Immune system
3
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Immune System is composed of
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Molecules: Antibodies
Cells:
B Cells → Bone marrow
T Cells → Thymus
Tissues: Lymphoid tissues
Organs: Thymus, Bone marrow
4
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2 Major Systems of the Immune System
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Lymphatic
Circulatory
5
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Ability to recognize and defend against specific pathogens or antigens
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Immunity
6
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Microorganisms that causes infectious diseases
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Pathogens
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2 Defense Mechanisms
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Humoral Immunity (Antibody-mediated)
Cellular Immunity (T cell-mediated)
8
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Specific defense; produces antibodies and lymphocytes targeting specific antigens.
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Immune Response (3rd Line)
9
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Physical & chemical barriers—skin, mucous membranes, secretions.
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First Line of Defense (Nonspecific)
10
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Internal defense—phagocytic WBCs (e.g., neutrophils), inflammation, cytokines, complement proteins.
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Second Line of Defense (Nonspecific)
11
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Adaptive immunity—lymphocytes and antibodies against specific pathogens.
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Third Line of Defense (Specific)
12
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Nonspecific Defense
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General protection—includes 1st and 2nd line defenses.
13
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Targeted response by lymphocytes and antibodies—3rd line of defense
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Specific Defense
14
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Highly resistant to disease due to humoral antibodies, cellular immunity or both
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Immune
15
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Condition of being immune; providing security against pathogens and toxins
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Immunity
16
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Inducing or triggers immune response and reacts with a specific antibody; molecules from pathogens or foreign organisms
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Antigen
17
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Gammaglobulin or immunoglobulin with unique amino acid sequence; binds only to the antigen triggered its production
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Antibody
18
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2 Types of Antigen
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Microbial
Non Microbial
19
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Capsules, cell walls, toxins, viral capsids, flagella
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Microbial
20
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Pollen, egg white (albumin), RBC surface molecules, serum proteins, transplanted tissue
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Non-Microbial
21
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Has N-acetylgalactosamine on red cell surface.
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Type A Antigen
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Has D-galactose on red cell surface.
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Type B Antigen
23
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Universal Acceptor
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AB+
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Universal Donor
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O-
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Minimum Size for Antigenicity
Must be ≥ 10,000 molecular weight to trigger immune response
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Lipids & Nucleic Acids as Antigens
Antigenic only when bound to proteins or polysaccharides.
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Antigenic determinants
This is a small part of an antigen that interacts with an antibody.
Each of these are recognized by different antibodies.
An antigen can have multiple types of these such as square, circle, triangle, rectangle etc.
Epitope
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Small foreign molecule that is not antigenic alone
This becomes antigenic only when attached to a carrier molecule (protein/polysaccharide)
Once antibodies are produced, they can recognize these independently
Hapten
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Examples of Hapten
Penicillin
Urushiol
Halothane
Hydralazine
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Toxin/foreign substance induce immune response → antibody production
Complete molecule
Can bind MHC Complex
Can bind Antibodies
Can trigger immune by itself
Antigens
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Small molecule requires carrier → elicit response
Incomplete antigen
Can NOT bind MHC Complex
Can NOT bind Antibodies
Can NOT trigger immune by itself
Hapten
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Gamma globulins that bind specific antigens with high specificity. Produced upon antigen exposure.
Antibodies (Immunoglobulins)
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The specific site on an ANTIGEN recognized by the antibody (antigen's binding site).
Epitope
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Specific site on an ANTIBODY that binds to the epitope.
Paratope
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Valence of an Antibody
Number of antigen-binding sites → most are bivalent (2 binding sites)
36
Single microbe/virus may have how many epitopes?
Multiple Epitopes, each targeted by different antibodies.
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Basic Structure of Antibodies
2 Light Chains
2 Heavy Chains
Held by disulfide bonds (L2H2 tetramer)
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Covalent bonds formed by cysteine residues, stabilizing the antibody's Y-shaped structure
Disulfide Bonds
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Located at the tips of the Y; made from the variable regions of both light and heavy chains.
Antigen-Binding Site
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Antibodies are glycoproteins due to attached carbohydrate groups.
Immunoglobulin Type
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Composition: More proteins than carbohydrates
Carbohydrate Type: Various carbohydrate types
Glycoprotein
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Composition: More carbohydrates than proteins
Carbohydrate Type: Glycosaminoglycans (mucopolysaccharides)
Proteoglycan
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Runs from N-terminal to C-terminal
Has a Variable Region (for antigen specificity)
Has a Constant Region (common within isotype)
Light Chain
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Why is the Light Chain Variable?
To allow recognition of diverse antigens, each antibody has a unique variable region.
45
Also runs from N-terminal to C-terminal
Contains both variable and multiple constant domains
Constant 2 domain helps bind complement proteins
Heavy Chain
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Antibody Binding Capabilities
Each Y-shaped antibody can:
1. Bind TWO epitopes on ONE antigen, or
2. Bind epitopes on TWO different antigens
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Antibody Monomer Structure
Y-shaped molecule made of 4 protein chains:
2 identical Light (L) chains
2 identical Heavy (H) chains
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Located at the tips of the Y arms
Contain the antigen-binding sites (Fab)
Identical on the same antibody
Vary between different antibodies
Variable Regions
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Found in the stem of the Y and lower arms
Define the class of antibody (IgG, IgA, etc.)
