Immune System, Lecture 2 Flashcards
Innate - inflammation
- inflammation or inflammatory response: local responses to tissue damage
- sources: pathogens, abrasions, chemical irritants, cell distortion or disturbance, extreme temperature (sun burn) → remarkably similar responses no matter source
- characteristic symptoms: redness, pain, heat, swelling (also loss of tissue function in damage area sometimes)
- often resident immune cells (like fixed macrophages) at injury location but may not be enough - cells will need to migrate to site
- goals: isolate, destroy or inactivate invader / remove debris / prepare for wound healing and tissue repair
Innate - inflammation (stage 1)
- release of inflammatory mediators (histamine, kinins, prostaglandins, complement proteins, cytokines, etc.)
trigger - local effects
- vasodilation microcirculation: increases blood flow for delivery of leukocytes, plasma proteins, nutrients, oxygen, etc. (outward signs: local redness, heat - good signs that you are getting vasodilation - tend to signify things coming into that area)
- increases permeability of blood vessels: endothelial cells contract opening spaces between them
trigger - non-local effects
- release of stored immune cells (spleen, lymph nodes) into circulation
- proliferation (increasing numbers) of new immune cells in bone marrow (make more immune cells)
my notes:
- increase in blood flow at local site of injury (vasodilation microcirculation) - not vasodilating a whole system - vessel becomes larger, so more circulation
- endothelial cells pulling a part from each other and creating a gap (things might migrate in those gaps in later stages)
- spleen contracts (contraction signal) and push cells into circulation
innate - inflammation (stage 2)
- phagocyte movement into injury site from blood (starts within an hour)
- neutrophils early (pretty quick - first ones to get there), later circulating monocytes (later, larger response) mature into wandering macrophages
stages - margination: phagocytes and local endothelium each form adhesion molecules (allow things to stick to particular location) for attachment to local area
- diapedesis: phagocyte migration through blood vessel walks into interstitial fluid
- chemotaxis: phagocyte migration to injury site guided by cytokines (chemoattraction)
◦ fluid follows; local distension (outward signs:
some edema/swelling, pain) - as cells move into
interstitial fluid, they bring some fluid along
◦ cytokines can come from a number of sources
and attract many needed things / timing of
release important to timing of attraction
my notes:
- migrate to injury site not the bloodstream (ex. where splinter is on diagram)
- wandering just means migrating to that location
- from circulating, they begin sticking to a particular location (accumalate a population of cells): stage 1
- immune cell actually going through the wall of blood vessel into interstitial fluid (stage 2)
- cytokines form chemoattraction that follows chemicals to where the injury site is
Innate - inflammation (stage 3)
- worn out, damaged, or dead cells replaced
- may include new network of blood vessels (angiogenesis - recreating some of the network of blood vessels) to help remove debris and deliver needed nutrients and oxygen
- tissue repair may leave no sign or in other cases a scar (scar tissue often less functional: denser collagen fibers, decreased elasticity, fewer blood vessels)
- remodelling may continue after initial repair (almost consider it stage 4, remodelling (long term) is not stage 3)
Adaptive Immune Responses
- specific / “lock and key”
- 3rd line of defense
- slower response, ultimate defense (big immune response)
- distinguishing adaptive from innate:
◦ recognize specific material to be attacked
‣ recognize/tolerate what is self
‣ recognize/reject what is foreign (non-self)
◦ memory for previous encounters (encounter a
specific pathogen, it will create memory cells the
first time so second time it can respond to it
differently, properly):
‣ even more rapid and strong immune
responses with subsequent encounters - antigen: any molecules that can trigger an adaptive immune response against itself or cell bearing it
◦ “recognition” often proteins on the pathogen
surface - lymphocytes are essential cells on adaptive system (mount some of the strongest responses)
Lymphocyte Development
B cells:
- arise and mature in bone marrow
T cells:
- arise in bone marrow and migrate to thymus as immature T cells
- mature in thymus to helper, regulatory and cytotoxic T cells
B and T cells:
- migrate to secondary lymphoid structures and form clonal populations:
- at this point they are naive lymphocytes
◦ not yet exposed to antigen (has not done any kind
of immune response)
◦ have one specific surface antigen receptor
(multiple copies)
◦ genetically developed (body puts receptor on
there based on genetics not based on any
encounter)
my notes:
- original cells will long be gone when they encounter something (instead the clones will that are left behind in secondary structures)
- never have multiple receptors, just the same one each time being cloned which gives us the “lock and key” concept
Lymphocyte Receptors - immunoglobulins
immunoglobulins (Ig):
- 2 types - B cell receptors / antibodies
- antigen able to recognize B cell receptors / antibodies as part of activation stage
structure - 4 chains - 2 heavy - 2 light
- constant end with stem binding site (always same within an Ig class)
- variable ends with 2 of same specific antigen binding sites (millions of different within an Ig class)
5 classes on immunoglobulins (Ig):
- IgG, IgA, IgM, IgE, IgD
IgG
bacteria and virus, largest class (main one attacking bacteria and virus)
IgA
sweat, saliva, breast milk, tears, mucus, gastrointestinal secretions (involved in a lot of secretions)
IgM
bacteria and virus, appear 1st, short lived (one of the first ones to be developed but does not last long)
IgE
allergic responses, parasites (tends to get overproduced in allergy reactions)
IgD
B cell activation
