Chapter 21A Immune System: Innate and Adaptive Defenses Slides by Barbara Heard and W. Rose. figures from Marieb & Hoehn 9 th ed. Portions copyright Pearson.

Chapter 21A Immune System: Innate and Adaptive Defenses

Slides by Barbara Heard and W. Rose.figures from Marieb & Hoehn 9th ed.

Portions copyright Pearson Education

Nobel Prizes for Immune System Discoveries2011 Beutler, Hoffmann, Steinman, "for their discoveries concerning the activation of innate immunity”; “for his discovery of the dendritic cell and its role in adaptive immunity”

[H: Toll receptors in fruit flies essential for innate immunity. B: Found Toll-like receptors in mammals & clarified their important role in innate immunity. S: Discovered dendritic cells & showed they have special ability to present antigens to & activate naïve T cells. Langerhans cells in skin are a subtype of DCs.] Dead fruit fly with fungus growing on it because it has mutant

Toll receptors. …&Hoffman, Cell, 1996.

Nobel Prizes for Immune System Discoveries

1996 Doherty, Zinkernagel“for their discoveries concerning the specificity of the cell mediated immune defence”[Discovered that killer T cells recognize virus-infected cells by simultaneous recognition of self & non-self markers. Explains benefits of HLA, which is a barrier to organ transplant.]

1987 Susumu Tonegawa"for his discovery of the genetic principle for generation of antibody diversity“[how to make millions of antibodiy proteins from a small number of genes by genetic shuffling]


1984 Jerne, Köhler, Milstein"for theories concerning the specificity in development and control of the immune system and the discovery of the principle for production of monoclonal antibodies"[Jerne: we are born with a full repertoire of antibodies and select the needed ones when we encounter a new pathogen. K. & M.: fused lymphocytes with tumor cells to create immortal cells (hybridomas) that make one antibody specifically]


1980 Benacerraf, Dausset, Snell"for their discoveries concerning genetically determined structures on the cell surface that regulate immunological reactions“[discovery & understanding of MHC (HLA in humans)]

1972 Edelman, Porter"for their discoveries concerning the chemical structure of antibodies“[Y shape, heavy & light chains, constant & variable regions]


1960 Burnet, Medawar"for discovery of acquired immunological tolerance“[Burnet: “immunological tolerance”; both showed how early immune system cells become self-tolerant]

1930 Landsteiner"for his discovery of human blood groups"[blood groups and blood typing]

1919 Bordet"for his discoveries relating to immunity"[antigens and antibodies]


1913 Richet"in recognition of his work on anaphylaxis“[Discovered & coined term for anaphylaxis & elucidated how it occurs.]

1908 Mechnikov, Ehrlich"in recognition of their work on immunity"[Mechinov discovered & coined the term phagocytosis & phagocytes; Erlich discovered antibodies]


1901 von Behring"for his work on serum therapy, especially its application against diphtheria, by which he has opened a new road in the domain of medical science and thereby placed in the hands of the physician a victorious weapon against illness and deaths“[von Behring discovered that when animals were injected with tiny doses of weakened forms of tetanus or diphtheria bacteria, their blood extracts contained chemicals released in response, which rendered the pathogens' toxins harmless.]

Immune System: Links to articlesTreating allergies with pills instead of shots NYT 20131206

The case against cleanliness: a skeptical review NYT 20120910

The boy with a thorn in his joints NYT 20130301 An interesting and moving article by a mother about her son, his juvenile idiopathic arthritis, and alternative medicine. Interesting comments too.

http://www.nytimes.com/2013/12/06/business/treating-allergies-with-pills-or-drops-instead-of-shots.html

http://www.nytimes.com/2012/09/11/science/an-epidemic-of-absence-review-seeing-hygiene-as-driver-of-disease.html

http://www.nytimes.com/2013/02/03/magazine/the-boy-with-a-thorn-in-his-joints.html

© 2013 Pearson Education, Inc.