Constant Regions
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"Fragment antigen-binding"
Contains the antigen-binding site
Formed by the variable regions of both light and heavy chains
Fab Region
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"Fragment crystallizable"
Located at the stem of the antibody
Responsible for binding to complement proteins or immune cells
Fc Region
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Light Chain Structure
Composed of 2 regions:
→ Variable Region (Vᶫ)
→ Constant Region (Cᶫ)
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Located at the N-terminal half
Site of antigen recognition
Contains the free alpha amino group
Variable Region of Light Chain (Vᶫ)
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Located at the C-terminal half
Contains the free alpha carboxyl group
Constant Region of Light Chain (Cᶫ)
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Types of Light Chains
Kappa (κ)
Lambda (λ)
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Each antibody has 2 identical light chains but never what?
Either 2 κ or 2 λ
❌ Never 1 κ and 1 λ
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Heavy Chain Structure
Made up of 2 regions:
→ Variable Region (Vʰ)
→ Constant Region (Cʰ)
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Located at the N-terminal, making up ¼ of the chain
Works with the light chain's variable region to form the antigen-binding site
Variable Region of Heavy Chain (Vʰ)
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Makes up ¾ of the chain, extending toward the C-terminal
Constant Region of Heavy Chain (Cʰ)
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Constant Region of Heavy Chain (Cʰ) is divided into three domains:
CH1
CH2 (binds complement proteins)
CH3
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Heavy Chain Type: Gamma (γ)
Most abundant in serum
Functions: Neutralization, opsonization, and activation of the complement system
IgG (Immunoglobulin G)
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Heavy Chain Type: Alpha (α)
Mainly found in mucosal areas (e.g., saliva, tears, and respiratory and gastrointestinal secretions)
Functions: Mucosal immunity, preventing pathogen adherence
IgA (Immunoglobulin A)
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Heavy Chain Type: Mu (μ)
First antibody produced in response to infection
Functions: Activation of the complement system, primary immune response
IgM (Immunoglobulin M)
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Heavy Chain Type: Delta (δ)
Found mainly on the surface of B cells
Functions: Initiates B cell activation, role in immune response modulation
IgD (Immunoglobulin D)
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Heavy Chain Type: Epsilon (ε)
Involved in allergic reactions
Functions: Mediates histamine release from mast cells and basophils
IgE (Immunoglobulin E)
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Responsible for binding to antigens, specific to each antibody.
Variable Region (VL)
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Consistent among antibodies of the same class, provides structural support.
Constant Region (CL)
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Determines the specificity for antigens, works with the light chain variable region.
Variable Region (VH)
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Determines the antibody class (IgG, IgM, etc.), and plays a role in effector functions.
Constant Region (CH)
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Maintains structural integrity of the antibody.
Helps hold together the heavy and light chains.
Influences antibody effector functions.
Contains disulfide bonds linking it to the constant region of the light chain
CH1
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Complement-binding site activates the complement system to enhance immune responses
CH2
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Site neutrophils and macrophages receptors
CH3
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Formed by:
Variable Heavy (Vₕ) region
Variable Light (Vₗ) region
The site where the antibody binds to the epitope on the antigen.
Antigen Binding Site
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Formed by:
Vₕ + Vₗ + Cₕ1 + Cₗ
Located at the tips of the Y-shaped antibody.
Responsible → directly binding antigen's epitope.
Each antibody → two Fab regions for binding antigens.
Fab (Fragment Antigen-Binding) Region
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Part of the antigen-binding site → interacts epitope of the antigen.
Involved antigen-antibody interactions → noncovalent bonds (e.g., hydrogen bonds, ionic bonds, van der Waals forces).
Hypervariable Regions (Complementarity-Determining Regions or CDR)
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Includes Cₕ2 and Cₕ3.
Includes Cₕ4 (specific to IgM and IgE).
Constant Region
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Functions of Constant Region
1. Complement Fixation
2. Transplacental Passage (IgG)
3. Allergic Responses (IgE)
4. Opsonization (Phagocytosis)
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Both light (L) and heavy (H) chains are _______, containing oligosaccharide units (carbohydrate chains).
Glycoproteins
79
Enzymes that are proven to have an effect on antibodies
1. Pepsin
2. Papain
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Proteolytic enzyme (protein-digesting enzyme) found in the human stomach.
Pepsin
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Action of Pepsin
Proteolysis →carboxyl terminus (hinge region) → near C₂ domain
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Products of Pepsin Digestion
Large Fab Fragment
Fc Fragment
Low Molecular Weight Peptides
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Proteolytic enzyme → digests antibodies → splitting the heavy chain.
Papain
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Action of Papain
Cleaves heavy chain → amino terminal side → interchain disulfide bonds → hinge region
85
Products of Papain Digestion
1. Two Identical Fab Fragments
- Antigen-binding site (formed by Vₕ + Vₗ + Cₕ1 + Cₗ).
- NO effector functions
2. One Fc Fragment
- CH2, CH3 domains
- Effector functions
86
Structure:
Monomeric
2 Heavy (H) chains
2 Light (L) chains.
2 Antigen-binding sites
Key Features:
✓ Most abundant Ig (~75% of total serum Ig).
✓ Secondary antibody response (~1 month after antigen recognition)
✓ Only Ig crosses placenta passive immunity.
✓ Binds viruses, bacteria, fungi.
