immunity chapter 23. smallpox vaccine before vaccines, smallpox had up to 50% death rates now...
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Immunity
Chapter 23
Smallpox Vaccine
• Before vaccines, smallpox had up to 50% death rates• Now smallpox is practically eradicated
Immunity
• Body’s ability to resist and combat diseases• Depends on mechanisms that recognize
proteins as self or nonself• Antigen– Any molecule the body recognizes as nonself and
provokes an immune response
Evolution of Defenses
• Innate immunity– Preset responses to nonself cues– Complement, phagocytes
• Adaptive immunity– Prepares defenses to specific pathogens
encountered during an individual’s lifetime– Cytokines, lymphocytes
Adaptive and Innate Immunity
Three Lines of Defense
• Physical barriers– exclude pathogens
• Innate immunity– begins as soon as antigen is detected
• Adaptive immunity– forms cells that fight infection and prevent
later infection
White Blood Cells
• Form in bone marrow• Participate in adaptive and innate responses• Release cytokines and other cell-to-cell
signaling molecules
Chemical Weapons
neutrophil eosinophil
mast cellbasophil
White Blood Cells
T lymphocyteB lymphocyteNK cell
White Blood Cells
dendritic cell macrophage
White Blood Cells
Surface Barriers
• Physical barriers– Intact skin
• Mechanical barriers– Mucus, cilia, flushing
• Chemical barriers – Protective secretions, low pH, lysozyme
Cilia in Airways
Bacterial Invaders
Table 23-3, p.385
Innate Immune Response
• Phagocytosis• Complement• Fever• Acute inflammation
Complement
• Many types of circulating proteins • Activated by binding to antigen– Triggers reactions that activate more complement
• Attract phagocytic cells
Membrane Attack Complexes
antibody activatedcomplement
bacterial pathogen
lipid bilayer of pathogen
Activation Cascade reactions
Formation of attack complexes
Lysis of target
one membrane attack complex (cutaway view)
hole in the plasma membrane of an unlucky baterium
Fig. 23-6, p.388
lipid bilayer of one kind of pathogen
Acute Inflammation
• Nonspecific response to foreign invasion, tissue damage
• Destroys invaders, removes debris• Symptoms are redness, swelling, warmth,
and pain
Inflammation
• Mast cells release histamine• Capillaries dilate and leak• Complement proteins attack bacteria• White cells attack invaders and clean up
a Bacteria invade atissue and directly kill cells or releasemetabolic productsthat damage tissue.
b Mast cells in tissue releasehistamines, which then triggerarteriole vasodilation (henceredness and warmth) as well asincreased capillary permeability.
c Fluid and plasmaproteins leak out ofcapillaries; localizededema (tissue swelling) and pain result.
d Complementproteins attackbacteria. Clottingfactors wall offinflamed area.
e Neutrophils, macrophages, engulf invaders and debris.Some macrophage secretions kill targets,attract more lymphocytes, and call for fever.
Fig. 23-7, p.388
Fever
• Temperature up to 39°C (102°F)• Enhances immunity, increases rates of enzyme
and phagocyte activity• Accelerates tissue repair
Features of Adaptive Immunity
• Self/nonself recognition • Specificity• Diversity • Memory
Antigens
• “Nonself” markers on foreign agents and altered body cells such as tumors
• Trigger division of B and T cells
Memory and Effector Cells
• When a B or T cell is stimulated to divide, it produces 2 cell types
• Memory cells: set aside for future use • Effector cells: engage and destroy the current
threat
Key Components of Immune Response
• MHC markers• Antigen-presenting cells• T cells• B cells • Natural killer (NK) cells
antigen fragments
MHC molecule
antigen–MHC complex
Formation of Antigen–MHC
Complex
fragments of engulfed antigen
MHC markerthat the cell already made
antigen-MHC complex displayed at surface of plasma membrane
Fig. 23-9, p.390
Antibody-MediatedImmune Response
naive B cells+
antigen+
complement
Cell-MediatedImmune Response
antigen-presenting cells
naive helper T cells
effectorhelper T cells
+memory
helper T cells
naivecytotoxic T cells
effector cytotoxic T cells+
memory cytotoxic cells
activatedB cells
effector B cells+
memory B cells
Fig. 23-10, p.390
Key Interactions
Antigen Interception
• Antigen-presenting T cells are trapped in lymph nodes
• Macrophages, dendritic cells, and B cells bind, process and present antigen
Fig. 23-11a, p.391
TONSILS
RIGHT LYMPHATIC DUCT
THYMUS GLAND
THORACIC DUCT
SPLEEN
SOME OF THE LYMPH VESSELS
SOME OF THE LYMPH NODES
BONE MARROW
Fig. 23-11b, p.391
arrays of lymphocytes
valve (prevents backflow)
Antigen Receptors
• Antibodies– Synthesized by B cells– Bind to one specific antigen
• Mark pathogen for destruction by
phagocytes and complement proteins
Antibody Structure
• Consists of four polypeptide chains
• Parts of each chain are variable; provide antigen specificity
antigen binding site
constant region
variable region
variable region(dark green)of heavy chain
binding site for antigen
variable region of light chain
constant region (bright green) of heavy chain, that includes a hinged region
Fig. 23-12a, p.392
binding site for antigen
antigen on bacterial cell(not to scale)
binding site on one kind of antibody molecule for a specific antigen
Fig. 23-12b, p.392
Fig. 23-12c, p.392
antigen on virus particle
binding site on anotherkind of antibody moleculeFor a different antigen
Immunoglobins (Igs)
• Five classes of antibodies– IgG– IgA– IgE– IgM– IgD
a As a B cell matures, different segments of antibody-coding genes recombine at random into a final gene sequence.