Immunity

• Resistance to disease

• Immune system– Two intrinsic systems

• Innate (nonspecific) defense system• Adaptive (specific) defense system


Immune System

• Functional system rather than organ system

• Innate and adaptive defenses intertwined• Release and recognize many of same

defensive molecules• Innate defenses do have specific

pathways for certain substances• Innate responses release proteins that

alert cells of adaptive system to foreign molecules


Immunity

• Innate defense system has two lines of defense– First - external body membranes (skin and

mucosae)– Second - antimicrobial proteins, phagocytes,

and other cells • Inhibit spread of invaders • Inflammation most important mechanism


Immunity

• Adaptive defense system – Third line of defense attacks particular foreign

substances• Takes longer to react than innate system


Figure 21.1 Overview of innate and adaptive defenses.

Innatedefenses

Surface barriers• Skin• Mucous membranes

Internal defenses• Phagocytes• Natural killer cells• Inflammation• Antimicrobial proteins• Fever

Adaptivedefenses

Humoral immunity• B cells

Cellular immunity• T cells


Innate Defenses

• Surface barriers ward off invading pathogens– Skin, mucous membranes, and their

secretions • Physical barrier to most microorganisms• Keratin resistant to weak acids and bases,

bacterial enzymes, and toxins• Mucosae provide similar mechanical barriers


Surface Barriers

• Protective chemicals inhibit or destroy microorganisms– Acidity of skin and secretions – acid mantle –

inhibits growth – Enzymes - lysozyme of saliva, respiratory

mucus, and lacrimal fluid – kill many microorganisms

– Defensins – antimicrobial peptides – inhibit growth

– Other chemicals - lipids in sebum, dermcidin in sweat – toxic


Surface Barriers

• Respiratory system modifications– Mucus-coated hairs in nose – Cilia of upper respiratory tract sweep dust-

and bacteria-laden mucus toward mouth

• Surface barriers breached by nicks or cuts - second line of defense must protect deeper tissues


Internal Defenses: Cells and Chemicals

• Necessary if microorganisms invade deeper tissues– Phagocytic cells– Natural killer (NK) cells– Antimicrobial proteins (interferons and

complement proteins)– Fever– Inflammatory response (macrophages, mast

cells, WBCs, and inflammatory chemicals)


Phagocytic cells

• Neutrophils most abundant but die fighting– Become phagocytic on exposure to infectious material

• Macrophages develop from monocytes – chief phagocytic cells


Mechanism of Phagocytosis

• Phagocyte must adhere to particle– Some microorganisms evade adherence with

capsule • Opsonization marks pathogens—coating by

complement proteins or antibodies

• Cytoplasmic extensions bind to and engulf particle in vesicle


Figure 21.2a Phagocytosis.

Innate defenses Internal defenses

A macrophage (purple) uses its cytoplasmicextensions to pull rod-shaped bacteria(green) toward it. Scanning electronmicrograph (4800x).


Figure 21.2b Phagocytosis. Phagocyte adheres to pathogens or debris.

1

Phagocyte forms pseudopods that eventually engulf the particles, forming a phagosome.

Lysosome fuses with the phagocytic vesicle, forming a phagolysosome.

Lysosomal enzymes digest the particles, leaving a residual body.

Exocytosis of the vesicle removes indigestible and residual material.

2

3

4

5

Phagosome(phagocyticvesicle)

Lysosome

Acidhydrolaseenzymes

Events of phagocytosis.

