MICR 130 Chapter 17.pdf - Laulima!

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M I C R O B I O L O G Y a n i n t r o d u c t i o n ninth edition TORTORA FUNKE CASE Chapter 17 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings PowerPoint ® Lecture Slide Presentation prepared by Christine L. Case Adaptive Immunity: Specific Defenses of the Host

Transcript of MICR 130 Chapter 17.pdf - Laulima!

M I C R O B I O L O G Ya n i n t r o d u c t i o n

ninth edition TORTORA FUNKE CASE

Chapter 17

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

PowerPoint® Lecture Slide Presentation prepared by Christine L. Case

Adaptive Immunity:Specific

Defenses of the Host

The Adaptive Immunity

� Innate immunity - defenses against any pathogen

� Reacts the same way every time

� Adaptive (specific) immunity – induced, and adapts to a

microbe or foreign substancemicrobe or foreign substance

� Has memory component, major difference from

innate immunity

� Two components to adaptive immunity

� Humoral immunity – immunity mediated by

antibodies (via B cells)

� Cellular immunity – immunity mediated by cells

Dual Nature of the Adaptive Immune System

� Cellular immunity – immunity mediated by cells

� T cells

Antigens and Antibodies

� Antigens – proteins or polysaccharides that stimulate

the immune system

� Often external structures of pathogens

� Or pollen, egg whites, cells & tissues� Or pollen, egg whites, cells & tissues

� Antigens in body are recognized by antibodies

The Nature of Antibodies

� Antibodies are aka “immunoglobulins” (Ig)

� Antibodies are made in response to an antigen

� Antigens = Antibody generator

� Recognize and bind to an antigen� Recognize and bind to an antigen

� Antibodies are “Y-shaped” proteins

Antibody Structure

Variable (V) region

Constant (C) region is same for a particular Ig

class

� Function of antibodies varies on class of Ig molecule

� 5 Ig classes

Immunoglobulin Classes

� IgG – monomer

� Most abundant, 80%

� Roams, protects body fluids, blood and

lymphlymph

� Protect against bacteria, viruses, toxins

in blood, enhance phagocytosis

� Can cross into tissue

� Crosses placenta, protects fetus

� Long lived

� IgM – pentamer (5)

� Stays in bloodstream

� First antibody produced in

response to infection, short-lived

Immunoglobulin Classes

response to infection, short-lived

� Used in diagnosing pathogen

in early stages of infection

� Effective in agglutinating antigen,

enhances phagocytosis

� IgA – monomers or dimers

� 10-15%

� Most common in mucous

membranes and body secretions

Immunoglobulin Classes

membranes and body secretions

� Prevent adherence of microbes

to mucosal surfaces

� Protection is short-lived

� IgD - monomer

� 0.2% of serum antibodies

� No well defined function

Immunoglobulin Classes

� IgE - monomer

� 0.002%

� Bind to mast cells, basophils

� Involved in allergic reactions

Immunoglobulin Classes

� Involved in allergic reactions

� Stimulates histamine release

� Attracts phagocytes, causes

hay fever

� Binds to parasitic worms

B cells and humoral immunity

Humoral Immunity

� Protection mediated by antibodies

� Produced by lymphocytes, B cells

� Production of antibodies starts with exposure to “free” � Production of antibodies starts with exposure to “free”