b The final sequence is transcribed into mRNA.
c Processing yields a mature mRNA transcript (e.g., introns excised, exons spliced).
d mRNA is translated into one of the polypeptide chains of an antibody molecule.
Stepped Art
Fig. 23-13, p.393
Antigen Receptor Diversity
Antibody-Mediated Immune Response
• B cell responds to one particular extracellular pathogen or toxin
• Activated B cell forms clones that differentiate into effector and memory cells
• Effector B cells secrete antibodies that tag antigens for destruction
Antibody-Mediated Response
antigen
Antigen binds only to antibody specific to it on a naive B cell.
clonalpopulationof effectorB cells
Effector B cells secrete antibodies.
Fig. 23-15a, p.395
B Cell Division
First exposure to antigen provokes aprimary immune response.
Anotherexposure to the same antigenprovokes secondaryresponse.
effector cells memory cells
naive B cell
effector cells memory cells
Fig. 23-15b, p.395
B Cell Differentiation
Fig. 23-15c, p.395
Secondary Immune Response
Cell-Mediated Immune Response
• Cytotoxic T cells target altered body cells that evade antibody-mediated immune response
• Antigen-presenting dendritic cells activate helper T cells
Fig. 23-16, p.396
Cell-Mediated Immune Response
• Helper T cells secrete cytokines– Induce formation of cytotoxic T cells– Proliferate NK cells – Enhance macrophage activity
• Destroy infected or altered cells
cytotoxic T-cell
tumor cell
Cell-Mediated Immune Response
Immunization
• Process that induces immunity• Active immunization:– Vaccination with antigen– Long-lasting immunity
• Passive immunization:– Purified antibody is injected– Protection is short lived
Allergies
• Immune reaction to harmless proteins (allergens)
• IgE binds to mast cells, causing inflammatory response
• Histamine release causes symptoms
Anaphylactic Shock
• Life-threatening allergic reaction• Caused by histamine released by many mast
cells• Airways constrict• Blood pressure drops as fluid leaks out of
capillaries
Autoimmune Disorders
• Failure of immune system to distinguish between self and nonself– produces antibodies against self
• Graves’ disease • Multiple sclerosis
Deficient Immune Responses
• Primary immune deficiencies– Present from birth
• Secondary immune deficiencies– Acquired by exposure to agent such as HIV
HIV Replication
reversetranscriptase
core proteins(two layers)
integrase
viral RNAenters cell
reversetranscriptionof viral RNA
host cell
viral DNA
viral genes are integrated
into the host DNADNA is
transcribed
viral RNAviral
proteins
budding
viral RNA
lipid envelopewith proteins
viral coatproteins
c The viral DNA becomes integrated into host cell’s DNA.a viral RNA
enters a T cell.
b Viral DNA forms by reverse transcription of viral RNA.
f Virus particles that bud from the infected cell may attack a new one.
d DNA, including the viral genes, is transcribed
viral DNA
Viral RNAviral
proteins
viral RNA
viral enzyme (reverse transcriptase)
25-30m
e Some transcripts are new viral RNA, others are translated into proteins. Both self-assemble as new virus particles.
Fig. 23-20, p.396
nucleus
HIV Infection
• HIV infects immune system cells– Macrophages, dendritic cells, helper T cells
• T cells are killed• Cytokine IL-4 is released• Immune system destroys itself• Secondary infections and tumors cause death
Table 23-4, p.399
HIV Transmission
• Virus transmitted by– Sex– Infected mothers– Shared needles
• Not transmitted by causal contact
Treatment
• No cure • AZT and other drugs slow disease and
increase life span• Traditional vaccines do not work• Researchers continue to work
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