chapter 21 - immunity

8/2/2019 Chapter 21 - Immunity

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Chapter 21

Nonspecific Body Defenses andImmunity

G.R. Pitts, J.R. Schiller, and James F. Thompson, P


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Defense Systems1.Innate(nonspecific)defenses External body

membranes

Inflammation

Antimicrobialproteins,phagocytes andother cells

2.Adaptive(specific)defenses T cells and B cells


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Innate Defense System

Surface Barriers First line of defense: mechanical and chemical protection

1. Skin

2. Mucosal Membranes

Internal Nonspecific Defenses Second line of defenses

1. Phagocytes

2. Natural Killer cells (NK lymphocytes)3. Inflammation

4. Antimicrobial proteins

5. Fever


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Skin and Mucosal Membranes

Mechanical Protection Epidermis

nose hairs, nails

Mucous membranes - line certain organ systems

mucus prevents drying, traps foreign things

respiratory tract cilia sweep mucus out

Lacrimal apparatus -- tear glands and ducts

wash the eye to dilute microbial growth

Saliva - dilute microbes on the oral cavity

Urine - flow dilutes, and acid pH helps kill, microorganisms

Defecation and vomiting - expel toxins and microbes


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Skin and Mucosal Membranes

Chemical Protection: reduce bacterialgrowth Skin

sebum (unsaturated FAs) forms oily layer

perspiration has fatty acids, salts (NaCl), and mildly acid pH

Lysozyme

in perspiration, tears, saliva, nasal secretions, other tissue fluids

enzyme breaks down bacterial cell walls

Hyaluronic acid

gel-like matrix in most connective tissues

slows the spread of many infectious agents

Gastric juice - stomach nearly sterile due to acid pH, ~2

Vaginal secretions mildly acid pH


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Innate Defense: Phagocytes

Macrophages (derived from monocytes) are the

chief tissue phagocytic cells Free macrophages wander through tissues in search

of microbes and cellular debris

Fixed macrophages: Kupffer cells (liver), microglia(brain), dust cells (lungs)

Neutrophils become phagocytic when

encountering infectious material Eosinophils are weakly phagocytic, deploy

destructive granules against parasitic worms


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Mechanism of Phagocytosis Chemotaxis

Adherence recognitionof external carbohydratesand proteins

Aided by opsonins

Ingestion

Killing and digestion


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Innate Defense: Natural Killer Cells

Distinct group of large granular lymphocytes (NK

lymphocytes = Null Killer lymphocytes)

Nonspecific killers respond to the lack of self-antigens and to the presence of certain surface

oligosaccharides Kill virus-infected body cells and some tumor cells

by releasing various defensive molecules not byphagocytosis

Act before the antigen-specific immune system isactivated

Secrete potent chemical signals that enhance the

inflammatory response


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Innate Defense: Inflammation

1. Inflammation Signs:

1. Redness

2. Heat

3. Swelling

4. Pain5. Loss of Function

Function:

1. Prevent spread ofdamage

2. Dispose of pathogensand debris

3. Set stage for tissuerepair


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InflammationStage 1: Vasodilation andincreased vessel permeability Macrophages and cells lining the

gastrointestinal and respiratory tractscarry Toll-Like Receptors (TLRs) thatrecognize specific classes of microbes

TLReceptor activation causes cytokinerelease

promotes inflammation & chemotaxis

Mast cells secrete histamine

Other cells secrete various regulatory

factors Histamine, kinins, prostaglandins,

leukotrienes, complement

Cause local vasodilation

Increase capillary permeability resulting in

edema

http://www.komabiotech.co.kr/technical/review/toll_like_receptor.gif


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Inflammation: Stage 1

Edema increased plasma filtrate seeps intotissue spaces bringing some immune proteins

Helps to dilute harmful substances

Increases supply of oxygen and nutrients neededfor metabolism, inflammation and repair

Allows entry of clotting proteins, which reduces thespread of mibrobes


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InflammationStage 2. Phagocytemoblization

1. Leukocytosis-inducingfactors: increaseneutrophil production

2. Margination(pavementing)

3. Diapedesis (amoeboidmovement)

4. Chemotaxis of WBCs neutrophils rapid arrival

monocytes slower arrival


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Inflammation

Stage 3. Tissuerepair Tissue regrowth and

repair of damage orscar formation

Pus dead phagocytes and

other WBCs, damagedtissue, and perhapsmicrobes

if too numerous foreffective removal byphagocytes, an abscessmay develop


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Effects of Inflammation

Increased blood

flow results inincreased localtemperature andlocal cellular

metabolism

Increased capillarypermeability and

phagocyticmigration to theinjured tissue

I D f A i i bi l


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Innate Defense: AntimicrobialProteins

