immunology Flashcards
physiological conditions causing a secondary immune deficiency
extremes of life
- ageing
- prematurity
infections causing a secondary immune deficiency
HIV
measles
treatment interventions causing a secondary immune deficiency
immunosuppressive therapy
anti-cancer agents
corticosteroids
malignancy causing a secondary immune deficiency
cancer of the immune system- lymphoma, leukaemia, myeloma
metastatic tumours
biochemical and nutritional disorders
malnutrition
renal insufficiency/dialysis
type 1 and type 2 diabetes
specific mineral deficiencies eg iron, zinc
what is a granuloma
an organised collection of activated macrophages and lymphocytes
what can trigger the formation of a granuloma
non-specific inflammatory response triggered by diverse antigenic agents or by inert foreigh materials
how is a granuloma formed
the triggered response results in activation of T lymphocytes and macrophages
failure of removal of the stimulus results in persistent production of activated cytokines
end result is organised collection of persistently activated cells
differential diagnosis of lung granuloma
sarcoidosis
mycobacterial disease (TB, leprosy)
berylliosis, silicosis and other dust diseases
chronic stage of hypersensitivity pneumonitis
foreign bodies
presentation of antibody deficiencies
recurrent bacterial infection (recurrent respiratory tract infections, GI infections)
antibody mediated autoimmune diseases
- idiopathic thrombocytopaenia
- autoimmune haemolytic anaemia
common primary antibody deficiences
Common variable immune deficiency
selective IgA deficiency
what is common variable immune deficiency
low IgG, IgA and IgM
recurrent bacterial infections esp respiratory
often associated with autoimmune disease
what is selective IgA deficiency
very common
2/3rd individuals are asymptomatic
1/3rd have recurrent respiratory tract infections
genetic component
Hypogammaglobulinaemia
reduced serum immunoglobulin levels
primary causes of recurrent bacterial infections and hypogammaglobulinaemia
antibody deficiency
- common variable immune deficiency
- specific antibody deficiency
other conditions, rare in adults (bruton’s agammaglobunaemia)
secondary differential diagnoses of recurrent bacterial infections and hypogammaglobulinaemia
protein loss
- protein losing enteropathy
- nephrotic syndrome
failure of protein synthesis
- lymphoproliferative disease (chronic lymphocytic leukaemia, myeloma, NHL)
function of natural killer cells
kill cells that lack MHC (molecules on surface)
- no need for antigen specifity
no long term memory
part of innate immunity
moa of biologic drugs
most are artificial antibodies that block the body’s own proteins
so they act just like passive immunisation and have to be injected every couple of weeks
what is adalimub
targets anti-TNF
is an antiinflammatory
used in rheumatic and inflammatory diseases
what is pembrolizumab
acts of anti-PD1
activates T cells
used against cancer
what is secukinumab
acts on anti-interleukin 17
main action: blocks one inflammation pathway
used in psoriaisis, arthritis, MS
types of transplant rejection
hyperacute rejection
acute cellular rejection
acute vascular rejection
chronic allograft failure
pathology of hyperacute rejection
takes minutes to hours to show
thrombosis and necrosis
type II hypersensitivity
management of hyperacute rejection
none
pathology of acute cellular rejections
5-30 days
cellular infiltration
type IV hypersensitivity
CD4 and CD8, T cells
treatment of acute cellular rejection
immunosuppression
advantages of inactivated vaccines
can be made quickly
elicit good antibody responses
easy to store
usually safe
disadvantages of inactivated vaccines
not very potent
- doesnt stimulate clonal expansion of B and T cells > requiring multiple injections
how are neutrophils attracted to site
by release of cytokines (TNFa)
complement system activation
antigen-antibody binding called C1 complex which in turn activate C3 convertase
alternative pathway
C3b production leads to more C3 convertase activation
- C3b binds to pathogen surface and associates with other complement proteins, forming C5 convertase
what are C3b and C5b
proinflammatory mediators
what can happen with a complement deficiency
predisposes to bacterial infections (esp meningitis)
what are TLRs
toll like receptors
- respond to PAMPS
- expressed on phagocytes and dendrites as built-in burglar alarm for microbes
outcome of TLR activation
pro-inflammatory cytokines and type 1 interferon secretion
TLR dysfunction
can lead to immunodeficiency (too little)
autoimmunity (too much)
TLR dysfunction
can lead to immunodeficiency (too little)
autoimmunity (too much)
what is TNF alpha
immediate early fire alarm signal response to many stressors
how to vaccinations work
produce memory in B cells and T cells
long lived memory B cells are generated during primary immune responses that can survive for many years even after the antigen has been eliminated
memory B cells rapidly re-activate in response to second encounter with that specific antigen
(clonal expansion, differentiated into plasma cells, antibody production)
