© 2012 Pearson Education, Inc. Figure 22-11 Innate Defenses (Part 1 of 2) Innate Defenses Physical...

© 2012 Pearson Education, Inc.

Figure 22-11 Innate Defenses (Part 1 of 2)

Innate Defenses

Physical barrierskeep hazardousorganisms andmaterials outsidethe body.

Phagocytesengulf pathogensand cell debris.

Immunologicalsurveillanceis the destruction ofabnormal cells by NKcells in peripheral tissues.

Interferonsare chemical messengersthat coordinate thedefenses against viralinfections.

Duct of eccrinesweat gland Hair

Fixedmacrophage Neutrophil

Freemacrophage

Naturalkiller cell

Lysedabnormalcell

Eosinophil Monocyte

Secretions

Epithelium

Interferons released by activatedlymphocytes, macrophages, orvirus-infected cells

p. 779


Figure 22-12 How Natural Killer Cells Kill Cellular Targets (Step 1)

Recognition andAdhesion

NK cell Golgi apparatus

Abnormalcell

p. 781



Realignment of Golgi apparatus

p. 781



Secretion of Perforin

Perforinmolecules

NKcell

Abnormalcell

Pores formedby perforincomplex

p. 781



Lysis of Abnormal Cell

p. 781



Innate Defenses

Physical barrierskeep hazardousorganisms andmaterials outsidethe body.

Phagocytesengulf pathogensand cell debris.

Immunologicalsurveillanceis the destruction ofabnormal cells by NKcells in peripheral tissues.

Interferonsare chemical messengersthat coordinate thedefenses against viralinfections.

Duct of eccrinesweat gland Hair

Fixedmacrophage Neutrophil

Freemacrophage

Naturalkiller cell

Lysedabnormalcell

Eosinophil Monocyte

Secretions

Epithelium

Interferons released by activatedlymphocytes, macrophages, orvirus-infected cells

p. 779


Figure 22-13 Interferons

Alpha ()-interferons areproduced by cells infectedwith viruses. They attractand stimulate NK cells andenhance resistance to viralinfection.

Beta ()-interferons,secreted by fibroblasts,slow inflammation in adamaged area.

Gamma ()-interferons,secreted by T cells and NKcells, stimulatemacrophage activity.

p. 782



Complementsystemconsists of circulatingproteins that assistantibodies in thedestruction of pathogens.

is a localized, tissue-levelresponse that tends tolimit the spread of aninjury or infection.

Inflammatoryresponse

is an elevation of bodytemperature that acceleratestissue metabolism and theactivity of defenses.

Fever

Mast cell

Complement

Lysedpathogen

Body temperature rises above 37.2ºC inresponse to pyrogens

1. Blood flow increased2. Phagocytes activated3. Capillary permeability increased

7. Adaptive defenses activated

4. Complement activated5. Clotting reaction walls off region6. Regional temperature increased

Innate Defenses

p. 779


Figure 22-14 Pathways of Complement Activation (Part 2 of 3)

The most rapid and effective activationof the complement system occursthrough the classical pathway.

Activation and Cascade

C3b Attachment(classical pathway)

C3b Attachment(alternate pathway)

The classical pathwayends with the conversionof an inactive C3 to anactivated C3b thatattaches to the cell wall.

The attached C1 proteinthen acts as an enzyme,catalyzing a series ofreactions involving othercomplement proteins.

C3b

C3bC3b

C3C2

C1

C1 attachment

Classical Pathway

Antibody Binding andC1 Attachment

Antibody binding

Antibodies

Bacterialcell wall

C4

p. 783


Figure 22-14 Pathways of Complement Activation (Part 1 of 3)

The alternativepathway is importantin the defenseagainst bacteria,some parasites, andvirus-infected cells.

Alternative Pathway

C3

C3b

The alternative pathway beginswhen several complementproteins, notably properdin,interact in the plasma. Thisinteraction can be triggered byexposure to foreign materials,such as the capsule of abacterium. The end result is theattachment of an activated C3bprotein to the bacterial cell wall.