Slide 1


Mechanism of Phagocytosis

• Pathogens killed by acidifying and digesting with lysosomal enzymes

• Helper T cells cause release of enzymes of respiratory burst, which kill pathogens resistant to lysosomal enzymes by– Releasing cell-killing free radicals

– Producing oxidizing chemicals (e.g., H2O2)

– Increasing pH and osmolarity of phagolysosome

• Defensins (in neutrophils) pierce membrane


Natural Killer (NK) Cells

• Nonphagocytic large granular lymphocytes

• Attack cells that lack "self" cell-surface receptors– Induce apoptosis in cancer cells and virus-

infected cells

• Secrete potent chemicals that enhance inflammatory response


Inflammatory Response

• Triggered whenever body tissues injured

• Prevents spread of damaging agents

• Disposes of cell debris and pathogens

• Alerts adaptive immune system

• Sets the stage for repair



• Cardinal signs of acute inflammation:1. Redness

2. Heat

3. Swelling

4. Pain

(Sometimes 5. Impairment of function)



• Begins with chemicals released into ECF by injured tissues, immune cells, blood proteins

• Macrophages and epithelial cells of boundary tissues bear Toll-like receptors (TLRs)

• 11 types of TLRs recognize specific classes of infecting microbes

• Activated TLRs trigger release of cytokines that promote inflammation



• Inflammatory mediators– Kinins, prostaglandins (PGs), and

complement • Dilate local arterioles (hyperemia)

– Causes redness and heat of inflamed region

• Make capillaries leaky• Many attract leukocytes to area• Some have inflammatory roles


Inflammatory Response: Edema

Capillary permeability exudate to tissues– Fluid containing clotting factors and

antibodies– Causes local swelling (edema)– Swelling pushes on nerve endings pain

• Pain also from bacterial toxins, prostaglandins, and kinins

– Moves foreign material into lymphatic vessels– Delivers clotting proteins and complement



• Clotting factors form fibrin mesh– Scaffold for repair– Isolates injured area so invaders cannot

spread


Figure 21.3 Inflammation: flowchart of events.Innate defenses Internal defenses

Initial stimulus

Physiological response

Signs of inflammation

Result

Arteriolesdilate

Local hyperemia(increased blood

flow to area)

Heat Redness

Release of inflammatory chemicals(histamine, complement,

kinins, prostaglandins, etc.)

Increased capillarypermeability

Capillariesleak fluid

(exudate formation)

Leaked protein-richfluid in tissue spaces

Pain Swelling

Possible temporaryimpairment of

function

Locally increasedtemperature increasesmetabolic rate of cells

Tissue injury

Attract neutrophils,monocytes, andlymphocytes to

area (chemotaxis)

Leaked clottingproteins form interstitialclots that wall off area

to prevent injury tosurrounding tissue

Temporary fibrinpatch forms

scaffolding for repair

Healing

Release of leukocytosis-inducing factor

Leukocytosis (increased numbers of whiteblood cells in bloodstream)

Leukocytes migrate toinjured area

Margination (leukocytes cling to

capillary walls)

Diapedesis (leukocytes pass through

capillary walls)

Phagocytosis of pathogensand dead tissue cells

(by neutrophils, short-term;by macrophages, long-term)

Pus may form

Area cleared of debris


Phagocyte Mobilization

• Neutrophils lead; macrophages follow– As attack continues, monocytes arrive

• 12 hours after leaving bloodstream macrophages

• These "late-arrivers" replace dying neutrophils and remain for clean up prior to repair

• If inflammation is due to pathogens, complement will be activated; cells of adaptive immunity will arrive


Phagocyte Mobilization

• Steps for phagocyte mobilization1. Leukocytosis: release of neutrophils from

bone marrow in response to leukocytosis-inducing factors from injured cells

2. Margination: neutrophils cling to walls of capillaries in inflamed area in response to CAMs

3. Diapedesis of neutrophils4. Chemotaxis: inflammatory chemicals

(chemotactic agent) promote positive chemotaxis of neutrophils


Figure 21.4 Phagocyte mobilization.


Inflammatorychemicals diffusing from the inflamed site act aschemotactic agents.

Leukocytosis.Neutrophils enter blood from bone marrow.

Margination.Neutrophils clingto capillary wall.

Diapedesis.Neutrophils flattenand squeeze out of capillaries.

1 2 3

Chemotaxis.Neutrophils follow chemical trail.

