the concept of immunity
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Copyright © 2010 Pearson Education, Inc.
The Concept of Immunity
Immunity: Latin immunis, exempt Susceptibility: Lack of resistance to a disease,
also known as Vulnerability Innate immunity: Inborn Adaptive immunity: Acquired, resistance to a
specific pathogen
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An Overview of the Body’s Defenses
Figure 16.1
ANIMATION Host Defenses: The Big Picture
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First Line of Defense: I. Skin & Mucous Membranes
Skin Keratin, a protective protein
Mucous membranes Hairs Cilia Tears, Saliva, Urine,
Vaginal secretions Lysozyme
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Ciliary Escalator
Figure 24.7
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II. Normal Microbiota
Normal microbiota compete with pathogens for nutrients
Keep pH unfavorable for disease microbes
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Red Blood Cells Transport O2 and CO2
White Blood Cells:Neutrophils Phagocytosis
Basophiles Histamine
Eosinophils Kill with toxin
Second Line of DefenseI. Blood components
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Macrophage Phagocytosis
Dendritic cells Phagocytosis
Natural killer cells Destroy target cells by apoptosis
T cells Cell-mediated immunity
B cells Produce antibodies
Platelets Blood clotting
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Percentage of each type of white cell in a sample of 100 white blood cells
Early and late in infection: Neutrophil then Macrophage
Neutrophils 60–70%
Basophils 0.5–1%
Eosinophils 2–4%
Monocytes 3–8%
Lymphocytes 20–25%
Differential White Cell Count
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II. Lymphatic SystemTissue + Fluid
Figure 16.5a
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III. Phagocytosis
Neutrophils
Macrophage Presents Ag Secret cytokines
(lymphokines + interleukins)
Figure 16.6
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IV. Inflammation
Releasing histamine Vasodilation (histamine, kinins, prostaglandins,
and leukotrienes) Redness Swelling Pain Heat
Tissue repair and wall-off
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Fever
Abnormally high body temperature Body’s defensive mechanism
Increase enzyme activity and cytokine activity Increase blood flow Some bacteria can not survive at higher temperature
Disadvantage: Tachycardia Acidosis Dehydration 44–46°C fatal
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V. Antimicrobial Substances ComplementsC3a + C5a cause inflammationC5b + C6 + C7 + C8 + C9 cause cell lysis
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Interferons a- and b- interferon: Virus infected cells to produce AVPs g- interferon: Neutrophils and macrophages
Limitations: Side effects Short lived Only prevents, not stop viral synthesis No effect on a number of cancers
Ion-binding Proteins AMPs: Natural antibiotics
V. Antimicrobial Substances
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Types of Adaptive Immunity
Naturally acquired active immunity Resulting from infection
Naturally acquired passive immunity Transplacental or via colostrum
Artificially acquired active immunity Injection of Ag (vaccination)
Artificially acquired passive immunity Injection of Ab
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Copyright © 2010 Pearson Education, Inc.Dua
l Nat
ure
of A
dapt
ive
Imm
unity
Figure 17.8
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Dual Nature of Adaptive Immunity
Humoral immunity: B-cells Ag-Ab
Cellular immunity T-cells Cytokines
ANIMATION Humoral Immunity: Overview
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I. Antigens
It has to be large Ag determinants = epitopes Hapten and Carrier
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Antigens
Figure 17.1
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Haptens
Figure 17.2
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II. Antibodies
They are immunoglobulins (Ig) The antigen-binding sites recognize epitope and
determine valence Constant Region / Variable Region Heavy Chain / Light Chain
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Antibodies
Figure 17.3a,b
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Monomer Most common and abundant (80%) Fix complement Cross placenta Enhance phagocytosis; neutralize toxins and
viruses; protects fetus and newborn Half-life = 23 days
IgG Antibodies
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Pentamer Agglutination Fix complement Agglutinates microbes; first Ab
produced in response to infection Half-life = 5 days
IgM Antibodies
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IgA Antibodies
Dimer 10–15% of serum Abs In secretions Mucosal protection Half-life = 6 days
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Monomer In blood, in lymph, and on B cells On B cells, initiate immune response Half-life = 3 days
IgD Antibodies
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Monomer Allergic reactions; lysis of
parasitic worms Half-life = 2 days
IgE Antibodies
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Diversity Self – non-self discrimination Memory
III. B Cells
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1st exposure to Ag