ProperdinFactor BFactor D

Bacterialcell wall

p. 783







Fever

Mast cell

Complement

Lysedpathogen





Innate Defenses

p. 779


Figure 22-15 Inflammation and the Steps in Tissue Repair (Part 1 of 2)

Tissue Damage

Mast Cell Activation

Chemical changein interstitial fluid

Release ofhistamine andheparin frommast cells

p. 784


Figure 22-15 Inflammation and the Steps in Tissue Repair (Part 2 of 2)

Redness, Swelling, Warmth, and Pain Phagocyte Attraction

Attraction ofphagocytes,especiallyneutrophils

Release ofcytokines

Dilation ofblood vessels,increased bloodflow, increasedvesselpermeability

Clotformation(temporaryrepair)

Removal ofdebris byneutrophilsand macro-phages;stimulation offibroblasts

Activation of specificdefenses

Pathogenremoval, cloterosion, scartissue formation

Tissue Repair

p. 784







Fever

Mast cell

Complement

Lysedpathogen





Innate Defenses

p. 779


Figure 22-17 An Overview of the Immune Response

Adaptive Defenses

Cell-MediatedImmunity

Direct Physical andChemical Attack

Antibody-MediatedImmunity

Attack by CirculatingAntibodies

Destructionof antigens

Phagocytesactivated

T cellsactivated

Communicationand feedback

Antigen presentationtriggers specificdefenses, or animmune response.

Activated Bcells give riseto cells thatproduceantibodies.

Activated T cells findthe pathogens andattack them throughphagocytosis or therelease of chemicaltoxins.

p. 787


Figure 22-16 Forms of Immunity

Immunity

Response to threats on anindividualized basis

Adaptive Immunity

Active Immunity Passive Immunity

Adaptive immunity is not present at birth; youacquire immunity to a specific antigen only whenyou have been exposed to that antigen or receiveantibodies fromanother source.

Develops in responseto antigen exposure

Develops afterexposure toantigens inenvironment

Develops afteradministration ofan antigen toprevent disease

Conferred bytransfer of maternalantibodies across placenta or inbreast milk

Conferred byadministration ofantibodies tocombat infection

Naturally acquiredactive immunity

Artificially inducedactive immunity

Naturally acquiredpassive immunity

Artificially inducedpassive immunity

Geneticallydeterminednoprior exposure orantibodyproductioninvolved

Innate Immunity

Produced by transferof antibodies fromanother source

p. 786


Figure 22-18a Antigens and MHC Proteins

Antigen presentationby Class I MHCproteins is triggered byviral or bacterialinfection of a body cell.

The infection resultsin the appearance ofabnormal peptides inthe cytoplasm.

The abnormal peptidesare incorporated intoClass I MHC proteinsas they are synthesizedat the endoplasmicreticulum.

Plasma membrane

Viral or bacterialpathogen

Transportvesicle

Endoplasmicreticulum

Nucleus

The abnormalpeptides aredisplayed by Class IMHC proteins on theplasma membrane.

After export to theGolgi apparatus, theMHC proteins reachthe plasmamembrane withintransport vesicles.

Infected cell

p. 789


Figure 22-18b Antigens and MHC Proteins

Antigenic fragments aredisplayed by Class IIMHC proteins on theplasma membrane.

Antigenic fragments are bound to Class IIMHC proteins.

The endoplasmicreticulum producesClass II MHC proteins.

Plasmamembrane

Endoplasmicreticulum

NucleusLysosome

Phagocytic antigen-presenting cell

Lysosomal actionproduces antigenicfragments.

Phagocytic APCsengulf the extracellularpathogens.

p. 789

p. 771

Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings © 2012 Pearson Education, Inc.


Figure 22-5 Classes of Lymphocytes (Part 1 of 2)

Classes of Lymphocytes

subdivided into

can differentiate into

T Cells

Approximately 80% ofcirculating lymphocytes areclassified as T cells.

CytotoxicT Cells

Helper T Cells

Cytotoxic T cellsattack foreign cellsor body cellsinfected by viruses.

