specific

Report
chapter 17:
specific/adaptable defenses of the host:
the immune response
defense against infection & illness
body defenses
innate/
adaptable/
non-specific
specific
epithelium, fever, inflammation,
complement, interferon,
macro/DCs
“immunity”
lymphoid cells
humoral
cell-mediated
non-self Ag
altered self Ag
Ab & B cells
APCs & T cells
lymphoid cells: B cells & T cells
naïve lymphocytes
• highly specific (Ag)
• >106 at a time
• billions made/day
• live weeks to months
lymphoid cell activation: B cells & T cells
Ag travels to lymph node
alone (B) or attached to APC (B/T)
Ag encountered by lymphocyte
lymphocyte is activated
bloodstream
lymphocyte clonally expands
activated T cells bloodstream
B cell Ab bloodstream
extravasation at infection site
adaptable cells bind Antigen (Ag), not PAMP
Ag: bound by WBC receptors
• BCR
• TCR
• Ig/Ab
getting info to lymphocytes
naïve B cells and T cells live in lymph nodes, Ag comes to them
humoral immunity
T cell independent response: weak, short,  affinity
• activation takes several h
• plasma cells w/in 1 wk
• memory cells w/in 2 wks
antibodies (Ab)
memory
acute
phase
results of Ag-Ab binding
Ab-dependent cell-mediated cytotoxicity (ADCC)
• Ab-bound target cell lysed by natural killer (NK) cells & eosinophils
large parasites are too big for phagocytosis &
integument is resistant
1. IgE coats parasites
2. Fc receptor of eosinophil recognizes IgE
3. helminth-bound IgE causes the eosinophil to
degranulate (release cytotoxins from granules)
NK cells activated by antibodies
1.
NK Fc receptor recognizes the Fc portion of Ab bound to target cell
2.
NK cell releases cytokines and cytotoxic granules
3.
these enter the target cell and trigger apoptosis
cell-mediated immunity:
Major HistoCompatibility molecules
& T cell receptors
CD8 TC cells & MHC Class I molecules
ALL body cells
MHC class I molecules & Cytotoxic T (Tc) cells
perforin
production
granzyme
production
CD4 TH cells & MHC Class II molecules
APCs only
TH cell activation by APCs: MHC Class II
T cell memory
the “helper” T cell
lymphocyte response
Pathogen
group
adaptive response
Ab (B cell)
TC cells (CTLs)
TH cells
extracellular
bacteria
bound Ab initiates
total immune
response*
not effective
B cell expansion
no direct role in elimination
intracellular
vesicular
bacteria
internal pathogen
renders Ab useless
cytosolic replication
of bacteria can cause
TC response
hyperactivation of
macrophages*
viruses
free viruses are
bound & neutralized
TC cells kill virallyinfected cells*
activate B cell vs. free viruses
& NK cells vs. infected cells
no direct role in elimination
helminths
antibody-mediated
cell-dependent
cytotoxicity (ADCC)*
not effective
B cell expansion
no direct role in elimination
enhance ADCC
comparing the innate & adaptive responses
Innate
Adaptive
phagocytes, NK cells, eosinophils, mast cells
T cells and B cells
response present from birth
response develops in first year of life
responds to infection within minutes to hours
responds to infection after a few days
PRRs on phagocytes recognize common
pathogen structural patterns
BCR & TCRs recognize specific epitope structures
all cells of one type have the same receptors
each B cell or T cell has a different Ag specificity
not clonal– react to common pathogen ligands
clonal response by Ag-specific effector T &
plasma B cells
defense in any connective tissue in body
defense generated in 2o lymphoid tissue
no memory generated
generates memory
coordinated innate & immune attack
coordinated humoral & cell-mediated attack
chapter 17 learning objectives
1.
What kinds of pathogens do the humoral and cell-mediated branches of the immune system target? How do the terms self,
non-self and altered-self relate to this discussion?
2.
What are the differences between T cells and B cells, in terms of place of maturation and receptors?
3.
What is the lymph system? What is the difference between lymph, interstitial fluid and blood?
4.
Where are MHC class I, MHC class II, BCRs and TCRs found?
5.
In class, we discussed three ways that B cells can be activated and clonally selected. Understand how each of these results in
the production of both plasma cells and memory cells.
6.
Both macrophages and dendritic cells are members of the innate defenses that routinely phagocytize pathogens. How are they
different?
7.
Draw and label the structure of an antibody molecule. Include the following components: light chain, heavy chain, variable
region, constant region, disulfide bonds, antigen binding site, and antigen. Compare and contrast IgG and IgM.
8.
What five things result from the binding of Ab to Ag? How do the two types of Ab-dependent Cell-mediated cytotoxicity
discussed in class differ?
9.
What kind of cells produce MHC class I molecules? Which produce MHC class II? Which T cells interact with these and what does
the interaction between T cell and MHC molecule cause?
10.
Compare and contrast the Helper T cell and the Cytotoxic T cell (cytotoxic T lymphocyte)
11.
How is memory produced in the cell mediated branch of the immune system?
12.
Distinguish between the antibody-mediated (humoral) immune system and T cell-mediated immune system. Know the steps
and key players in both.
13.
Which is the best lymphocyte response for: extracellular bacteria, intracellular vesicular bacteria, viruses and helminths?
14.
Compare and contrast innate and adaptable defenses for: response time, specificity, memory, & location of defense

similar documents