Week 10: Host Defense Flashcards
innate immunity
• Physical and chemical barriers that exists to prevent infection from occurring in the first
place
• Non-specific, primary response mechanisms
adaptive immunity
• Highly coordinated and specific response to a particular pathogen
Anatomical Barriers:
Physical • Skin • Mucus • Cilia Chemical • Stomach acid • Enzymes in tears • Gland secretions
Pattern recognition receptors (PRR)
recognize structures that are shared by a class of microbes
Toll-like receptors (TLRs),
expressed on Macrophages and Dendritic cells,
recognize different classes of microbial structures; 10 unique TLRs exist;
When PRRs recognize their target molecule,
the macrophage or the dendritic cell will
release cytokines into the environment.
The cytokines released by a macrophage or dendritic cell are specific
to
the type of PRR that was triggered, and thus is specific to the type/ class of pathogen.
Interferons
signal to neighbouring cells that a viral infection is present. This shuts down
the neigbouring cells’ ability to synthesize proteins so that viral replication is inhibited
and spread is slowed in the area
If the innate response isn’t sufficient to reduce the infection,
the
adaptive response is activated
The bridge between the innate and the adaptive immune response
are the
antigen presenting cells (APCs).
Now loaded with antigen,
the APC must present
antigen to a
lymphocyte to
stimulate an adaptive
response
T cells develop from
lymphocyte precursor cells in the bone marrow
and complete their maturation in the thymus (hence, T-cell)
There are two types of T-cells
- Th cells – Helper T-cells
* Tc cells – Cytotoxic T-cells
If the TCR recognizes the antigen,
the
Th cell is activated
Upon activation Th cells
Proliferate Begin to produce effector cytokines that support either the • Cell-mediated response • Humoral response
For intracellular pathogens (viruses, intracellular bacteria)
Th cells will release IL-12, among other cytokines, which will activate Tc cells
Upon activation, Tc cells
• Proliferate
• Circulate through the body and scan all
cells for antigen
• When the TCR recognizes its specific
antigen, it kills the infected host cell to
prevent further spread
Upon activation, most Th and Tc cells become
effector T-cells;
however, some become memory T-cells
Effector T-cells
Elicit the primary response and mediate their effects immediately
Memory T-cells
- Do not respond immediately; are mostly inactive
* Long lived cell
B cells develop from
lymphocyte precursor cells in
the bone marrow and complete their maturation in
there as well
B-cells require two signals to
activate it
• Specific antigen-antibody interaction
• Cytokines secreted by Th cells;
generally IL-4 and IL-5
Activated B-cells will proliferate and
develop into either:
• Effector B-cells; called plasma cells
which secrete antibodies
• Memory B-cells; long-lasting cells
Neutralization
• Binds to the surface of pathogens, effectively
blocking their access to infect other cells
Agglutination
• Because antibodies have two binding sites, they
can bind to two antigens. Clumping of several
antibody-antigen complexes is called
agglutination
• Pathogens stuck in these clusters are unable to
infect host cells
Opsonization
• Antibodies have a binding site for phagocytic cells;
as a result they enhance phagocytosis of
antibody-bound antigens
IgM
Initial antibody secreted by plasma cells
IgG
• Follows IgM production, but is the type that is most
abundantly produced during a humoral response
• Due to its size it can cross the placenta and enter breast
milk; important in newborn immunity
IgA
- Offers protection in the mucous membranes
- Tears, saliva, GI tract
- Can also enter into breast milk for newborn immunity
IgE
• Most often associated with allergy
inductive period
time between the
initial infection and the onset of the adaptive
response (usually measured by antibody
production)
Regulatory T-cells (Tr cells) help to slow the adaptive
response after an infection is cleared
• Effector T-cells and plasma cells (effector B-cells) are
eliminated
• Memory T-cells and memory B-cells persist
A secondary exposure to
the same pathogen
typically results in
faster and stronger
response due to the
presence of Memory T
cells and B cells
Inactivated, or Heat-killed vaccine
- Made from killed pathogen
- Generally develops a weaker response and less protection
- Regarded as highly safe – no chance of mutation
Attenuated
• Made from weakened pathogens
• Generally develops a more robust response, more memory cells and better long-term protection; but, in some cases they are
regarded as less safe. Since it is a live, albeit weakened, form of the pathogen there is always a slight risk that mutation could
result in infection
Subunit
- Made from subunits of the pathogen (antigens/ proteins)
- Generally develops a weaker response and less protection
- Regarded as highly safe – no chance of mutation