1. Attack microorganisms directly

2. Interfere with microbial reproduction

The most important are:

1. Interferons

2. The Complement System3. Transferrins which bind Fe2+ in plasma,

inhibiting bacterial growth


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Interferons (IFNs)

Produced by most tissue cellswhen infected by a virus

Diffuses to uninfected cells andbinds to surface receptors stimulates macrophages and

natural killer lymphocytes

stimulates production ofantiviral proteins which blockviral replication

inhibits growth of virally infectedcells

suppresses growth of tumor cells

A lpha I FN is used against: hepatitis C virus

herpes virus (genital warts)


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The Complement System

20 plasma and cell membrane proteins thatexist as inactive precursors

When activated, the complement systemfunctions to complement or enhance certainimmune, inflammatory, and allergic responses

Kills bacteria and certain other microbial celltypes (our cells normally are protected from

complement attack) Stimulates chemotaxis in leuckocytes

Enhances the effectiveness of both nonspecific

and specific defenses


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Classical Pathway is triggered by the specificimmune system Requires binding of antibodies to antigens of

invading organisms

Complement C1 then binds to the antigen-antibody

complexes (complement fixation)

Alternative Pathway is triggered by non-specific interaction among factors B, D, and P,and microbial cell wall polysaccharides(complement fixation)

Both pathways involve an enzyme cascade

Complement Pathways


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ComplementPathways

Both pathways convergeon C3, which cleavesinto C3a and C3b

C3b initiates formation ofa membrane attackcomplex (MAC)

MAC causes cell lysis bycreating many hundredsof microscopic holes inthe cells plasmalemma

C3b is also an opsonin

f


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Innate Defense: Fever

Pyrogens reset the temperature set-point in thehypothalamus

Inhibits some microbes from growing

Increases bodys metabolic rate, which speeds up

immune defenses and tissue repair Increases effects of antimicrobial substances

produced by the immune system

Stimulates liver and spleen to sequester iron and zinc(needed by microorganisms)

High fevers are dangerous

f S


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Innate Defense System: Review

Surface Barriers

1. Skin

2. Mucosal membranes

Internal Nonspecific Defenses1. Phagocytes

2. Natural Killer cells (NK lymphocytes)

3. Inflammation4. Antimicrobial proteins

5. Fever


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Adaptive Defense The adaptive immune system:

Acts to immobilize, neutralize, or destroy foreignsubstances and cells

Amplifies the inflammatory response and activatescomplement

Is antigen-specific*, systemic, and has memory *Recognizes specific foreign molecules

Has two interdependent arms

Humoral, or antibody-mediated immunity (AMI)

Cellular, or cell-mediated immunity (CMI)

Ad ti D f


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Adaptive Defense

Definitions:

Immunity: the ability of the body to defend itselfagainst specific foreign invaders (molecules or cells)

Immunogenicity: the ability to stimulateproliferation of specific lymphocytes and specificantibody production

Reactivity: the ability of activated lymphocytes andtheir products, antibodies, etc., to interact withspecific antigens

Ad ti D f


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Adaptive Defense

Definitions:

Specificity: the antigen triggers focused immunedefenses (from particular lymphocytes lineages)that respond only to the antigens of this foreignsubstance/cell

Memory: the immune system produces clones ofspecific memory lymphocytes (T & B) which reactrapidly when the particular foreign substance/cell isencountered again

Specificityand memorydifferentiate this system

from the nonspecific (innate) defenses

Ad ti D f


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Adaptive Defense

Antigen any substancewhich provokes specificimmune responses

Antigenic determinants Parts of antigens that trigger

the specific immune

responseAn antigen may be an entire

microorganism or only smallstructures or subregions of

large molecules

Most antigens arecomplex and express

multiple types of antigenicdeterminants.