✓ Not first antibody produced upon antigen exposure.
Immunoglobulin G (IgG)
87
Most ABUNDANT IgG subclass.
Effective at complement activation.
BEST at crossing the placenta.
IgG1
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Short hinge region.
POOR complement activator.
LIMITED placental transfer.
IgG2
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LARGEST hinge region.
Most EFFICIENT at complement activation.
Crosses placenta effectively.
IgG3
90
Short hinge region.
Poor complement activator.
MODERATE placental transfer
IgG4
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Complement Fixation Efficiency
Order (Best to Least)
IgG3 > IgG1 > IgG2
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Placental Transfer Efficiency
Order (Best to Least)
IgG1 > IgG3 > IgG4
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Key features:
✓ Secondary antibody
✓ ~15% of total serum Ig.
✓ Exocrine secretions.
Found in mucous secretions along the:
✓ Respiratory tract
✓ Gastrointestinal tract (GIT)
✓ Genitourinary tract
Present in:
✓ Tears
✓ Saliva
✓ Colostrum (first milk)
✓ Intestinal juice
✓ Vaginal fluid
✓ Prostate secretions
✓ Respiratory epithelium secretions
Immunoglobulin A (IgA)
94
Protective Factors of Colostrum
Complement
Macrophages
Lymphocytes
Lactoferrin, lactoperoxidase, lysozymes.
95
Functions of IgA
✓ Vital role in mucosal immunity
✓ Resistant to enzyme degradation (intestinal juice)
✓ Secretory IgA (IgA2) → dimer form.
✓ Poor complement activator
✓ Weak opsonizer.
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Structure:
✓ 5 monomeric units linked by disulfide bonds → pentamer.
✓ single J chain for stability
✓ pentameric IgM → 10 antigen-binding sites
Key Features:
✓ Primary antibody against A and B antigens on RBCs.
✓ Main antibody → blood transfusion reactions.
✓ FIRST antibody produced during the PRIMARY immune response.
Location:
✓ Serum due to its large size.
✓ CANNOT cross the basement membrane of blood vessels.
Function:
✓ Highly effective complement activation → Cₕ2 region.
Immunoglobulin M (IgM)
97
Percentage in Plasma Membrane:
✓ ~1% of plasma membrane proteins immature B lymphocytes.
Structure:
✓ Monomer antibody (like IgG).
Function:
✓ Acts as a signal for young B cells to activate.
Immunoglobulin D (IgD)
98
✓ Allergies and Type 1 Hypersensitivity.
✓ Triggers powerful immune reactions (anaphylaxis)
Involved in immune responses against:
✓ Parasitic worms (e.g., Hookworms, Ascaris).
✓ Protozoan parasites (e.g., Plasmodium falciparum).
Immunoglobulin E (IgE)
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Mediator: IgE
Mechanism: IgE binds to mast cells & basophils → Histamine release
Onset: Seconds to minutes
Examples: Allergies, anaphylaxis, asthma
Type I – Anaphylactic (Immediate)
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Mediator: IgG or IgM
Mechanism: Antibodies bind to cell surface antigens → Cell destruction
Examples:
Hemolytic anemia
Rh incompatibility
Graves’ disease
Type II – Cytotoxic
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Mechanism: Antigen-antibody complexes deposit in tissues → Inflammation
Examples:
Systemic lupus erythematosus (SLE)
Rheumatoid arthritis
Type III – Immune Complex-Mediated
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Mediator: T cells (no antibodies involved)
Mechanism: T cells release cytokines → Tissue damage
Onset: 24–72 hours
Examples:
Tuberculin skin test (PPD)
Contact dermatitis
Graft rejection
Type IV – Delayed (T-cell Mediated)
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Ability to develop an immune response when exposed to an antigen; Normal state.
Immunocompetence
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Weakened/attenuated immune response caused by immunosuppressive drugs (steroids), chemotherapy, irradiation (rad therapy), malnutrition (kwashiorkor, marasmus) and disease processes (cancer)
Immunocompromised
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Deficiency in immune response, mediated by a humoral antibody or immune lymphoid cells (responsible for cellular immunity) or both
Immunodeficiency
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Most abundant antibody (70–75%); monomeric; first antibody in secondary immune response; crosses placenta (except IgG2); fixes complement.
IgG
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Monomeric form of IgA found in serum; anti-inflammatory; part of mucosal defense; fixes complement.
IgA1
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Dimeric form found in secretions (tears, saliva, breast milk); protects mucosal surfaces; resistant to enzymatic degradation; fixes complement
IgA2
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Pentameric structure with 10 antigen-binding sites; first antibody produced in primary immune response; most efficient at complement activation; does not cross placenta.
IgM
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Monomer; found on immature B cells; functions as a signal for B cell activation; does not fix complement or cross the placenta.
IgD
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Monomer; involved in allergic (Type I hypersensitivity) reactions and defense against parasitic infections; binds to mast cells and basophils; does not fix complement or cross placenta.
IgE
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Forms when an antibody binds to its specific antigen.
Antigen-Antibody Complex
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Strength of Ag-Ab binding
Affinity
114
CLUMP of antigens (like microbes or RBCs) by antibodies
✓ IgM (decavalent = 10 binding sites)
✓ IgG (bivalent, 2 binding sites)
Seen in blood typing and transfusion reactions.