Helper T cellsstimulate theactivation andfunction ofboth T cellsand B cells.

Suppressor Tcells inhibitthe activationand functionof both Tcells and B cells.

Memory T cellsare a subset ofT cells thatrespond to a previouslyencountered antigen.

Memory T Cells

SuppressorT Cells

p. 770


Figure 22-5 Classes of Lymphocytes (Part 2 of 2)

subdivided into

B Cells

Plasma Cells

When stimulated,B cells candifferentiate intoplasma cells, whichproduce and secreteantibodies.

B cells make up1015% of circulatinglymphocytes.

NK cells makeup the remaining510% ofcirculatinglymphocytes.

NK Cells

Classes of Lymphocytes

p. 770


Figure 22-19 Antigen Recognition by and Activation of Cytotoxic T Cells (Steps 1-3)

Antigen Recognition Activation andCell Division

Infected cell

InactiveCD8

T cell

Viral orbacterial antigen

Antigen recognition occurswhen a CD8 T cell encountersan appropriate antigen on thesurface of another cell, boundto a Class I MHC protein.

Antigen recognition resultsin T cell activation and celldivision, producing active TC

cells and memory TC cells.

Active TC cell

Memory TC cells(inactive)

Infectedcell

CD8protein

Class IMHC

T cellreceptor

CD8T cell

Antigen

Costimulationactivates

CD8 T cell

Before activationcan occur, aT cell must bechemically orphysicallystimulated bythe abnormaltarget cell.

Costimulation

p. 790


Figure 22-19 Antigen Recognition by and Activation of Cytotoxic T Cells (Steps 4)

Destruction of Target Cells

The active TC cell destroys theantigen-bearing cell. It may useseveral different mechanisms tokill the target cell.

Lysedcell

Perforin release Destruction ofplasma membrane

Stimulation ofapoptosis

Disruption of cellmetabolism

Cytokine release

Lymphotoxin release

p. 790


Figure 22-21a A Summary of the Pathways of T Cell Activation

Activation by Class I MHC proteins

Antigen bound toClass I MHC protein

Indicates that the cell is infectedor otherwise abnormal

CD8 T Cells

Cytotoxic T Cells Memory TC Cells

Attack and destroyinfected and

abnormal cellsdisplaying antigen

Awaitreappearanceof the antigen

Control or moderateimmune response by

T cells and B cells

Suppressor T Cells

p. 792


Figure 22-20 Antigen Recognition and Activation of Helper T Cells (Part 1 of 2)

Antigen Recognition by CD4 T Cell

Foreign antigen

Antigen-presentingcell (APC)

Class II MHCAPC

Antigen

T cell receptor

Costimulation

CD4 protein

TH cell

InactiveCD4 (TH)cell

p. 791


Figure 22-20 Antigen Recognition and Activation of Helper T Cells (Part 2 of 2)

CD4 T Cell Activation and Cell Division

Memory TH cells(inactive)

Active TH cells

Cytokines

Active helper T cells secretecytokines that stimulate bothcell-mediated andantibody-mediated immunity.

Cytokines

Cytokines

p. 791


Figure 22-21b A Summary of the Pathways of T Cell Activation

Activation by Class II MHC proteins

Helper T Cells

Stimulate immuneresponse by

T cells and B cells


Memory TH Cells

CD4 T Cells

Indicates presence of pathogens,toxins, or foreign proteins

Antigen bound toClass II MHC protein

p. 792

Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings © 2012 Pearson Education, Inc.

p. 771


Figure 22-22 The Sensitization and Activation of B Cells (Step 1)