Capillary wallBasementmembraneEndothelium

4

Slide 1


Antimicrobial Proteins

• Include interferons and complement proteins

• Some attack microorganisms directly

• Some hinder microorganisms' ability to reproduce


Interferons

• Family of immune modulating proteins– Have slightly different physiological effects

• Viral-infected cells secrete IFNs (e.g., IFN alpha and beta) to "warn" neighboring cells– IFNs enter neighboring cells produce

proteins that block viral reproduction and degrade viral RNA

– IFN alpha and beta also activate NK cells


Interferons

• IFN gamma (immune interferon)– Secreted by lymphocytes– Widespread immune mobilizing effects– Activates macrophages

• Since IFNs activate NK cells and macrophages, indirectly fight cancer

• Artificial IFNs used to treat hepatitis C, genital warts, multiple sclerosis, hairy cell leukemia


Figure 21.5 The interferon mechanism against viruses. Slide 1


VirusViral nucleic acid

New viruses

Antiviral proteinsblock viralreproduction.

Interferon genes switch on.

DNA

AntiviralmRNA

Nucleus

mRNA forinterferon

Cell produces interferon molecules. Interferon

Interferonreceptor

Host cell 1Host cell 2

Infected by virus;makes interferon;is killed by virus

Binds interferonfrom cell 1; interferoninduces synthesis ofprotective proteins

Virus enters cell. 5

Interferon binding stimulates cell toturn on genes for antiviral proteins.

4

1

2

3


Complement System (Complement)

• ~20 blood proteins that circulate in inactive form

• Include C1–C9, factors B, D, and P, and regulatory proteins

• Major mechanism for destroying foreign substances

• Our cells contain complement activation inhibitors


Complement

• Unleashes inflammatory chemicals that amplify all aspects of inflammatory response

• Kills bacteria and certain other cell types by cell lysis

• Enhances both innate and adaptive defenses


Complement Activation

• Three pathways to activation– Classical pathway

• Antibodies bind to invading organisms and to complement components

• Called complement fixation• First step in activation; more details later

– Lectin pathway– Alternative pathway


Complement

Lectin pathwayLectins: proteins produced by liver

Some bind to mannose (sugar) residues found on surface of many pathogens.

When lectin binds, it can activate other proteins in the complement pathway.


Complement

Alternative pathwayComplement system is in a continuous low level of activation

Complement regulatory proteins on host cells (i.e. our own cells) keep complement system in check

Many pathogens lack complement regulatory proteins, so their presence allows complement to become activated



• Each pathway involves activation of proteins in an orderly sequence

• Each step catalyzes the next

• Each pathway converges on C3, which cleaves into C3a and C3b

• Common terminal pathway initiated that– Enhances inflammation, promotes

phagocytosis, causes cell lysis



• Cell lysis begins when– C3b binds to target cell insertion of complement

proteins called membrane attack complex (MAC) into cell's membrane

– MAC forms and stabilizes hole in membrane influx of water lysis of cell

• C3b also causes opsonization• C3a and other cleavage products amplify

inflammation – Stimulate mast cells and basophils to release

histamine– Attract neutrophils and other inflammatory cells


Figure 21.6 Complement activation.

Classical pathwayActivated by antibodiescoating target cell

Lectin pathwayActivated by lectinsbinding to specific sugarson microorganism’s surface

Alternative pathwayActivated spontaneously. Lack ofinhibitors on microorganism’ssurface allows process to proceed

Together with other complementproteins and factors

Opsonization:Coats pathogen surfaces, which enhances phagocytosis

MACs form from activated complement components (C5b and C6–C9) that insert into the target cell membrane, creating pores that can lyse the target cell.

Enhances inflammation:Stimulates histaminerelease, increases blood vessel permeability,attracts phagocytes bychemotaxis, etc.

Pore

Complementproteins(C5b–C9)

Membrane of target cell

C3

C3b

C3b

C5b

C6

C7

C8

C9

C3a

C5a

MA

C


Fever

• Abnormally high body temperature

• Systemic response to invading microorganisms

• Leukocytes and macrophages exposed to foreign substances secrete pyrogens

• Pyrogens act on body's thermostat in hypothalamus, raising body temperature


Fever

• Benefits of moderate fever– Causes liver and spleen to sequester iron and

zinc (needed by microorganisms)– Increases metabolic rate faster repair(?)


