the concept of immunity

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


An Overview of the Body’s Defenses

Figure 16.1

ANIMATION Host Defenses: The Big Picture


First Line of Defense: I. Skin & Mucous Membranes

Skin Keratin, a protective protein

Mucous membranes Hairs Cilia Tears, Saliva, Urine,

Vaginal secretions Lysozyme


Ciliary Escalator

Figure 24.7


II. Normal Microbiota

Normal microbiota compete with pathogens for nutrients

Keep pH unfavorable for disease microbes


Red Blood Cells Transport O2 and CO2

White Blood Cells:Neutrophils Phagocytosis

Basophiles Histamine

Eosinophils Kill with toxin

Second Line of DefenseI. Blood components


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


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


II. Lymphatic SystemTissue + Fluid

Figure 16.5a


III. Phagocytosis

Neutrophils

Macrophage Presents Ag Secret cytokines

(lymphokines + interleukins)

Figure 16.6


IV. Inflammation

Releasing histamine Vasodilation (histamine, kinins, prostaglandins,

and leukotrienes) Redness Swelling Pain Heat

Tissue repair and wall-off


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


V. Antimicrobial Substances ComplementsC3a + C5a cause inflammationC5b + C6 + C7 + C8 + C9 cause cell lysis


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


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

Copyright © 2010 Pearson Education, Inc.Dua

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Figure 17.8


Dual Nature of Adaptive Immunity

Humoral immunity: B-cells Ag-Ab

Cellular immunity T-cells Cytokines

ANIMATION Humoral Immunity: Overview


I. Antigens

It has to be large Ag determinants = epitopes Hapten and Carrier


Antigens

Figure 17.1


Haptens

Figure 17.2


II. Antibodies

They are immunoglobulins (Ig) The antigen-binding sites recognize epitope and

determine valence Constant Region / Variable Region Heavy Chain / Light Chain


Antibodies

Figure 17.3a,b


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


Pentamer Agglutination Fix complement Agglutinates microbes; first Ab

produced in response to infection Half-life = 5 days

IgM Antibodies


IgA Antibodies

Dimer 10–15% of serum Abs In secretions Mucosal protection Half-life = 6 days


Monomer In blood, in lymph, and on B cells On B cells, initiate immune response Half-life = 3 days

IgD Antibodies


Monomer Allergic reactions; lysis of

parasitic worms Half-life = 2 days

IgE Antibodies


Diversity Self – non-self discrimination Memory

III. B Cells


1st exposure to Ag

2nd exposure to Ag

First Clones


T-independent Activation of B Cells

Figure 17.6


T-dependent Activation of B Cells

Figure 17.4


Ag Response Ig Memory

T-dependent Proteins Strong IgG Yes

T-independent Polymers(Lipid orPolysaccharides)

Weak IgM No


Clonal Selection

Figure 17.5

ANIMATION Humoral Immunity: Clonal Selection and Expansion


Clonal deletion: eliminates harmful B cells


Immune Responses to an Antigen

Figure 17.16


Immune Responses to an Antigen


Monoclonal Ab Production


The Results of Ag-Ab Binding

Figure 17.7

1. Destroy2. Made unavailable


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)


T Helper Cells

CD4+ or TH cells (When activated) Produce cytokines Help in B cell and Tc cell activation


T Cytotoxic Cells CD8+ or TC cells Target cells are self carrying endogenous

antigens Activated into cytotoxic T lymphocytes (CTLs) CTL causes apoptosis


T Cytotoxic Cells

Figure 17.11


T Regulatory Cells

Treg cells CD4 and CD25 on surface

Suppress T cells against self


Antigen-Presenting Cells

Digest antigen Ag fragments on APC surface with MHC

B cells Dendritic cells Activated macrophages

ANIMATION Antigen Processing and Presentation: MHC


A Dendritic Cell

Figure 17.13


Activated Macrophages

Figure 17.14


Granular leukocytes destroy cells that don’t express MHC I

Kill virus-infected and tumor cells Attack parasites

Natural Killer (NK) Cells


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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