2.2 - Adaptive Immunity Flashcards
Key Features of Adaptive Immunity
- destruction of infectious microorganisms that evade the 1st and 2nd line of defence/ resistant to inflammation
Features
1) Inducible - activated in response to a specific pathogen
2) Specific - targets specific pathogens
3) Long-lived - provides immunity for a long time
4) Has memory - remembers previous pathogens to allows for faster response upon re-exposure
2 Elements if Adaptive Response
1) Antigens - molecules found on patthgens that trigger the immune response
2) Lymphocytes
Humoral Vs. Cellular Immunity
Humoral Immunity
- antibodies (produced by B cells) bind to antigens on pathogens
- marks cells for destruction
Cellular
- T cells either 1) directly kill cells or 2) stimulate leukocytes to enhance the response
- destroys infected cells
Active VS Passive Immunity
Active
- developed by exposure to antigens
- ex. Vaccine, Infection
Passive
- developed when antibodies are transferred from 1 person to another
ex. from mother to baby
Antigens and Immunogens
Antigens
- sit on the surface of the pathogen
- bind to antibodies
Immunogens
- type of antigen
- induce production of antibodies, T and B cells
- all immunogens are antigens (bind to receptors), but not all antigens are immunogens (some antigens bind but dint produce response)
Haptens
- small molecules that can not cause an immune response on their own
- only become immunogenic when combined with larger molecules
What are Immunoglobulins
- antibodies produced by B cells
Immunoglobulin G: IgG
- most abundant
** can cross placenta and provide immunity to fetus** - accounts for most protection against infections
Classes
1) IgG 1 - involved in parasitic infxns
2) IgG 2 - detects bacteria
3) IgG 3 - activates complement
4) IgG 4 - involved in allergic response
Immunoglobulin A: IgA
2 Types
1) IgA
- in blood
- targets pathogens that enter the bloodstream
2) IgA2 (secretory)
- found in bodily secretions: breastmilk, saliva, tears, mucous
- prevents pathogens from adhering to epithelial layers
- forms protective barrier on mucosal surfaces
Immunoglobulin M: IgM
- largest antibody
- 1st antibody produces in response to an antigen
- synthesized in neonatal life (provides protection for newborns)
Immunoglobulin D: IgD
- low concentration in blood
- expressed on surface of immature B cells
Molecular Structure of Antibody
Y - shaped
Tip of Y = fab region
- where antigens bind
Arms of Y = 4 Polypeptide chain
- each chain has a Variable region and constant region
- variable region allows antibodies to recognize various antigens
Stem of Y - fragment crustibale
- rects with other immune cells
Hinge region - between stem and arms
- allows flexibility in shape to enable better binding
Epitope VS Paritope
Epitope - determinant
- part of the antigen that is RECOGNIZED by antibodies
Paratope - binding site
- binds to corresponding site on antigen (tip of Y)
Functions of Antibodies
Direct (NAP)
1) Neutralization
- neutralizes toxins: antibody binds to pathogen to prevent it from binding with other cells
2) Agglutination
- antibodies clump pathogens together
- makes it easier to be detected by immune system
3) Precipitation
- antibodies bind to antigens that form insoluble complexes
- the complexes can not join tissue so it gets removed
Indirect - antibody activates other components of immune response
1) Inflammation
- binding of antibody to antigen releases inflammatory mediators
2) Phagocytosis
- antibody binds to phagocyte receptors and stimulates them to engulf pathogens
3) Complement
- binding initiates cascade leading to more inflammation
Immunoglobulin E - IgE
- defends against parasites (by attracting eosinophils)
- binds to allergens: triggers allergy symptoms
- binds to mast cells and cause degranulation
- histamine gets released and attracts eosinophils and kills parasites
Secretory/Mucosal Immunity
- lymphoid tissues protect against pathogens that enter through external surfaces
- IgA 2 is the dominant immunoglobulin in mucosal secretions
Why is Clonal Diversity Needed?