Ch i l N t f A ti


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Chemical Nature of Antigens Complete Ag: complex

macromolecules - usually proteins(nucleo-, lipo-, glyco-) --sometimes carbohydrates or lipids

Are immunogenic & reactive

Incomplete Ag: smallermolecules (haptens)

react with antibodies but cannot

cause an immune response withoutaid (protein carrier)

e.g., poison ivy, drug allergies

Ad ti D f


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Adaptive Defense Antigen receptor diversity

>1 billion different antigenic

determinants are recognized by thebody

Genetic recombination shuffles andreorganizes different Ab genes

Major histocompatibility complexantigens (MHC) unique to each individuals cells;

help in identifying what is selfversus foreign

2 classes of MHC antigens

(markers) class I MHC found on all body cells

except RBC's

class II MHC - only on antigenpresenting cells (APCs), thymuscells, and activated T cells

A ti P ti C ll (APC )


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APCs phagocytize, process, and present antigens tolymphocytes

APCs do not respond to specific antigens

APCs contribute to coordinating specific immunity Macrophages

Dendritic (Langerhans) cells

B lymphocytes

The major initiators of adaptive immunity are APCs,which actively migrate to the lymph nodes andsecondary lymphoid organs and present antigens to T

and B cells

Antigen-Presenting Cells (APCs)

Cl I MHC P t i


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Found on all cells, except RBCs

Recognized by Tlymphocytes and APCs

Display peptides from endogenous antigens

Endogenous antigens are:

Associated with body cells

Degraded by proteases and enter the endoplasmic

reticulum Transported through special membrane channels

Bound with MHC class I molecules on the ER membrane

Migrate to the cell membrane as a complex: Ag -- MHC

class I molecule

Class I MHC Proteins

MHC Class I Proteins


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MHC Class I Proteins

Cancer cells often do something quite similar to the virus-infected cells.

(Foreign MHC Class I Ags are the source of tissue transplant rejections.)

This is a form of Antigen Presentation

MHC Cl II P t i


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1. Immune cell identity markers found only on mature Bcells, some T cell classes, and antigen-presenting

cells2. MHC Class II proteins are synthesized in the ER

3. A phagosome containing a pathogen (withexogenous antigens) merges with a lysosome

1. MHC Class II proteins migrate into the phagosome

where the antigen macromolecules are degraded andparticular antigen peptides are bound to the MHCClass II markers

2. Ag-- MHC class II complexthen migrates to the cell

membrane and displays antigenic peptide for

MHC Class II Proteins



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This is a key function of our APCs in most Ag-specific defenses.

L h t P id A S ifi it


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B and T lymphocytes developin bone marrow

Lymphocytes mature and

develop immunocompetence(ability to recognize specificantigen) in different locations

B cells mature in the bonemarrow and provideAb-mediatedimmunity

T cells mature in the thymusand provide cell-mediated

immunity

Lymphocytes Provide Ag Specificity

I t t B T ll


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Naive cells display a unique surface receptor for a

specific antigen once mature

Receptor expression occurs before a cell encountersthe foreign antigen it may later attack

It is genes, not antigens, that determine which foreignsubstances our immune system will recognize and resist

Naive cells circulate to secondary lymphoid tissue

where they may encounter antigens later

B and T cells become fully functional only after bindingwith their recognized antigen

Immunocompetent B or T cells

I t t T C ll


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T cells mature in the thymusunder positive and negativeselection pressures

Positive selection outer thymiccortex

Selects functional T cells which becomeboth immunocompetent and potentiallyself-tolerant

Non-selected cells die via apoptosis

Negative selection inner thymiccortex

Kill or regulate off T cells that react withself-antigens

Immunocompetent T Cells

Survive

Apoptosis

Apoptosis

I t t B C ll


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B cells become immunocompetent and self-

tolerant in bone marrow Some self-reactive B cells are killed by apoptosis

(clonal deletion)

Some self-reactive B cells can modify their anti-selfproperties (receptor editing)

Some self-reactive B cells are released from thebone and are inactivated by negative regulation(anergy)

Immunocompetent B Cells

Cell Mediated Imm nit


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CMI is involved in most aspects of specific

immune defense Three populations of T lymphocytes

regulate specific immunity

Helper TH cells which carry CD4+ markers

Suppressor TS cells

Memory T cells

cytotoxic TC cells which carry CD8+ markers

destroy tumor cells and virus-infected cells;

they also attack transplanted cells and tissues

Cell-Mediated Immunity

Cell Mediated Immunity


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Cell -Mediated Immunity

Basic steps1. Recognition by T lymphocytes of antigen

presented by an antigen-presenting cell withmatching MHC Class II markers

1. Proliferation and differentiation of T cells onceactivated

1. Production ofclones of identical effector T cellscapable of recognizing a specific antigen1. Appropriate action (help, attack, memory,

suppression) from T cell subclones

T Cell


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T CellActivation-Step 1:

Antigen

Bindingand AntigenPresentation

T Cell Activation Step 2: Co Stimulation


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T cells must bind to

MHC Class II surfacereceptors on an APC

After co-stimulation

with cytokines, T cellsenlarge, proliferate,and form clones

Activated T cellsdifferentiate andperform functionsaccording to their T

cell class

T Cell Activation- Step 2: Co-Stimulation

T Lymphocyte Activity


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Primary T cell response usually peaks within a

week

T cells then undergo apoptosis within a month

Reduced activity parallels elimination of antigen

This is a negative feedback control

A few Memory T cells remain to respond to anyfuture exposure to the same antigen

T Lymphocyte Activity

Helper T Lymphocytes


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Regulatory cells that play acentral management role in

the immune response

Once primed by APC antigenpresentation, TH cells:

Stimulate proliferation of otherT cell classes

Stimulate B cells that havealready become bound to

antigen

There is N O coordinatedimmune response without TH

cell function

Helper TH Lymphocytes

Helper T Lymphocytes


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TH cells interact directly with B cells that have antigen

fragments on their surfaces bound to MHC Class IIreceptors

TH cells express CD4+ cell identity markers

T

H

cells stimulate B cells to divide more rapidly and

begin antibody formation

B cells may be activated without TH cell help by

binding to T cellindependent antigens (certain

microbial polysaccharides)

Most antigens, however, require TH co-stimulation to

activate B cells

C t ines re e se m if n ns ecific efenses

Helper TH Lymphocytes

Cytotoxic T Lymphocytes


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TC cells express CD8+ cell identity markers

TC cells, or killer T cells, are the only T cells that candirectly attack and kill other cells

They circulate throughout the body in search of bodycells that display the antigen to which they have beensensitized

Their targets include:Virus-infected cells Cells with intracellular bacteria or parasites Cancer cells Foreign cells from blood transfusions (WBCs and platelets) or

Cytotoxic Tc Lymphocytes

Cytotoxic T Lymphocytes


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Bind to self/anti-self complexes on any body

cell

Infected or abnormal cells can be destroyed aslong as appropriate antigen and co-stimulatoryregulators (e.g., IL-2) are present

[In contrast, Natural Killer cells activate their

killing machinery when they bind to a differentMHC-related cell surface marker on cancercells, virus-infected cells, and transplantedcells]

Cytotoxic Tc Lymphocytes

Cytotoxic T Lymphocyte Actions


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Secrete perforins which cause cell lysis by creatingtransmembrane pores

Secrete lymphotoxin which fragments the target cells DNA Secrete gamma interferon which stimulates macrophage attack

Cytotoxic Tc Lymphocyte Actions

Suppressor T Lymphocytes


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TS cells immune regulatory cells which releasecytokines that suppress the activity of both T cellsand B cells

Generated when other specific T cell clones aregenerated

Negative feedback control to bring the body back tonormal after the battle has been won

Suppressor Ts Lymphocytes

Antibody Mediated Immunity


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Antigen challenge the first encounter

between an antigen and a naive B lymphocyte

Antigen presentation usually occurs in the

spleen or a lymph node, but can occur in anylymphoid tissue

Antigen presentation usually made by amacrophage, but some B cells can reactdirectly against certain bacterial antigens

Binding of the antigen to the B cells specific

Ag receptor activates the B cell

Antibody-Mediated Immunity

Primary Response


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Most clone cells become

plasma cells that secretespecific antibodies

Clones that do notbecome plasma cells

become B memory cellsthat can respond tosubsequent exposures tothe same antigen

Primary ResponseActivated B cells grow and divide, forming clones bearing the sameantigen-specific receptors and secreting the same antigen-specificAb

Primary Response


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Initial B cell differentiation, proliferation, and

Ab synthesis requires time after the first Agexposure

Lag period: 3 to 6 days after antigen challenge

Peak plasma levels of antibody are achieved in~10 days

Antibody molecules also reach the interstitial

fluids, especially where inflammation exists

Antibody levels then decline gradually if thereis no additional Ag exposure

Primary Response

Secondary Response


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Any subsequent exposure to thesame antigen

Sensitized memory cells (B andT) respond within hours

Antibody levels peak in 2 to 3

days at higher plasma levelsthan in the primary response

Activated B subclones generateantibodies that bind withgreater affinity

Plasma antibody levels canremain high for weeks tomonths

Secondary Response

Primary and Secondary Antibody Responses


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Primary and Secondary Antibody Responses

