MedEd Immuno 1 Flashcards
cells of innate immunity (6)
neutrophils
basophils
eosinophils
macrophages
natural killer cells
dendritic cells
cells of adaptive immunity (2)
B and T cells
which type of immunity is fast vs slow
innate = fast
adaptive = slow
soluble components of the innate immune system
complement
acute phase proteins
cytokines / chemokines
describe activation of the innate immune system
produce phagocytes and release them into blood
endothelial cells express adhesion molecules - allows cells to stick and migrate
phagocytosis
oxidative / non oxidative killing
macrophages communicate to t cells
neutrophils die and form pus
which immune cells is pus mainly composed of
neutrophils
what is the point of dendritic cells in terms of the 2 types of immunity
mediate the transition from innate to adaptive immunity
what type of cell is a dendritic cell
phagocyte
what do dendritic cells do after phagocytosis (3)
upregulate expression of HLA
express costimulatory molecules
migrate via lymphatics to lymph nodes
what receptor do dendritic cells use to migrate to lymph nodes
CCR7 receptor
what do B and T cells do in primary vs secondary lymphoid organs
primary - developed and mature
secondary - interaction with pathogens
which organs are primary vs secondary lymphoid organs
primary - bone marrow and thymus
secondary - spleen, lymph nodes, MALT
what is humoral vs cellular immunity
humoral = deals with antigens from freely circulating pathogens (outside cell)
cellular = deals with clearing the infected cell
lifecycle of a T cell
pre T cells made in thymus
selection in thymus
CD4 or CD8 T cells made
lifecycle of B cell
produced in BM: pro B cell –> pre B cell
develop into IgM secreting B cells
then develop into plasma cells or undergo class switching to make IgG / IgE / IgA
how does T cell selection work in the thymus
low affinity for HLA –> not selected (inadequate reactivity)
intermediate affinity for HLA –> selected
high afifnity for HLA –> not selected (autoreactivity)
what % of produced T cells are selected in the thymus
10%
which T cells go on to make CD4 t cells and which go on to make Cd8 T cells
cd4 = affinity for HLA II
cd8 = affinity for HLA I
what are cd4 T cells aka
T helper cells
what are cd8 T cells aka
T killer cells
3 functions of cd 4 / t helper cells
recognise extracellular protein peptides presented on HLA2
help development of full B cell response
help development of some cd8 t cell response
3 functions of cd8 / t killer cells
reconise intraceullar protein peptides presented on HLA1
kill cells
2 ways cd8 / t killer cells can kill
via perforin / granzyme
via Fas ligand expression
describe B cell selection in the BM
no recognition of self = survive
recognition of self = not selected
what are the 2 fates of a B cell selected in the BM
become IgM secreting plasma cell
undergo class switching to become IgG/A/E B cell
which pathway of the B Cell (IgM or class switching) requires T cells and which is T cell independent
IgM = T cell independent
class switching = T cell dependent
what reaction do B cells undergo to become IgG/A/E B cells
germinal centre reaction
describe the germinal centre reaction
dendritic ells prime CD4+ T cells
CD4+ T cells help B cell differentiation
B cell proliferation with somatic hypermutation isotype switching
what do CD4+ T cells require to help B cell differentiation
CD40L:CD40
2 roles of ABs
identification of pathogens and toxins
interaction with and activation of other immune componnets to remove pathogens
which part of the AB is needed to identify pathogens
Fab
which part of the AB is needed to activate other immune components and remove the pathogen
Fc
which cell exists in immature form in periphery where they recognize pathogens, then mature and become adapted for presenting antigens to T cells in lymph nodes?
dendritic cells
what is the complement cascade
sequence of reactions that enhances the rest of the immune system
what is the starting point of the complement cascade
inactive circulating proteins
what is the activation stage of the complement cascade
proteases cleave the protein and initiate the cascade
what is the end point of the complement cascade
membrane attack complex (MAC) - attacks the pathogen cell membrane
fragments released during the complement cascade have 4 other effects, what are they?
increase vascular permeability
opsonise immune complexes and pathogens
activate phagocytes
promote mast cell and basophil degranulation
name the pathways of the complement cascade
classical or alternative or MBL
–> C3
–> final common pathway
–> MAC
what are the components of the classical pathway
C1 / C2 / C4
what are the components of the MBL pathway
C4 / C2
what are the components of the final common pathway
C5 / C9
how does the classical pathway kill pathogens
Ag-AB complexes
how does the alternative pathway kill pathogens
bacterial cell wall attack
how does the MBL pathway kill pathogens
attacks microbial cell surface and carbs
name 3 broad classes of immunodeficiencies
primary
secondary
physiological
3 classes of primary immune deficiencies
innate
adaptive
complement
4 classes of causes of secondary immune deficiencies and 2 examples of each
infections - HIV, measles
biochemical disorders - malnutrition, renal impairment
malignancy - leuakaemia, lymphoma
drugs - steroids, cytotoxics
3 physiological states of immune deficiency
neonates
pregnancy
old age
name 3 PIDs of failure to produce neutrophils
reticular dysgenesis
kostmann syndrome
cyclical neutropaenia
inheritance pattern of reticular dysgenesis
AR
inheritance pattern of kostmann
AR
inheritance pattern of cyclical neutropaenia
AD
mutation in kostmann
HAX1 protein
mutation in cyclical neutropaenia
ELA-2
PC of cyclical neutropaenia
episodic neutropaenia every 4-6 weeks
Tx for PIDs of failure to produce neutrophils
G-CSF
PID of defect of phagocyte migration
leukocyte adhesion deficiency
3 PC of leukocyte adhesion deficiency
high neutrophil count
absent pus formation
delayed umbilical cord sloughing
pathogenesis of leucocyte adhesion deficiency
deficient in CD11a/18 (expressed on neutrophils, binds to ICAM-1 on endothelial cells)
deficiency = neutrophils can’t exit bloodstream
Tx of leukocyte adhesion deficiency
haematopoietic stem cell transplant
PID of defect of oxidative killing
chronic granulomatous disease
pathogenesis of chronic granulomatous disease
deficiency of NADPH oxidase complex –> impaired killing
4 clinical signs of chronic granulomatous disease
granulomas
lymphadenopathy
hepatosplenomegaly
pus