Sensitization

SensitizedB cell

Antigenbinding

Antigens bound toantibody molecules

Antigens

Class II MHC

Antibodies

Inactive B cell

p. 793



Activation

Cytokinecostimulation

Helper T cell

T cell

SensitizedB cell

B cell

Class II MHC T cell receptor

Antigen

p. 793



Division and Differentiation

Plasma cells

ANTIBODYPRODUCTION

Activated B cells

Memory B cells(inactive)

p. 793


Figure 22-21b A Summary of the Pathways of T Cell Activation

Activation by Class II MHC proteins

Helper T Cells

Stimulate immuneresponse by

T cells and B cells


Memory TH Cells

CD4 T Cells

Indicates presence of pathogens,toxins, or foreign proteins

Antigen bound toClass II MHC protein

p. 792


Figure 22-23a Antibody Structure and Function

Antigenbinding

site

Variablesegment

Constantsegments

of lightand heavy

chains

Heavy chain

Disulfidebond

Antigenbinding site

Light chain

Complementbinding site

Site of bindingto macrophages

A diagrammatic view of the structure of an antibody.

p. 794


Figure 22-23c Antibody Structure and Function

Antigen

Antigenicdeterminant

sites

Antibodies

Antibodies bind to portions ofan antigen called antigenicdeterminant sites, or epitopes.

p. 794


Figure 22-23d Antibody Structure and Function

Antibody molecules can bind ahapten (partial antigen) once it hasbecome a complete antigen bycombining with a carrier molecule.

Completeantigen

HaptenCarrier

molecule

p. 794


Table 22-1 Classes of Antibodies (Part 1 of 2)

p. 795


Table 22-1 Classes of Antibodies (Part 2 of 2)

Secretorypiece

p. 795


Figure 22-24a The Primary and Secondary Responses in Antibody-Mediated Immunity

Time (weeks)

IgGIgM

An

tib

od

yco

nce

ntr

atio

n i

n s

eru

m PRIMARYRESPONSE

p. 796


Figure 22-24b The Primary and Secondary Responses in Antibody-Mediated Immunity

Time (weeks)

IgM

SECONDARYRESPONSE

IgG

p. 796


Figure 22-25 The Course of the Body’s Response to a Bacterial Infection

Neutrophils Macrophages Plasma cells

Antibodytiter

CytotoxicT cells

Naturalkiller cells

Time (weeks)

Nu

mb

er o

f ac

tive

im

mu

ne

cell

s

p. 797


Figure 22-27a Defenses against Bacterial and Viral Pathogens

BACTERIA

Phagocytosis bymacrophages and APCs

Antigenpresentation

Activation ofcytotoxic T cells

Activation ofhelper T cells

Activation of B cells

Antibodyproduction byplasma cells

Destruction ofbacteria bycell lysis or

phagocytosis

Opsonizationand phagocyte

attraction

Formation ofantigenantibody

complexes

Defenses against bacteria involve phagocy-tosis and antigen presentation by APCs. p. 799


Figure 22-27b Defenses against Bacterial and Viral Pathogens

Release of interferons

Infection oftissue cells

Appearance of antigenin plasma membrane

Infection of or uptakeby APCs

VIRUSES

Antigenpresentation

Activation ofhelper T cells

Activation of B cells

Antibodyproduction byplasma cells

Destruction ofviruses or

prevention ofvirus entry into cells

Increasedresistance toviral infection

and spread

Stimulationof NK cells

Activation ofcytotoxic T cells

Destruction ofvirus-infected cells

Defenses against viruses involves direct contact with virus-infected cellsand antigen presentation by APCs. p. 799


Figure 22-29 The Mechanism of Anaphylaxis (Part 1 of 2)

FirstExposure Allergen fragment

AllergensMacrophage

B cell sensitizationand activation

TH cell activation

Plasma cell

IgE antibodies

p. 804


Figure 22-29 The Mechanism of Anaphylaxis (Part 2 of 2)

IgE

Granules

Massivestimulation of

mast cellsand basophils

Sensitization ofmast cells andbasophils

SubsequentExposure

Release of histamines, leukotrienes,and other chemicals that

cause pain and inflammation

Capillary dilation, increased capillarypermeability, airway constriction,mucus secretion, pain and itching

Allergen

p. 804

© 2012 Pearson Education, Inc. Figure 22-11 Innate Defenses (Part 1 of 2) Innate Defenses Physical...

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