Immunological Memory


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Immunological Memory Immunization is

possible becausememory B cells andmemory T cellspersist after the

initial Ag exposure

with any subsequent exposure, the immune system

responds more quickly, forcefully secondary response - antibodies produced during

subsequent exposures are produced in greaterquantities and have a greater attraction for antigen

Antibodies


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Are unique soluble proteins secreted by

activated B cells and plasma cells in responseto an antigen

Are capable of binding specifically with thatantigen

Constitute much of the gamma globulin fractionof plasma proteins

Also called immunoglobulins

Antibodies

Basic Antibody Structure


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Basic Antibody Structure

Four polypeptide chainslinked together with disulfidebonds

The four chains boundtogether form an antibodymonomer

Each chain has a variable (V)region at one end and aconstant (C) region at theother

Variable regionsVariable regionsof the heavyand light chains combine toform the antigen-bindingsite

Ag

Antibody Structure


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Antibodies responding to different antigens

have different V regions but the C region is thesame for all antibodies in a given antibody class

C regions form the stem of the Y-shapedantibody monomer and determine:

the class of the antibody

the cells and chemicals to which the antibody canbind

how an antibody class functions in eliminating

antigens

Antibody Structure

Classes of Antibodies


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IgD: monomer attached to the surface of B cells,important in B cell activation

IgM: pentamer released by plasma cells during theprimary immune response

IgG: monomer that is the most abundant and diverseantibody in primary and secondary responses; crossesthe placenta and confers passive immunity

IgA: dimer that helps prevent attachment ofpathogens to mucosal surfaces

IgE: monomer that binds to mast cells and basophils,causing histamine release when activated

Classes of Antibodies

Antibody Functions


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All antibodies form an antigen-antibody (immune)

complex

Antibodies do not directly destroy antigen, though

they may immobilize or inactivate Ag

Antibodies act as opsonins and tag Ag for immuneattack and destruction

Defensive mechanisms triggered by antibodies includeneutralization, agglutination, precipitation,

opsonization, and complement fixation

Antibody Functions

Antibody Mechanisms of Action


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1. Neutralization: Antibodies bind to and blockspecific sites on viruses or exotoxins, thus preventingthese antigens from binding to receptors on tissuecells

Antibodies bind to the same determinant on more thanone antigen forming antigen-antibody complexesthat are cross-linked into large lattices

2. Agglutination: Cellular antigens are cross-linked,causing cell clumping

2. Precipitation: Soluble molecules are cross-linkedinto large insoluble complexes




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4. Opsonization: Bound Abs facilitatephagocyte adherence

5. Complement Fixation: IgM and IgGantibodies bound to cellular Ags bindcomplement via the Classical Pathway

The complement cascade causes chemotaxis,opsonization, phagocytosis and cell lysis

Complement activation enhances the inflammatoryresponse


Summary of Antibody Actions


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Summary of Antibody Actions

Figure 21.13

Monoclonal Antibodies


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Monoclonal antibodies are purified tissue

culture preparations of a specific antibody for asingle antigenic determinant which areproduced from descendents of a single B cell

Commercially prepared monoclonal antibodiesare used:

To provide passive immunity

In research applications In clinical laboratory testing

In the treatment of certain cancers

Monoclonal Antibodies

Adaptive Immunity: Summary


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A defensive system with two interdependentarms (CMI & AMI) that uses lymphocytes,

APCs, and specific molecules to recognize anddestroy foreign substances

Adaptive immune responses depend on theability of its cells to: Distinguish foreign from self molecules

React with foreign substances (antigens) by bindingto them

Communicate with one another to effect acoordinated protective response specific to those

antigens




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To start an immune response, APCs, B and Tlymphocytes must recognize foreign antigen

Antigen-Presenting Cells and some B cellsrecognize and immediately bind to certainantigens in the blood, the extracellular fluid(ECF), or other tissue spaces

More often, B and T cells on l y recognizeantigen (protein fragments) when Ag ispresented by the macrophages in combinationwith MHC Class II surface markers and

stimulation is provided by Th lymphocytes


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Summary of

the ImmuneResponse

Clinical Classification of Immunity


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Active Immunity: the bodys own B and T lymphocytesencounter antigens and produce specific responses againstthem; immunological memory does occur

Natural ly Acquired response to a microbial or parasitic infection Artificial ly Acquired response to a vaccine of dead or attenuated