Purpose:
✓ Enhances phagocytosis
✓ Reduces number infectious units
Mechanism:
✓ Y-shaped antibodies bind to multiple antigens → large clumps → easier removal immune cells
Agglutination
115
COAT a microbe easier for phagocytes (like neutrophils and macrophages) to recognize and engulf it.
Mechanism:
✓ Fab region antibody → antigen
✓ Fc region → Fc receptors
✓ Phagocytosis → entire Ag-Ab complex
Effect:
✓ Enhances phagocytosis
✓ Promotes antigen destruction
Opsonization
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Defense mechanism: IgG antibodies bind to viruses or toxins
Preventing activity and BLOCKING infection or toxicity.
Mechanism:
✓ Blocks pathogen adhesion to mucosal surfaces (respiratory, intestinal, genitourinary)
✓ Binds toxin active sites, neutralizing harmful effects
Effect:
✓ Forms free-flowing Ag-Ab complexes
✓ Prevents microbes and toxins from penetrating mucosal barriers
Neutralization
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ELIMINATES large extracellular pathogens (e.g., parasitic worms) → using antibodies to recruit immune cells.
Mechanism:
✓ Antibodies coat the target organism
✓ Fc region binds to receptors on neutrophils and eosinophils
✓ Cells release enzymes, cytokines, and toxic chemicals
✓ Target is damaged, destroyed
Effect:
✓ Efficient elimination of large pathogens
Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC)
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Defense Mechanism: Antibody-antigen complexes → IgG and IgM → enhances immune response.
Mechanism:
✓ IgG & IgM → antigens and activate the complement cascade
Cascade leads to:
✓ Pathogen lysis (rupture)
✓ Inflammation
✓ Recruitment of immune cells
Effect:
✓ Destroys pathogens
✓ Enhances immune response
Complement Activation
119
All enhance phagocytosis by macrophages.
Neutralization
Opsonization
Agglutination
Precipitation
120
Body's ability to resist infections and diseases through defense mechanisms.
Immunity
121
2 category of Immunity
Innate (nonspecific)
Adaptive (specific)
122
Present at birth, first line of defense, rapid but nonspecific.
Provides immediate protection against pathogens.
Mechanisms:
✓ Physical barriers: Skin, mucous membranes
✓ Chemical barriers: Enzymes (saliva), stomach acid
✓ Cellular components: Macrophages, neutrophils, NK cells
Example:
✓ Humans immune to canine distemper
✓ Mice immune to poliovirus
Innate Immunity
123
Type of Cells under Innate Immune Cells
Neutrophils → First responders, phagocytosis
Macrophages → Engulf pathogens, APCs
Dendritic Cells → Bridge innate and adaptive
Natural Killer (NK) Cells → Kill virus-infected/cancerous cells
Eosinophils → defend against parasites, allergic reactions
Basophils & Mast Cells → Release histamine, trigger inflammation
124
Develops over time, highly specific to pathogens, and has memory for a stronger response upon re-exposure.
Example:
Immunity to measles after infection or vaccination.
Adaptive Immunity
125
2 Types of Adaptive Immunity
1. Humoral Immunity: B cells & antibodies
2. Cell-Mediated Immunity: T cells
126
Types of Cells under Adaptive Immune Cells
B Cells → Produce antibodies (humoral immunity) form memory cells
Helper T Cells (CD4+) → Activate B cells & immune response
Cytotoxic T Cells (CD8+) → Kill infected/abnormal cells
Regulatory or Suppressor T Cells (Tregs) → prevent autoimmunity
127
Exposure pathogen triggers body to generate an immune response, providing long-lasting immunity.
Examples:
✓ Lifelong immunity: Chickenpox, mumps
✓ Temporary immunity: Influenza, intestinal infections
Naturally Acquired Active Immunity
128
Antibodies transferred from mother to infant through the placenta or breastfeeding. Provides short-term protection until the infant's immune system develops.
Examples:
✓ IgG: Crosses the placenta
✓ IgA: Found in colostrum (breast milk)
Naturally Acquired Passive Immunity
129
Immune response mediated by antibodies produced by B cells.
Targets:
✓ Bacteria
✓ Extracellular pathogens
Role:
Primary defense against bacterial infections
Humoral Immunity
130
Immune response where T cells directly attack infected or abnormal cells.
Targets:
✓ Viruses
✓ Fungi
✓ Intracellular bacteria (e.g., Mycobacterium tuberculosis)
✓ Tumors
Role:
Delays allergic reactions, helps with transplant rejection.
Cellular Immunity
131
Involves B cells producing antibodies against antigens, secreted by plasma cells (activated B cells).
Antibodies are found in extracellular fluids like plasma, lymph, and mucus.
Defends Against:
✓ Bacteria
✓ Toxins
✓ Free-floating viruses (before they enter cells)
Humoral (Antibody-Mediated) Immunity
132
Process in which cells self-destruct when they are not properly activated.
✓ B cells that do not receive antigen stimulation undergo this process.
✓ Virus-infected cells may also undergo this process to prevent viral replication
Programmed cell death (apoptosis)
133
Involves T cells that recognize antigens on infected cells → T cells directly attack infected or abnormal cells.