2nd exposure to Ag
First Clones
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T-independent Activation of B Cells
Figure 17.6
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T-dependent Activation of B Cells
Figure 17.4
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Ag Response Ig Memory
T-dependent Proteins Strong IgG Yes
T-independent Polymers(Lipid orPolysaccharides)
Weak IgM No
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Clonal Selection
Figure 17.5
ANIMATION Humoral Immunity: Clonal Selection and Expansion
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Clonal deletion: eliminates harmful B cells
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Immune Responses to an Antigen
Figure 17.16
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Immune Responses to an Antigen
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Monoclonal Ab Production
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The Results of Ag-Ab Binding
Figure 17.7
1. Destroy2. Made unavailable
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IV. Cellular Immunity
T cells mature in the thymus Thymic selection eliminates many immature T cells
T cells respond to Ag by T-cell receptors (TCRs) T cells require antigen-presenting cells (APCs)
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T Helper Cells
CD4+ or TH cells (When activated) Produce cytokines Help in B cell and Tc cell activation
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T Cytotoxic Cells CD8+ or TC cells Target cells are self carrying endogenous
antigens Activated into cytotoxic T lymphocytes (CTLs) CTL causes apoptosis
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T Cytotoxic Cells
Figure 17.11
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T Regulatory Cells
Treg cells CD4 and CD25 on surface
Suppress T cells against self
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Antigen-Presenting Cells
Digest antigen Ag fragments on APC surface with MHC
B cells Dendritic cells Activated macrophages
ANIMATION Antigen Processing and Presentation: MHC
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A Dendritic Cell
Figure 17.13
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Activated Macrophages
Figure 17.14
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Granular leukocytes destroy cells that don’t express MHC I
Kill virus-infected and tumor cells Attack parasites
Natural Killer (NK) Cells
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Cells Communicate via CytokinesCytokine Representative ActivityInterleukin-1 (IL-1) Stimulates TH cells in presence of antigens; attracts
phagocytesInterleukin-2 (IL-2) Proliferation of antigen-stimulated CD4+ T helper cells,
proliferation and differentiation of B cells; activation of CD8+ T cells and NK cells
Interleukin-12 (IL-12) Inhibits humoral immunity; activates TH1 cellular immunity
Cytokine Representative ActivityLymphokines Induce the migration of leukocytes
TNF-α Promotes inflammation
Hematopoietic cytokines
Influence differentiation of blood stem cells
IFN-a and IFN-b Response to viral infection; interfere with protein synthesis
IFN-g Stimulates macrophage activity
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Immunological Disorders Hypersensitivity
– Type I: Immediate or anaphylactic– Type II: Cytotoxic– Type III: Complex– Type IV: Delayed or Cell-mediated– Autoimmune
Immunodeficiency– Primary: Genetic, developmental defects– Secondary: Due to infection, cancer,
malnutrition / stress
Type I Hypersensitivity (Anaphylactic)
IgE Histamine
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Type II Cytotoxic• ABO blood types• Hemolytic disease of the newborn:
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Hemolytic Disease of the Newborn
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Type III: Immune Complex
Arthus Reaction:
Serum Sickness:
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Type IV: Delayed (Cell-mediated)
Contact dermatitis: Poison ivy Tuberculin skin test Feature: Always localized
Type I Type II Type III Type IV
Main Mediator IgE IgG, IgM IgG, IgM T cells
Therapy Desensitization, antihistamines , steroids, epinephrine
Steroids Steroids Steroids
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Autoimmune Disease
Rhumatoids
Examples
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Transplantation Issues
Rejection
Tolerance
Immunosuppression
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Immunodeficiency Disorders
Primary– Agammaglobulinemia: No Ig– DiGeorge syndrome: Thymus undeveloped,
no T cell– Severe combined immunodeficiency (SCID):
Defect in IL12 gene Secondary
– AIDS– Leukemia
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Precipitation Tests
Precipitation
Immunodiffusion
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Agglutination Tests
Agglutination
Hemagglutination
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Complement Fixation
Ab/Ag complex competition
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Immunological Tests (cont.)
Neutralization Immuno-
fluorescence
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ELISA Tests
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Western Blots
Protein profiling
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