(weakened) pathogens

Passive Immunity: An outside source of immune cells ormolecules is provided to a recipient; immunological memorydoes not occur; protection ends when the donated materials arenaturally eliminated from the body

Natural ly Acquired the mother to her baby via the placenta (IgG) orvia lactation (colostrum/milk) (IgM & IgA)

Artificial ly Acquired the injection of serum, gamma globulin, orleukocyte transfusion




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Organ and Tissue Transplants


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The four major types of grafts are:

Autograft graft transplanted from one site on the body toanother in the same person

Isograft graft between identical twins (or clones);individuals with the same genotype

Allograft graft between individuals that are not identicaltwins, but belong to same species

Xenograft grafts taken from another animal species

Organ and Tissue Transplants

Prevention of Graft Rejection


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Donors are selected to minimize differences in MHC

Class I antigens = HLA (human leukocyte antigens) Unnecessary for routine blood transfusions since RBCs lack

HLAs

Prevention of rejection is accomplished by usingvarious immunosuppressive drugs

Survival and longevity of grafts have varying success

Immunosuppressive drugs depress the patientsimmune system so it is less effective in defendingagainst pathogens and cancer

Prevention of Graft Rejection

Pathologies: Immunodeficiencies


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g

Human Immunodeficiency Virus HIV enters certain cell types by receptor

mediated endocytosis

infects primarily helper T cells

attaches to the CD4 protein on cell surface

A retrovirus

carries its genetic material as RNA inserts its genetic material into host cell DNA with

the enzyme reverse transcriptase cell makes copies of the virus, releases them for

further infection

May be carried silently in cells for years, beingpassed on during ordinary mitosis

Activation of HIV life cycle destroys THelper cells

Weakened immune response to all foreigninvaders, benign or aggressive

Pathologies: Autoimmune Diseases


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g

Multiple Sclerosis (MS) myelin sheath(white matter) attacked and destroyed

Myasthenia Gravis ACh receptors atneuro-muscular junction of skeletal muscle

attacked and destroyed

Graves Disease thyroid cells TSH receptorattacked and stimulated causing excess thyroid

hormone (T3 & T4) production

Type I Diabetes - destruction of pancreaticislet cells eliminates insulin secrection

Pathologies: Autoimmune Diseases


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g

Systemic Lupus Erythematosus (SLE) generalized attack on connective tissues andnuclear antigens

Glomerulonephrit is - destruction of theglomerular capillaries causes impaired renalfunction

Rheumatoid Arthrit is - destruction of thesynovial membranes in joints

Pathologies: Cancer


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g The immune system probably evolved first to

respond to cancer cells when a new cancer cell develops, new surface

marker proteins (tumor antigens) often appear

if the immune system recognizes these new surfacemarkers as non-self, it will destroy the cellexpressing them

this immune surveil lance is most effective ineliminating virus-induced tumor cells because theytend to express viral antigens which are not self

Leukemias and Lymphomas cancers ofleukocytes

Pathologies: Hypersensitivities


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g yp Immediate hypersensitivities (allergies)

First exposure merely sensitizes one to an allergen(penicillin, venoms, dust, mold, pollen, etc.)APCs digest and inappropriately present the allergen

Subclones of B cells secreting IgE predominate in response

Anti-allergen IgE attaches to mast cells and basophils

Later exposures produce dramatic responsesAntigen binds to IgE on mast cells and basophils

Ag-IgE binding triggers these cells to release muchhistamine and other inflammatory molecules

Local reactions swelling, rashes, erythema, itching

Systemic reactions asthma, anaphylactic shock, death

Pathologies: Subacute


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gHypersensitivities

Caused by IgG and IgM

Occurs 1-3 hr after exposure and lasts 10-15 hr

Cytotoxic reactionsAb bind to Ag on specific cells causing phagocytosis and

complement-activated lysis May occur after transfusion of mismatched blood

Immune-complex hypersensitivities

Ags are widely distributed or insoluble Ag-Ab complexes cantbe removed

Intense inflammation

Severe damage to local tissue

Also involved in autoimmune diseases

Pathologies: Delayed Hypersensitivities


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Pathologies: Delayed Hypersensitivities

Occurs 1-3 days after exposure

Cell-mediated immune response

Causes mild swelling to serious cytotoxic tissue

damage (contact dermatitis, e.g., TB skin test,poison ivy, latex gloves, etc.)

[Note: Sometimes allergies may be temporarilytransferred by blood or plasma transfusions.]


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End Chapter 21

chapter 21 - immunity

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