Adaptive Defenses

• Adaptive immune (specific defense) system– Protects against infectious agents and

abnormal body cells – Amplifies inflammatory response– Activates complement– Must be primed by initial exposure to specific

foreign substance• Priming takes time


Adaptive Defenses

• Specific – recognizes and targets specific antigens

• Systemic – not restricted to initial site

• Have memory – stronger attacks to "known" antigens

• Two separate, overlapping arms– Humoral (antibody-mediated) immunity– Cellular (cell-mediated) immunity


Humoral Immunity

• Antibodies, produced by lymphocytes, circulating freely in body fluids

• Bind temporarily to target cell– Temporarily inactivate– Mark for destruction by phagocytes or

complement

• Humoral immunity has extracellular targets


Cellular Immunity

• Lymphocytes act against target cell– Directly – by killing infected cells– Indirectly – by releasing chemicals that

enhance inflammatory response; or activating other lymphocytes or macrophages

• Cellular immunity has cellular targets


Antigens

• Antibody Generators

• Substances that can mobilize adaptive defenses and provoke an immune response

• Targets of all adaptive immune responses

• Most are large, complex molecules not normally found in body (nonself)


Complete Antigens

• Important functional properties– Immunogenicity: ability to stimulate

proliferation of specific lymphocytes– Reactivity: ability to react with activated

lymphocytes and antibodies released by immunogenic reactions

• Examples: foreign protein, polysaccharides, lipids, and nucleic acids


Haptens (Incomplete Antigens)

• Small molecules (haptens) not immunogenic by themselves– E.g., peptides, nucleotides, some hormones

• May be immunogenic if attached to body proteins and combination is marked foreign

• Cause immune system to mount harmful attack

• Examples: poison ivy, animal dander, detergents, and cosmetics


Antigenic Determinants

• Only certain parts (antigenic determinants) of entire antigen are immunogenic

• Antibodies and lymphocyte receptors bind to them as enzyme binds substrate


Antigenic Determinants

• Most naturally occurring antigens have numerous antigenic determinants that– Bind to different antibodies– Mobilize several different lymphocyte

populations

• Large, chemically simple molecules (e.g., plastics) have little or no immunogenicity


Figure 21.7 Most antigens have several different antigenic determinants.

Antibody A

Antigen-bindingsites

Antibody BAntibody C

Antigenic determinants

Antigen


Self-antigens: MHC Proteins

• Protein molecules (self-antigens) on surface of cells not antigenic to self but antigenic to others in transfusions or grafts

• Example: MHC glycoproteins– Coded by genes of major histocompatibility

complex (MHC) and unique to individual


Cells of the Adaptive Immune System

– Two types of lymphocytes• B lymphocytes (B cells)—humoral immunity• T lymphocytes (T cells)—cellular immunity

– Antigen-presenting cells (APCs)• Do not respond to specific antigens• Play essential auxiliary roles in immunity


Adaptive defensesHumoral immunityCellular immunity

Primary lymphoid organs(red bone marrow and thymus)

Secondary lymphoid organs(lymph nodes, spleen, etc.)

Origin• Both B and T lymphocyte precursors originate in red bone marrow.

Maturation• Lymphocyte precursors destined to become T cells migrate (in blood) to the thymus and mature there.• B cells mature in the bone marrow.• During maturation lymphocytes develop immunocompetence and self-tolerance.

Seeding secondary lymphoid organs and circulation• Immunocompetent but still naive lymphocytes leave the thymus and bone marrow.• They “seed” the secondary lymphoid organs and circulate through blood and lymph.

Antigen encounter and activation• When a lymphocyte’s antigen receptors bind its antigen, that lymphocyte can be activated.