Defends Against:
✓ Intracellular bacteria & viruses
✓ Fungi, protozoa, helminths
✓ Cancer cells
✓ Transplanted tissues
Cell-Mediated Immunity
134
2 Types of Cell-Mediated Immunity
1. Helper T Cells: Coordinate the immune response by activating other immune cells.
2. Cytotoxic T Cells: Destroy infected or abnormal cells.
135
Key Difference Between Humoral and Cell-Mediated Immunity
Humoral Immunity: Attacks pathogens in body fluids (extracellular) 💧
Cell-Mediated Immunity: Attacks infected or abnormal cells directly 🔬
136
Fetal Development of the Immune System
Lymphocyte Precursors → bone marrow.
Thymus: Precursor cells develop into T lymphocytes (T cells) → cell-mediated immunity.
Fetal Liver (before birth) & Bone Marrow (after birth): Precursor cells develop into B lymphocytes (B cells) → antibody-mediated immunity.
137
Immune System Composition (B Cells vs T Cells)
B Cells → Humoral Immunity (antibody production).
T Cells → Cellular Immunity (directly attacking infected cells).
138
B Cell Development & Maturation
Origin: B cells → stem cells in bone marrow (adults) or liver (fetuses).
Migration: After maturation, B cells migrate to lymphoid organs (e.g., lymph nodes, spleen).
139
Clonal Selection & Activation of B Cells
B cells recognize → specific antigen.
Activation: Stimulated B cells undergo rapid division (clonal expansion).
Differentiation: B cells → plasma cells (secrete antibodies)
140
Specificity of B Cells
Each B cell produces antibodies → one specific antigenic determinant (epitope).
141
Clonal Diversity: Numerous clonally derived lymphocytes exist → each recognizing a specific antigenic determinant
Antigen-Driven Activation: antigen selects → activates a pre-existing clone
Clonal Expansion: Activated B/T cells proliferate → many identical clones.
Differentiation: Clones → plasma (effector) cells or memory cells.
Immune Memory: Some clones persist as memory cells → future, faster responses.
Clonal Selection Hypothesis
142
B and T cells that react against self-antigens are destroyed during fetal development.
Clonal Deletion
143
Prevents antibodies → targeting self-antigens and causing autoimmune diseases
Immune system does not produce antibodies against self-antigens → immune tolerance.
Clonal Deletion → only lymphocytes recognizing foreign antigens survive.
Self-Tolerance
144
Clonal Deletion Process
Occurs in primary lymphoid organs:
→ T Cells: Thymus
→ B Cells: Bone marrow
Exact mechanism is not fully understood but is crucial for preventing self-reactivity.
145
Concentration of antibodies in the blood serum.
Used to measure immune response against an antigen.
Antibody Titer
146
Primary Immune Response (First Exposure to an Antigen)
1️⃣ Lag Phase: No antibodies detected in serum for several days.
2️⃣ IgM appears first, followed by IgG.
3️⃣ Gradual increase in antibody levels.
4️⃣ Most B cells become plasma cells (secrete antibodies), while some become memory B cells for future responses.
5️⃣ Antibody levels decline after the peak response.
147
Secondary Immune Response (Subsequent Exposure)
1️⃣ Faster and stronger antibody production than primary response.
2️⃣ Memory B cells quickly differentiate into plasma cells, producing large amounts of IgG.
3️⃣ Higher and longer-lasting antibody levels, providing more effective immunity.
💡 Key Takeaway: Immunological memory ensures stronger and quicker responses to repeat infections.
148
Primary Immune Response Timeline
1️⃣ IgM rises first 📈
Detectable: 4–7 days
Peaks: 7–10 days
2️⃣ IgG follows 📈
Starts rising: 7–14 days
Peaks: 2–3 weeks after exposure
3️⃣ Slower and weaker response compared to secondary exposure.
4️⃣ Antibody levels decline as the antigen is eliminated.
149
Secondary Immune Response Timeline
1️⃣ Memory B cells react quickly 🧬
2️⃣ IgG rises rapidly ⚡
Detectable: 1–3 days
Peaks: much higher and faster than primary response
3️⃣ IgM shows only a minor increase.
4️⃣ Provides stronger and longer-lasting protection against reinfection.
150
Hematopoietic Stem Cells differentiate into 2 progenitor cells
1. Lymphoid Progenitor Cells
2. Myeloid Progenitor Cells
151
are the precursors of all blood cells and differentiate into either lymphoid or myeloid progenitor cells.
They are essential for the production of immune cells that defend the body against infections and diseases.
Hematopoietic Stem Cells
152
Lymphoid progenitor cells differentiate into 3 cells
(Adaptive)
1️⃣ B Cells → Plasma cells (produce antibodies).
2️⃣ T Cells:
✓ CD4+ Helper T cells → Activate the immune response.
✓ CD8+ Cytotoxic T cells → Kill infected cells.
3️⃣ Natural Killer (NK) cells → Innate immune defense against virus-infected and cancer cells.
153
Myeloid progenitor cells differentiate into 5 cells
(Innate)
1️⃣ Granulocytes (PMNs - Polymorphonuclear Leukocytes):
✓ Neutrophils → Most abundant, phagocytose bacteria 🦠.
✓ Eosinophils → Combat parasites and mediate allergic reactions 🦠.
✓ Basophils → Release histamine, involved in allergies.
2️⃣ Mast Cells → Reside in tissues, release histamine (from histidine via decarboxylation).
3️⃣ Monocytes → Circulate blood; become macrophages in tissues.