or “extracellular” antigens

Activation of B cells

� B cells carry antibodies on cell surface

� 100,000+ antibodies, all bind to same antigen

� Each B cell (antibody) binds to unique antigen

� Binding of antigen “activates” cell� Binding of antigen “activates” cell

B cell activation

2 - Activated B cell undergoes “clonal

expansion”3 - Clones are

identical to each other, carry same

antibody as activated B cell

1 - Antigen binding activates B cell

activated B cell

4 - Most clones become plasma

cells ���� antibody producers

5 - Some clones become memory cells ���� long-lived, provide memory

Ig Classes

IgM1. First produced during infection

���� blood2. Agglutination

1. Activate basophils, mast cells ����inflammation

2. EosinophilsIgE

2. Eosinophils

IgG

1. No known functionIgD

1. Found in blood, tissue2. Bacteria, viruses, toxins

1. Found in mucous membranes2. Prevent adherence

IgA

B cells and humoral immunity

� T-dependent antigens – require TH

to activate B cells

� Generally stronger than …

� T-independent antigens –activate

B cells without THB cells without TH

� B cells are capable of creating

virtually an infinite number of different

antibodies

� Provides protection against

almost any antigen

� Any B cell that reacts with “self” is

deleted

Antigen-antibody binding and its results

� Antigen-antibody complex – antibody bound to antigen

� Antibody binding is highly specific

� Bind to unique antigen

� Antibody-antigen binding results in a number of � Antibody-antigen binding results in a number of

responses

The Results of Antibody Binding

Agglutination

� Reduces number of

particles to clean-up

� Enhances phagocytosis� Enhances phagocytosis

Opsonization

� Enhancement of

phagocytosis

Antibody-dependent cell-

mediated cytotoxicity

� Destruction by cells that

remain external to target

The Results of Antibody Binding

remain external to target

Neutralization

� Inactivation of viruses, toxins

by blocking adherence

Activation of complement

� Causes inflammation,

The Results of Antibody Binding

� Causes inflammation,

cell lysis

Immunological Memory

� Antibody titer – amount of antibody in serum

� Indicator of intensity of humoral response

� Two responses:

� Primary response� Primary response

� Slow, relatively weak

� Secondary response

� Fast, intense

� Due to memory cells

� Response is similar for T cells

Immunological Memory

Primary response

� No antibodies for 4-7 days

� Slow rise in antibody titer

� Peaks in about 10-17 days

Secondary response aka “memory”

� Reached peak in 2-7 days

� Lasts many days

� Greater in magnitude

Humoral Immunity

� Intracellular antigens (viruses, some bacteria) are not

exposed to antibodies

� Evade humoral defense mechanisms

� T cells help combat intracellular pathogens

T Cells and Cellular Immunity

� Also recognize “non-self” cells – cancer, foreign cells

� T cells specific to antigens via “T cell receptor” (TCR)

� Found in lymphoid tissue

T Cells and Cellular Immunity

� T cells recognize antigens processed by “antigen-

presenting cells” (APC)

� Include macrophages, dendritic cells

� APC phagocytose antigen, process it, put it on surface� APC phagocytose antigen, process it, put it on surface

� “Present it” to T cells in lymph tissue

� Response of T cells depends on class of T cell

activated

T Cells and Cellular Immunity

APC ingests antigen, processes antigen

APC “presents” antigen on

surface of cellBinding of TCR activates T cell

Helper T cells, TH

� Activated TH

coordinate adaptive

immune response

� Release cytokines that

recruit, activate

immune cells

� Simulate eosinophils,

B cells

Activated TC becomes cytotoxic T lymphocyte, CTL

TC can be activated by TH, virus infected

cell, tumor cell

CTL recognize and kill specific target cells

Activation of Cytotoxic T cells

� Kill by inducing apoptosis � programmed cell death

� Cell shrinks, implodes

� Easier to clean-up, less messy than cell lysis

� Doesn’t further stimulate immune response

� Remains digested by macrophages

Apoptosis

B cell undergoing apoptosis

Normal B cell

Cell-mediated Immunity

Cytokines: Chemical Messengers

� Immune cells communicate with each other via

cytokines

� TH cells are important producers

� Interleukins – serve as communicators between WBC� Interleukins – serve as communicators between WBC

� IL-1 activates TH cells

� Chemokines – induce migration of leukocytes

� IL-8 attracts immune cells, phagocytes

� Interferons – protect against viral infected cells

� α-TNF – important in inflammation, toxic to tumor cells

Critical Thinking

1. Antivenin is used to neutralize the effects of a snake

bite. What is antivenin?

� Antibodies that neutralize the venom

2. AIDS is a virus that affects TH cells. These people 2. AIDS is a virus that affects TH cells. These people

have trouble making antibodies. Why?

� TH cells are required for making TH-dependent

antibodies

3. Can AIDS patients make any antibodies?

� B cells can make TH-independent antibodies