Proliferation and differentiation• Activated lymphocytes proliferate (multiply) and then differentiate into effector cells and memory cells.• Memory cells and effector T cells circulate continuously in the blood and lymph and throughout the secondary lymphoid organs.

Red bone marrowRed bone marrow

Lymphocyteprecursors

Thymus

Red bone marrow

Lymph node

Antigen

1

2

3

4

5

Slide 1Figure 21.8 Lymphocyte development, maturation, and activation.


Maturation

• "Educated" to become mature; B cells in bone marrow, T cells in thymus– Immunocompetence – lymphocyte can

recognize one specific antigen by binding to it• B or T cells display only one unique type of antigen

receptor on surface when achieve maturity – bind only one antigen

– Self-tolerance• Lymphocytes unresponsive to own antigens


T cells

• T cells mature in thymus under negative and positive selection pressures ("tests")– Positive selection

• Selects T cells capable of recognizing self-MHC proteins (MHC restriction); failures destroyed by apoptosis

– Negative selection• Prompts apoptosis of T cells that bind to self-

antigens displayed by self-MHC• Ensures self-tolerance


Cellular immunityAdaptive defenses

1. Positive Selection

T cells must recognize self major histocompatibilityproteins (self-MHC)Antigen-presentingthymic cell

DevelopingT cell

Failure to recognize self-MHC results in apoptosis(death by cell suicide).

T cell receptorSelf-MHCSelf-antigen

Recognizing self-MHCresults in survival.Survivors proceedto negative selection.

2. Negative Selection

T cells must not recognize self-antigens

Recognizing self-antigenresults in apoptosis. Thiseliminates self-reactiveT cells that could causeautoimmune diseases.

Failure to recognize (bindtightly to) self-antigenresults in survival andcontinued maturation.

Figure 21.9 T cell education in the thymus.


B cells

• B cells mature in red bone marrow

• Positively selected if successfully make antigen receptors

• Those that are self-reactive – Eliminated by apoptosis (clonal deletion)


Seeding Secondary Lymphoid Organs and Circulation

• Immunocompetent B and T cells not yet exposed to antigen called naive

• Move from primary lymphoid organs (bone marrow and thymus) to "seed" secondary lymphoid organs (lymph nodes, spleen, etc.)


Antigen Encounter and Activation

• Clonal selection– Naive lymphocyte's first encounter with

antigen selected for further development – If correct signals present, lymphocyte will

complete its differentiation


Proliferation and Differentiation

• Activated lymphocyte proliferates exact clones

• Most clones effector cells that fight infections

• A few remain as memory cells– Able to respond to same antigen more quickly

second time

• B and T memory cells and effector T cells circulate continuously


Antigen Receptor Diversity

• Genes, not antigens, determine which foreign substances immune system will recognize– Immune cell receptors result of acquired

knowledge of microbes likely in environment

• Lymphocytes make a billion or more different types of antigen receptors– Coded for by ~1,000 genes– Gene segments are shuffled by somatic

recombination


Table 21.3 Overview of B and T Lymphocytes


Antigen-presenting Cells (APCs)

• Engulf antigens

• Present fragments of antigens to T cells for recognition

• Major types– Dendritic cells in connective tissues and

epidermis– Macrophages in connective tissues and

lymphoid organs– B cells


Dendritic Cells and Macrophages

• Dendritic cells phagocytize pathogens, enter lymphatics to present antigens to T cells in lymph node– Most effective antigen presenter known– Key link between innate and adaptive

immunity

• Macrophages widespread in lymphoid organs and connective tissues– Present antigens to T cells to activate

themselves into voracious phagocytes that secrete bactericidal chemicals


Adaptive Immunity: Summary

• Uses lymphocytes, APCs, and specific molecules to identify and destroy nonself substances

• Depends upon ability of its cells to– Recognize antigens by binding to them– Communicate with one another so that whole

system mounts specific response


Activation and Differentiation of B Cells

• B cell activated when antigens bind to its surface receptors

• Causes proliferation and differentiation into effector cells (mostly plasma cells, a few memory B cells)


Fate of the Clones

• Most clone cells become plasma cells– Secrete specific antibodies at rate of 2000

molecules per second for four to five days, then die

– Antibodies circulate in blood or lymph• Bind to free antigens and mark for destruction by

innate or adaptive mechanisms


Fate of the Clones

• Clone cells that do not become plasma cells become memory B cells– Provide immunological memory– Allow stronger, faster response to future

exposures to same antigen


Figure 21.11a Clonal selection of a B cell.