4️⃣ Dendritic Cells → Antigen-presenting cells (APCs) that activate T cells
5️⃣ Megakaryocytes → Fragment into platelets, involved clotting and inflammation.
154
Innate immune cells (no prior antigen exposure, non-specific).
Kill: Virus-infected & cancerous cells.
Mechanism:
✓ Activating Receptors → Trigger NK cell activation.
✓ Inhibitory Receptors → Detect Class I MHC (self-signal).
✓ Perforin → Creates pores in target cells.
✓ Granzymes → Induce apoptosis (cell death)
✓ Cytokine secretion → Antiviral & inflammatory response.
✓ Tissues: Blood, bone marrow, liver, spleen, mucosal tissues.
Natural Killer (NK) Cells
155
Function: Immune cell activation & antigen presentation.
Includes:
✓ Lymph nodes: Filter lymph (B-cell cortex, T-cell paracortex, medulla).
✓ Spleen: Filters blood (immune response in white pulp, removes old RBCs & pathogens in red pulp).
✓ Tonsils: Trap airborne & ingested pathogens.
Secondary Lymphoid Tissues (SLT)
156
Function: Protects mucosal surfaces from pathogens.
Includes:
✓ GALT (Gut-associated lymphoid tissue): Peyer's patches (intestines).
✓ BALT (Bronchus-associated lymphoid tissue): Lungs.
✓ Tonsils & Appendix.
Mucosa-Associated Lymphoid Tissue (MALT)
157
What happens when MHC Class I molecules are present on healthy cells?
[Strong Inhibition]
Strong inhibitory signals to NK cells → NK cells remain inactive, protecting healthy cells.
158
What occurs when virus-infected or tumor cells downregulate MHC I?
[Reduced Inhibition]
Reduced inhibitory signals → NK cells activated → NK cells attack abnormal cells.
159
What happens when activating ligands are upregulated on infected/transformed cells?
[Strong Activation]
Activating receptors override inhibitory signals → NK cells attack even with MHC I present.
160
NK Cells vs NKT Cells - Immunity Role
NK cells → Innate.
NKT cells → Bridge innate & adaptive.
161
NK Cells vs NKT Cells - Antigen Recognition
NK cells → Detect missing MHC I.
NKT cells → Recognize lipid antigens via CD1d.
162
NK Cells vs NKT Cells - TCR Expression
NK cells → No TCR.
NKT cells → Semi-invariant TCR
163
NK Cells vs NKT Cells - Cytokine Production
NK cells → Cytotoxic (perforin & granzymes).
NKT cells → Regulate immune response (Th1/Th2 balance).
164
Respond to lipid antigens (CD1d) and regulate immune response, not direct cytotoxicity.
NKT Cells
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Why are NKT cells considered a bridge between innate and adaptive immunity?
Combine NK cell speed (innate) with T cell specificity (adaptive) → fast response + immune regulation.
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How do NKT cells connect innate & adaptive immunity?
1. Fast response →
Cytokines
IFN-γ
IL-4
IL-17
2. Recognize lipid antigens → CD1d (not MHC)
3. Kill infected/cancerous cells
4. Activate T & B cells, balance Th1/Th2
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What do NKT cells recognize and how?
Lipid antigens → CD1d
NOT peptides → MHC like regular T cells.
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Functions of NKT cells
✓ Cytotoxicity (perforin, granzymes)
✓ Cytokine release (shapes immunity)
✓ T & B cell activation
✓ Immune balance (Th1 vs Th2)
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Immune cells that process & present antigens to T cells to initiate immune responses.
Antigen-presenting cells (APCs)
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4 Classical (professional) APCs.
1. Dendritic cells
2. Macrophages
3. Langerhans cells
4. B cells (present to CD4+ T cells)
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Which molecules present which types of antigens?
MHC II → Peptide antigens → CD4+ T cells
CD1d → Glycolipid antigens → NKT cells
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What's the activation sequence from microbe to NKT cell response?
🦠 Microbe →
🛡 APC (e.g., dendritic cell) →
🔗 CD1d presents antigen →
🚀 NKT cell activated →
🔥 Cytokine release (IL-4, IFN-γ, IL-17)
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Common locations of dendritic cells
🌬 Lungs
🧴 Skin
🍽 GI tract
👃 Nose
🛡 Sites exposed to external environment
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Professional APCs that link innate and adaptive immunity by capturing and presenting antigens to naïve T cells in lymphoid organs.
Dendritic cells (DCs)
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How do DCs capture antigens?
🧫 Phagocytosis
💧 Macropinocytosis
🎯 Receptor-mediated endocytosis
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Which MHC activates which T cell type?
MHC I → CD8+ T cells (viral/intracellular)
MHC II → CD4+ T cells (bacterial/extracellular)
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How do DCs activate naïve T cells?
1. Migrate to lymph nodes
2. Present antigen via MHC
3. Use CD80/CD86 + cytokines for full activation
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What happens after DC-T cell interaction?
No antigen → Keep circulating or apoptosis
With antigen → Become:
✓ Effector T cells (Helper or Cytotoxic)
✓ Memory T cells (long-term protection)
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Key cytokines secreted by DCs & their effects?
IL-12 → Stimulates Th1 (antiviral/intracellular)
IL-4 → Stimulates Th2 (parasites/allergy)
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Specialized dendritic cells in the skin & mucosal surfaces.
Antigen presentation, immune surveillance, and tolerance regulation.
