Immuno Exam 1 - Adaptive immunity - Extracellular Pathogens Flashcards
Give a brief summary of how macrophages and neutrophils initiate the immune response to extracellular pathogens
Microbes bind to neutrophils receptors → phagocyte membrane zips up around microbe → microbe ingested in phagosome → fusion of phagosome with lysosome → activation & killing of microbes by lysosomal enzymes in phagolysosomes & of phagocytosed microbes by ROS & NO
What kind of immunity does Th1 drive?
Th1 immunity referred to as a driver of cell mediated immunity – kicks off CD8+ T cells, activates macrophages other phagocytes
What kind of immunity does Th2 drive?
Th2 immunity drives the humoral antibody response – interacts with B cells, based on cytokine being secreted, what antibody is produced is determined
What antibody activates complement?
IgM
What antibody does INF-gamma activate?
IgG – Fc receptor-dependent phagocyte responses, complement activation, neonatal immunity
What antibody does IL-4 activate?
→ IgE – immunity against helminthes, mast cell degranulation
Describe stimulation of isotype switching
Antigen stimulated B cells may differentiate into IgM antibody-secreting cells CD40L and cytokines, or cells that produce different Ig heavy chain classes influence…
IFN-γ induces to IgG
IL-4 induces to IgE
Mucosal tissues, cytokines TGF-β induce to IgA
How can B cells be activated to produce antibody?
B cells produce antibodies but must become activated to do so; naïve cannot
Can be activated by binding to microbe
T cell independent antibody production – neutralize free floating pathogen
Complement activation → recognition by B cell → signals from Ig-CR2 complex
Soluble antigen is capable of activating B cells
Involves crosslinking of immunoglobulin receptor
Typically involves antigens with large repeating epitopes but not proteins
Primarily results in production of IgM (no class switching)
How long does it take for antibodies to develop after initial interaction
About a week
What antibodies are T-cell dependent and what is the consequence?
IgG is usually T-cell dependent – after more time of more circulation after exposure
Peaks at 10-14 days
What antibody is T-cell independent and what is the significance?
IgM can be, but not always, T-cell independent – less time of less circulation after exposure
Peaks at 3-5 days
How does exposure to microbes cause changes in phenotype and function of B cells?
- Increased survival, proliferation of B cells
- Increased expression of B7-1/B7-2
- Increased expression of cytokine receptors IL-4 and IL-2 (survival signal)
- Increased expression of CCr7 & migration from follicle to T cell areas
Describe the pathway of activated B cells clonally expanding
Activated B cell → clonal expansion
→ become plasma cell + IgM → antibody secretion
→ IgG-expressing B cell+ IgG → isotype switching
→ high-affinity Ig-expressing B cell + high affinity IgG → Memory B cell
Describe T and B cell interactions in lymph nodes (where abouts are they)?
T cells migrate to edge of T cell zone; B cells migrate to edge of follicle & into T cell zone
T cells activate B cells which then migrate back to follicle (to germinal center)
Activated → enlargement of lymph node
Is isotype class switching dependent on T cells
YES! AND CYTOKINES Isotype class switching is dependent T cell interactions and cytokines Antigen presentation to helper T cell → activation of T cell, expression of CD40 ligand and cytokine secretion → activation of B cell by cytokines & CD40 ligation → B cell proliferation & isotype switching induced by cytokines
What are the general sequential phases of the adaptive immune response?
Recognition of antigen by specific lymphocytes → activation of lymphocytes (proliferation & differentiation into effector cells) → effector phase of elimination of antigens
Response declines as antigen is eliminated & most of the antigen-stimulated lymphocytes die by apoptosis
Antigen-specific cells that survive are responsible for memory
Describe what is unique about IgA for dentists
IgA is the most prevalent antibody isotype in the mouth
Must be secreted onto mucosal surfaces
Dimer, connected by J chain& cleaved once in lumen
How do antibodies lead to lysis, phagocytosis, or inflammation?
(IgM, IgG, IgA) → neutralization of microbes & toxins
Bound IgG → opsonization & phagocytosis of microbes
→ Antibody-dependent cellular cytotoxicity via NK cells
IgM, IgG, IgA → complement activation → lysis, phagocytosis or inflammation
Where do antibody producing plasma cells reside?
Bone Marrow
Where do memory B cells reside?
In secondary lymph nodes
Describe active immunization
Induces adaptive immunity, immunological memory & protection
Involves ‘live’ or killed vaccines
Wide range of antigenic preparations is in use
Describe passive immunization
Passive immunization is accomplished by the passive injection of preformed antibodies
(Or passage to fetus from mother)
What are the 3 kinds of Live vaccines
- Attenuated
- Heterologous
- Recobinant
Describe Live attenuated vaccines
Live attenuated organisms – organisms whose virulence has been artificially reduced
Replication of the vaccine strain in the host reproduces many of the features of wild type infection, without causing clinical disease
Most successful viral vaccines belong to this group