Adaptive defenses Humoral immunity

Primary response(initial encounterwith antigen)

AntigenAntigen bindingto a receptor on aspecific B lymphocyte(B lymphocytes withnoncomplementaryreceptors remaininactive)

Proliferation toform a cloneActivated B cells

Plasma cells(effector B cells)

Memory B cell—primed to respondto same antigen

Secretedantibodymolecules


Immunological Memory

• Primary immune response– Cell proliferation and differentiation upon first

antigen exposure– Lag period: three to six days – Peak levels of plasma antibody are reached in

10 days– Antibody levels then decline


Immunological Memory

• Secondary immune response– Re-exposure to same antigen gives faster,

more prolonged, more effective response• Sensitized memory cells respond within hours• Antibody levels peak in two to three days at much

higher levels • Antibodies bind with greater affinity• Antibody level can remain high for weeks to

months


Adaptive defenses Humoral immunity

Primary response(initial encounterwith antigen)

Antigen

Antigen bindingto a receptor on aspecific B lymphocyte(B lymphocytes withnoncomplementaryreceptors remaininactive)

Proliferation toform a clone

Activated B cells

Plasma cells(effector B cells)

Memory B cell—primed to respondto same antigen

Secondary response (can be years later)

Clone of cellsidentical toancestral cells

Subsequentchallenge by sameantigen results inmore rapid response

Plasmacells


MemoryB cells


Figure 21.11 Clonal selection of a B cell.


Figure 21.12 Primary and secondary humoral responses.

Anti

body t

iter

(anti

body c

once

ntr

ati

on)

in p

lasm

a (

arb

itra

ry u

nit

s)

100

101

102

103

104

0 7 14 21 28 35 42 49 56

First exposureto antigen A

Second exposure to antigen A;first exposure to antigen B

Primary immuneresponse to antigenA occurs after a delay.

Secondary immune response toantigen A is faster and larger; primaryimmune response to antigen B issimilar to that for antigen A.

Time (days)

Anti-Bodiesto A

Anti-Bodiesto B


Active Humoral Immunity

• When B cells encounter antigens and produce specific antibodies against them

• Two types of active humoral immunity:– Naturally acquired—response to bacterial or

viral infection– Artificially acquired—response to vaccine of

dead or attenuated pathogens


Active Humoral Immunity

• Vaccines– Most of dead or attenuated pathogens– Spare us symptoms of primary response– Provide antigenic determinants that are

immunogenic and reactive


Passive Humoral Immunity

• Readymade antibodies introduced into body

• B cells are not challenged by antigens

• Immunological memory does not occur

• Protection ends when antibodies degrade


Passive Humoral Immunity

• Two types1. Naturally acquired—antibodies delivered to

fetus via placenta or to infant through milk

2. Artificially acquired—injection of serum, such as gamma globulin• Protection immediate but ends when antibodies

naturally degrade in body


Figure 21.13 Active and passive humoral immunity.

Humoralimmunity

Active Passive

Naturallyacquired

Infection; contact with pathogen

Artificiallyacquired

Vaccine; dead or attenuated pathogens

Naturallyacquired

Antibodies passed from mother to fetus via placenta; or to infant in her milk

Injection of exogenous antibodies (gamma globulin)

Artificiallyacquired

Chapter 21A Immune System: Innate and Adaptive Defenses Slides by Barbara Heard and W. Rose. figures from Marieb & Hoehn 9 th ed. Portions copyright Pearson.

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