Epidermis (stratum spinosum), mucosal tissues, lymph nodes, spleen, lungs, liver, and bone marrow.
Markers:
✓ Langerin (CD207)
✓ CD1a
✓MHC II
Unique Feature:
✓ Birbeck granules (antigen-processing organelles)
Immunity Role:
✓ Antigen Capture: Recognizes & engulfs pathogens (bacteria, viruses, fungi).
✓ Migration: After activation, migrates to lymph nodes, presenting antigens to T cells.
✓ Balance: Activates T cells for infection defense and maintains immune tolerance to prevent overreactions.
Langerhans Cells
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A set of cell surface glycoproteins essential for antigen presentation to T cells.
🔍 Function: Helps immune system recognize self vs. non-self
🧬 Encoded by HLA genes on chromosome 6
Major Histocompatibility Complex (MHC)
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MHC I – Who has it? What does it do?
📍 Found on: All nucleated cells
🎯 Presents to: CD8+ cytotoxic T cells
🦠 Antigen Type: Endogenous (intracellular: viruses, tumors)
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MHC II – Who has it? What does it do?
📍 Found on: APCs (macrophages, DCs, B cells)
🎯 Presents to: CD4+ helper T cells
🦠 Antigen Type: Exogenous (extracellular: bacteria, parasites)
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Where are lymphocytes formed and where do they reside?
📍 Formed in: Lymph nodes, thymus, spleen
🚪 Enter blood via: Lymphatics
💉 Blood presence: Only 2% (most in lymphoid organs)
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🔑 Function: Produce specific antibodies
🧬 Mechanism: Gene rearrangement enables recognition of billions of antigens
Lymphocytes
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🏠 Origin: Bone marrow
🎯 Function: Humoral immunity → Antibody production
B Lymphocytes (B Cells)
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2 B Cells
1. Plasma cells – Secrete antibodies
2. Memory B cells – Long-term protection
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🔒 Function: Cell-mediated immunity (e.g. graft rejection, tumor & viral defense)
T Lymphocytes (T Cells)
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Types of T Lymphocytes (T Cells)
CD8+ Cytotoxic T cells
CD4+ Helper T cells
Suppressor (Regulatory) T cells
Memory T cells
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What do Cytotoxic T Cells (CTLs) do and how do they kill?
💣 Kill virus-infected & transplanted cells
⚔ Mechanism:
✓ Perforin-granzyme pathway
✓ Fas-FasL interaction
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NKT vs. CTLs – How do they differ?
🧬 NKT Cells:
✓ Bridge between innate & adaptive immunity
✓ Recognize lipid antigens via CD1d
✓ Rapid responders (like innate cells)
✓ Release diverse cytokines: IFN-γ, IL-4, IL-17
✓ Function: Immune modulation + cytotoxic killing
✓Surface Markers: TCR + NK markers (e.g., CD161, NK1.1)
🎯 CTLs (CD8+ T Cells):
✓ Part of the adaptive immune system
✓ Recognize peptide antigens via MHC I
✓ Require priming/activation by APCs
✓ Release mainly cytotoxic cytokines: IFN-γ, TNF-α
✓ Function: Focused cytotoxic killing of infected cells
✓ Surface Markers: Have only TCR
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Function: Recognizes antigens on MHC molecules for adaptive immunity
Activation: Works with CD4/CD8 to activate T cells
Role: Provides immune memory for faster responses
Example: CD8+ T cells use TCR to recognize MHC-I, killing infected cells
TCR (T Cell Receptor)
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Detects and kills abnormal cells (virus/cancer) without prior activation
NK Markers (NK1.1, CD161, CD56, CD16)
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Triggers ADCC (NK-mediated killing)
CD16
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Regulates cytokine production
CD161/NK1.1
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NK activation & adhesion
CD56
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Function: Identifies Cytotoxic T Cells (CTLs)
Role: Binds MHC-I presenting intracellular peptides to kill infected cells
CD8 Marker
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Assist B cells (antibody production) & Cytotoxic T cells (cell-mediated immunity)
Antigen Recognition: MHC-II on APCs
Helper T Cells (CD4+)
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Types of Helper T Cells (CD4+)
Th1
Th2
Tfh
Th17
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Activates CTLs, targets intracellular pathogens (viruses, Mycobacterium)
Key Cytokines: IFN-γ, IL-2
Th1
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Assists B cells, targets extracellular pathogens (IgE production)
Key Cytokines: IL-4, IL-5, IL-13
Th2
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Matures B cells, promotes antibody production
Key Cytokines: IL-21, IL-4
Tfh
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Defends mucosal surfaces (skin, gut)
Key Cytokines: IL-17, IL-22
Th17
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Function: Regulate & suppress immune response to prevent autoimmunity and excessive inflammation
Key Cytokine: IL-10 (immunosuppressant)
Inhibition:
✗ Th1 (↓ Cell-mediated immunity)
✗ Th2 (↓ Antibody production)
✗ CD8+ T cells (↓ cytotoxic killing)
Suppressor T Cells (Tregs)
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Function: Provide long-term immunity after antigen exposure
Key Feature: Convert to effector T cells rapidly upon re-exposure to the same antigen
Importance: Faster & stronger immune response during reinfection
Memory T Cells
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Targets: Intracellular pathogens (viruses, bacteria, tumor cells)
Key Features:
Requires continuous antigen presence for activation
Not transferred to fetus (unlike humoral immunity)
T Cells & Cell-Mediated Immunity
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Chemical Messengers of Immunity
Over 100 types identified!