- our body can respond to all antigens with only 5 immunoglobulins bc of clonal diversity
- immune system’s ability to produce clones of lymphocytes that can recognize unique antigens
- lymphocytes develop their recognition capacity in thymus and bone marrow
- develops in fetal life
- naive cells remain in the body and are primed to become specific when they encounter an antigen - result in naive but immunocompetent cells
-immunocompetent bc these cells can produce an immune response, but naive bc they have not encountered the antigen and produced specific receptors
B and T cell Development
B Cell
- produced in bone marrow
- each B cell only recognizes 1 type of antigen
T cells
- produced in the thymus
- develop antigen specific t cell receptors that allow them to recognize specific pathogens
B and T Cells
- once mature, leave bone marrow/thymus travel to lymphoid tissues where they become immunocompetent
- undergo central tolerance: to ensure they dont attack bodys own tissues
Primary and Secondary Response
Primary
- occurs when 1st exposed to antigen
- IgM antibodies are detected 1st
- then IgG response
Secondary
- occurs after re-exposure to the same antigen
- response is more rapid bc memory cells have been previously sensitized (need less differentiation/activation)
- a lot of IgG is produced for longer-lasting immune response
Antigen Processing and Presentation
1) B cells and T cells encounter an antigen and get processed by APC’s such as macrophages, B cells
2) APC’s catch the antigen, break it down into smaller fragments, and present these on the surface of a histocompatibility complex (MHC )
3) While B cells process antigens, they differentiate into plasma cells (which then produce antibodies)
T cells differentiate into effector cells:
T - helper - coordinate immune response
T cytotoxic - destroy cells
Result:
B cells - antibody producing plasma cells
T cells - contribute to immune response and kill pathogens
Cell Interactions
- intrecellular collaborations result in the production of effector and memory cells
- requires 3 intracellular signalling events
1. Antigen specific recognition - T cells identify and bind to antigens presented by APC’s
2. Activation of adhesion molecules
3. Response to specific cytokines - cytokines propagate response to other immune cells
Function of T Helper Cells
- help drive the maturation of T and B cells
- amplify interactions bw APC’s and lymphocytes
2 Types
1) Th1
- develop cell-mediated immunity
- activate macrophages and cytotoxic cells (destroy pathogens)
2) Th2
- develop humoral immunity
- activate B cells to produce antibodies (mark antigens for destruction)
What are Super Antigens
- SAG binds to non-specific (variable) portion of T cell receptor
- the non-specific binding activates a lot of T cells = overwhelming immune response
- result is excessive cytokine production which causes fever, low BP, and shock
B Cell Clonal Selection
- when immunocompetent B cell encounter antigen for the 1st time, it is stimulated to differentiate and proliferate
- it differentiates into a plasma cell
- each plasma cell produces antibodies specific to antigens
- B cells undergo class switch: they can produce different classes of antibodies which allow a more targeted immune response
T Cell
- T cells are activated when an antigen binds to a T cell receptor
T cells either
1) directly kill abnormal cells
2) assist activation of other immune cells
T-regulatory cells
- prevent the immune system from attacking bodys own tissues
Memory T Cells
- remember previous encounters with antigens and allow for quick response
T Cytotoxic Cells
- destroy infected cells
Role of perforin and granzymes
- Perforin: creates pores in infected membrane
- Granzyme: enters cell and triggers apoptosis
Fetal Immunity
- fetus has sufficient IgM (produced in neonatal life)
- IgG passes from mother to fetus to provide immunity in 1st few months of life
- newborns are immunologically immature
- deficient antibody production,
phagocytotic actvity
- deficient antibody production,
Aging and Immune Function
1) Decreased T cell activity
- fewer T cells migrating to thymus (where they mature) = decreased function
2) Thymus Shrinks
- decreased production of thymic hormone which are required for T cell differentiation/maturation
- decreased T cell efficiency
3) Decreased ability for antibody to respond to antigens
- teeters: amt of antibodies in our system for certain illness
- teeters decrease overtime
- insufficient teeters can make us experience infection we were previously immue to
