Transcript Immunology - Canisteo-Greenwood Central School

Immunology
The Body’s Defenses
Chapter 33
I.
How Microbes Cause Disease
A.
pathogen
•
B.
antigens (ag)
•
C.
D.
any substance that triggers the immune system to respond
infections can be superficial or systemic, or one then the other
bacteria
1.
2.
3.
4.
5.
E.
adherence (with adhesions or fimbriae)
colonization  invasiveness
toxins: damage to cells/tissues  damage to host
enzymes: increase virulence, degrade cells/tissues, cause/dissolve clots
capsule: helps resist phagocytosis
viruses
•
F.
replication inside host cells (lytic and lysogenic cycles)
fungi
1.
2.
3.
G.
usually cause superficial infections through enzymes (e.g., keratinase)
allergic reactions
toxins
protists (protozoa)
1.
2.
H.
ingest host cells and fluids
invade rbc’s
algae
•
I.
any disease-causing organism
neurotoxins
disease transmission can be direct or indirect
II.
Host Defense
A.
nonspecific defenses
1. very general (broad spectrum)  work on any antigen
2. not as strong as specific defenses
3. first line
a. anatomical barriers
i.
intact skin and secretions of skin
ii. saliva and mucous
b. coughing and sneezing reflexes
c.
normal flora
i.
bacteria normally living in body  compete with pathogens
ii. slow down growth of pathogen or spread of antigen
4. second line
a. phagocytic leukocytes (wbc's)
i.
neutrophils: release some destructive chemicals
ii. eosinophils: defense against larger parasites
iii. monocytes: immature macrophages
iv. macrophages: act as antigen-presenting cells (APC's)
v.
dendritic cells: act as antigen-presenting cells (APC's)
Fig. 33.5 A macrophage engulfing multiple bacteria
b.
other nonspecific leukocytes (not phagocytic)
i.
basophils: release histamine and heparin
ii. natural killer (NK) cells: destroy viral-infected and tumor cells
c.
antimicrobial substances
i.
ii.
tears (lysozyme)
transferrins
•
•
iron-binding proteins in blood
reduce available Fe for pathogen
d. molecular defenses
i.
interferon
•
ii.
by
some antitoxins
•
iii.
neutralize toxins
complement system
•
•
e.
anti-viral protein produced
infected cells
20+ proteins in blood
many functions
inflammation and fever
i.
ii.
confine infection
raise temp. above pathogen’s normal
range
Fig. 33.6
Action of the complement
system against bacteria
Fig. 33.3
A summary of
nonspecific
defenses
B.
specific defenses (third line of defense)
1.
2.
3.
respond only to one antigen at a time (narrow spectrum)
stronger than nonspecific defenses
specific leukocytes (lymphocytes)
a.
b.
4.
T-cells
B-cells  plasma cells
antibodies (immunoglobulins; ab)
•
proteins that bind specifically (lock-and-key) to antigens (ag)
5. some antitoxins
III. Specific Immunity
A.
kinds of immunity
innate: genetics or 1st and 2nd line only
acquired: some way other than genetics; involves specific defenses
1.
2.
a.
active: body makes it’s own ab’s
i.
naturally acquired active: by having a disease
ii. artificially acquired active: through vaccine
•
weakened or dead form of antigen  causes immune response
b.
B.
passive: body obtains ab’s through external source
i.
naturally acquired passive: across placenta or in breast milk
ii. artificially acquired passive: through immune serum
antigens (ag)
1.
usually parts of pathogens
•
foreign proteins or carbs of certain size
C.
cells and tissues involved in specific immunity
1.
specific leukocytes (lymphocytes)
B-cells  produce ab
i.
become plasma cells  secrete ab
ii. memory cells  protect if invaded by same pathogen again
b. T-cells
i.
cytotoxic (Tc)
•
destroy viral-infected, tumor, or foreign cells
ii. helper (Th)
•
activate Tc, B-cells, and other immune cells
iii. suppressor (Ts)
•
turn immune system off after infection
iv. memory (Tm)
•
become Tc or Th to protect against same antigen
a.
2.
circulatory and lymphatic systems
a.
b.
c.
transport immune substances to site of infection
leukocytes concentrate and mature in lymph nodes
immune surveillance
•
lymph nodes, Tc, macrophages, NK cells
D. four general properties
•
recognition, specificity, heterogeneity, memory
Fig. 33.14 Action of cytotoxic T-cells
Cytotoxic T-cells attacking and destroying a cancer cell (target cell)
IV. Dual Nature of Immune System
A.
humoral immunity (antibody-mediated)
1.
a.
b.
2.
3.
a.
b.
4.
a.
b.
c.
d.
e.
consists of:
B-cells, plasma cells, memory cells
Ab circulating in blood
defends against extracellular pathogens and free ag
properties and structure of Ab’s
heavy vs. light chains
constant vs. variable regions
classes of Ab’s
IgG
IgM
IgA
IgE
IgD
Fig. 33.11
Structure of
an antibody
The five classes of antibodies
5. ab’s work by neutralizing an ag
a. neutralization  renders ag ineffective
b. ways of accomplishing this:
i. coat ag to prevent adherence
ii. enhance phagocytosis
• coat surface of ag
o opsonization
• clump many ag’s together
o agglutination
• precipitate soluble antigen
iii. act as antitoxins
iv. trigger inflammation and fever
v. activate complement system
The action and
work of antibodies
6.
T-cell influence
•
Th cells bring ag to B-cells  activate B-cells  ab produced
B. cell-mediated immunity
1.
consists of:
a. direct action of T-cells (esp., Th and Tc)
b. nonspecific leukocytes
•
phagocytic wbc’s, basophils, NK cells
2. defends against intracellular pathogens and cancer
3. process:
a. some macrophages act as antigen-presenting cells (APC's)
•
bring ag to Th cells  Th cells activated
b. Th cells bring ag to B-cells and Tc cells  B-cells and Tc cells activated
c. major histocompatibility complex (MHC)
•
protein on all of an individual’s cells that identifies “self” tissue
C.
immune cells communicate with each other through various chemicals
Fig. 33.7
A summary
of specific
defenses
V.
Sequence of Events Occurring During a Typical, First-Time Infection
•
pathogen (ag) invades and damages body  nonspecific defense activate
(2nd line)  macrophage phagocytizes a pathogen  macrophage
displays ag on its surface  macrophage presents (APC) ag to a Th cell 
Th cell brings ag to B-cells and activates other T-cells (esp., Tc cells)  Bcells produce ab in response to ag  some B-cells become plasma cells 
plasma cells release ab  ab’s and various T-cells begin attacking ag 
some B-cells and T-cells (Th, Tc) become memory cells near end of
infection  Ts cells turn immune system off
An overview of the immune response
VI. Immunologic Memory
A.
B.
immune system remembers what it has been exposed to previously
1. responds very quickly and efficiently to such ag’s
a. memory B-cells  become plasma cells  release large amts. of ab
b. memory T-cells (Tm)  become Th and Tc cells  quickly attack ag
2. most often, symptoms do not even occur
primary vs. secondary response
VII. Factors That May Modify the Immune Response
A.
B.
C.
D.
E.
F.
G.
compromised host
genetics
age
nutrition
effect of injury
environment
stress
Fig. 33.9
Primary and
secondary response