They stimulate/regulate immune responses.
Cytokines
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3 Types of Cytokines and their functions
Interleukins (ILs): Communication between WBCs
Interferons (IFNs): Protect against viral infections
Chemokines: Attract WBCs to infected areas
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Core players in cell-mediated immunity that needs TCR (T Cell Receptor) to recognizes specific antigens and requires MHC (Major Histocompatibility Complex) for antigen recognition
T Cells
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Location: All nucleated cells
Presents to: CD8+ Cytotoxic T Cells
Function: Presents intracellular antigens (e.g., viruses, tumors)
MHC I
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Location: APCs (e.g., dendritic cells, macrophages, B cells)
Presents to: CD4+ Helper T Cells
Function: Presents extracellular antigens (e.g., bacteria, fungi)
MHC II
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Process: Expands T cells that specifically recognize the antigen
Clonal Selection
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Source of Antigen: Inhaled, ingested, or injected (e.g., bacteria, toxins, fungi)
Processed by APCs:
✓ Phagocytic Cells: Dendritic cells & Macrophages
✓ B Cells: Present antigens but are not phagocytic
Exogenous Antigen Presentation
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Steps of Exogenous Antigen Presentation
1. Antigen Uptake: APC engulfs antigen via endocytosis
2. Processing: Endosome fuses with lysosome, breaking down the antigen
3. Peptide Generation: Antigen degraded into short peptides
4. MHC-II Loading: Peptides loaded onto MHC Class II
5. Presentation: MHC-II + peptide complex displayed on surface
6. T Cell Activation: Recognized by CD4+ Helper T Cells, initiating immune response
📌 Key Outcome: Activates CD4+ T cells, leading to B cell activation and antibody production
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Source of Antigen: Generated within the cell (e.g., viral proteins, tumor antigens)
Endogenous Antigen Presentation
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Steps of Endogenous Antigen Presentation
1. Protein Degradation: Intracellular proteins (e.g., viral or tumor proteins) broken down by proteasome
2. MHC-I Loading: Peptides are transported to the endoplasmic reticulum (ER) via TAP and loaded onto MHC Class I
3. Presentation: MHC-I + peptide complex displayed on cell surface
4. CD8 T Cell Recognition: Recognized by CD8+ Cytotoxic T Cells
5. Infected Cell Destruction: Activated CD8 T cells (CTLs) kill the infected cell using:
✓ Perforin: Pokes holes in target cell
✓ Granzymes: Enter cell and trigger apoptosis
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T cells (especially CD8+ Cytotoxic T cells) play a role in killing infected or abnormal cells.
T cells help in activating B cells to produce antibodies (humoral immunity).
Cell-Mediated Immunity
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B cells produce antibodies that neutralize pathogens and assist in pathogen destruction.
Antibody production is regulated by T-helper (Th) cells, particularly for T-dependent antigens.
Humoral Immunity
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Process:
1. Macrophage ingests and presents antigen to Th cell.
2. Th cell activates B cells, which then become plasma cells.
3. Plasma cells produce antibodies.
Antigens: Typically proteins found on:
✓ Viruses 🦠
✓ Bacteria 🧫
✓ Foreign RBCs 🩸
✓ Hapten-carrier molecules
T-Dependent Antigens (Require T cell help)
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B cells directly produce antibodies without needing T cell assistance.
Antigens: Mostly polysaccharides (e.g., bacterial capsules 🏰).
Response: Weaker immune response than T-dependent antigens.
T-Independent Antigens (No T cell help)
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How It Works:
✓ Target cell is coated with antibodies (via Fc region).
✓ NK cells and other immune cells bind to Fc region.
✓ NK cells attack the target and lyse it with toxic substances.
Purpose: This mechanism is crucial for large pathogens (e.g., parasites 🦠) that cannot be easily phagocytosed.
Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC)
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5 Cardinal features of Immune Response
1. Specificity
2. Diversity
3. Memory
4. Self-limitation
5. Discrimination
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Immune responses are specific to distinct antigens.
Key Term: Epitope (recognized by antibodies).
Specificity
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The immune system can recognize a vast array of antigens.
Key Fact: Discriminates between 10^9 epitopes.
Diversity
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The immune system "remembers" past antigens.
Key Fact: Secondary responses are faster and stronger.
Memory
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Immune responses wane after antigen is cleared.
Key Fact: Immune responses are temporary.
Self-Limitation
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Ability to distinguish foreign from self antigens.
Key Fact: Tolerance = unresponsiveness to self-antigens.
Discrimination
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3 Phases of Immune Response
1. Cognitive Phase
2. Activation Phase
3. Effector Phase
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Foreign antigens bind to specific receptors on mature lymphocytes before antigenic stimulation.
Key Point: Antigen recognition happens prior to activation
Cognitive Phase
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Antigen recognition triggers specific events in lymphocytes.
Key Events:
✓ Lymphocyte proliferation
✓ B cells → Plasma cells (antibody production)
✓ T cells → Activation of phagocytes & direct cytotoxicity
✓ Helper T cells promote activation
Activation Phase
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Activated lymphocytes (effector cells) eliminate the antigen.
Key Point: Lymphocytes perform their functions to destroy the pathogen
Effector Phase
