3-overview of immune system II Flashcards
Innate immunity
(Timing
Uses receptors to detect pathogens
Key cell types
Actions
Response to repeat infection
Major components )
1st line of defense
Fast
Nonspecific
Encoded in germline
Limite number of receptors
Unchanging
Phagocytic cells
Macrophages
Neutrophils
Dendritic cells
Others
Induces local inflammation
Key in immunity
Same each time
Short term memory
Barriers
Skin
Phagocytes
Pattern recognition molecules
Adaptive immunity
(Timing
Uses receptors to detect pathogens
Key cell types
Actions
Response to repeat infection
Major components )
Slow to develop (5-6+ days)
Use randomly generated antigen receptors
Huge diversity of receptor specificities
Highly specific to individual molecules
Lymphocytes
B & T cells
Responsible for specific (to epitopes) immune responses
Clear infections
Sometimes result in memory
More rapid & effective with each subsequent exposure
To be infected with same thing
T & B lymphocytes
Antigen-specific receptors
Antibodies
Phases of the immune response
-Many phases to immune response
Takes time
-Innate immune response:
Fast, Only last days
-Adaptative immune response
Last long – sometimes results in memory – up to lifelong immunity
Innate immune response: what happens first
Breach of epithelial cell layer
immune cells can sense patterns across pathogens
innate immune cells have PPR, what is PRR
-Pattern recognition receptors (PRRs)
Provide initial discrimination between self and non-self
Recognize broad categories of molecules that are commonly found in pathogens (PAMPs)
-PRR binds to PAMPs
what are PAMPs
Pathogen-associated molecular pattern (PAMPs)
Common foreign structures that characterize whole groups of pathogens
Part of microorganisms that is not found in host body.
EX: Cell wall of bacteria – category of pathogen
what happens when PRR binds to PAMP?
-Innate cell activation & local inflammation
-Activation of PRR on cells (macrophages) – directly induces effector functions in these cells. (phagocytosis)
-PRR bind PAMP – phagocyte
-Innate cells amplify immune response by production of inflammatory mediators
-Cytokines & chemokines
inflammatory mediators
cytokines & chemokines produce inflmmatory responses: Redness, heat, swelling, pain
inflammation response process:
1.Bacteria trigger macrophages to release chemokines & cytokines
2.Vasodilation – blood vessel loosens up – cell enter site of infection
Increase vascular permeability – cause redness/heat/swelling
3.Inflammatory cells migrate into tissue
Releasing inflammatory mediator – pain
what does pathogen detection lead to?
-Activation of immune cells
-Detect pathogens (PAMPs) using receptors (PRRs)
-one of those cells is: Dendritic cells
they Present antigens & Bridge innate/adaptive
how does DC become mature?
when their PRR is activated/when they have phagocytosed PAMP/pathogen
Once matured, they travel to secondary lymph organs (lymph nodes0
how does Dendritic cells link innate & adaptive immunity
DC travel from the site of infection – to local secondary lymphoid tissue (lymph nodes) – interacts & activate naive T cells (by presenting antigen)
where does T & B cell activation occur
in lymph node
T cells activated by 3 signals:
-Antigen-presenting cels (APCs) activate T cells through 3 signals
-Through interaction of specific molecules
-Receptor and cytokines
antigen presentation
-Epitope of an antigen – can be a piece of peptide buried within a protein
-Antigen/epitope – presented using specific molecule (MHC – Major Histocompatibility Complex) to T cell receptors
Adaptive immunity: Activation of adaptative immunity
-Antigen-specific cells – activated secondary lymphoid tissues (Lymphoid nodes)
-T cells
-B cells
There antigen specificity – determined by their receptors
-T cell receptor (TCR)
-B cell receptor (BCR – antibody (can be secreted) – immunoglobulin)
Antibodies (Ab)
-Secreted immunoglobulin (Ig) molecules
-Made by B lymphocytes & its progeny plasma cells
-Bind Antigens (Ag)
-Ab present circulating in serum = fluid component of blood
-2 Abs can recognize different epitopes on the same antigen (very specific)
3 Differences between B & T cells
-B cells arise and mature in the Bone marrow
T cells arise from bone marrow progenitors, but generates and mature in Thymus
-BCR can be membrane-bound or secreted (Ab/Ig)
TCR only exits as membrane-bound
-BCR can recognize Ag in its natural form
TCR can only recognize small pieces from Ag only when bound to molecules of MHC on the surface of APC (Antigen-presenting cells)
Specificity of BCR & TCR
-Individual B & T cells – each have an individual specificity for a single antigen/epitope
-Each lymphocyte expresses many identical copies of 1 receptor with 1 specificity for 1 Ag
-Huge diversity of lymphocytes/with their own specificity
-theoreticlly can respind to any antigen that can come along, by rearranging & editing the genomic DNA encoded by antigen receptor expressed by B&T cell
During development, if a lymphocyte reacts to self-antigen
-eliminated/removed
-A test if lymphocyte binds to the self-antigen
Clonal selection
-When B/T cell interacts with its specific antigen – it is selected and activated
-Activation = result in proliferation – produce many clones
-Each clone is reactive against the Ag initially stimulated by the original lymphocyte
-Proliferation & differentiation (no longer naive) of activated specific lymphocytes to form clones of effector cells
-Effector cells eliminate Ag
what happens when T & B cells are activated in lymphoid organs
-become effector cells that can fight infection
-Happens through both humoral & cell-mediated activities
-Clear infection – need to leave lymph nodes & enter site of infection
Humoral immunity
combats pathogens via antibodies
-Mediated by antibodies produced by B cells
-Contribute to adaptive immunity by producing specific antibodies
Ab:
-Diff. Types
-located in diff.locations
-Act in diff. Ways
-Involved in clearing and/or neutralizing antigen
Cell-mediated immunity
involves primarily T lymphocytes
-Mediated by T cells
-Many different T cell subsets can get activated – depends on situation & exert variety of effector functions
EX:Diff. T cells – diff. Function
-Some help activate B cells
-Some help activate macrophages
-Some kill infected cells directly
After clearing the infection:
clones of T lymphocytes left, no longer needed:
-Downregulation of lymphocytes
-and maybe immunological memory
Immunization
Deliberate induction of an adaptive immune response
active immunization
Active: working immune system
-Natural – natural infection – memory
-Induced – vaccination – activate immune response – memory
Passive immunization
Passive: with cells/molecules that mediate immunity (NOT immune response)
-Natural – mother-to-fetus transfer of antibodies
-Induced – monoclonal antibody therapy
