Immunology Flashcards
name physical barriers in which pathogens can breach
lungs, GI tract, reproductive tract, skin
where do T-lymphocytes mature?
thymus
what 3 cells leave the blood and take long-term residency in tissues?
dendritic cells, macrophages and mast cells
where do B and T lymphocytes spend most of their life?
secondary lymph organs
name the 5 secondary lymph organs
peyers patches, appendix, spleen, lymph nodes, tonsil
name the WBCs in the adaptive immune system
B and T lymphocytes
(other WBCs all innate)
what do B and T lymphocytes produce in the adaptive immune response?
B - antibodies
T - effector T cells
what are the 3 ways complement can be activated and how does each one work?
classic - antigen/antibody complexes
MB-lectin - lectin binding to pathogen surfaces
alternate - pathogen surfaces
what 3 things occur after complement activation?
inflammatory cell recruitment
opsonisation of pathogens
killing of pathogens
what is complement?
a cascade of proteins in serum
what is the mechanism pathway of innate immunity?
infection -> recognition by performed nonspecific effectors -> infectious agent removal
what is the mechanism pathway of the early induced response?
infection -> recruitment of effector cells -> recognition activation of effector cells -> infectious agent removal
what is the mechanism pathway of the adaptive response?
infection -> transport antigen to lymphoid organs -> recognition by naive B/T cells -> production of effector cells -> infectious agent removal
describe the characteristics of neutrophils
short lived (6-12 hours)
first line of defense
phagocytose pathogens
release soluble mediators
what do 1st degree granules in neutrophils contain?
bactericidal enzymes (lysozyme, neutral proteases, acid hydrolases, myeloperoxidase)
what do 2nd degree granules in neutrophils contain?
lysozyme, collagenase, lactoferrin, cathepsin B
what are the 4 steps to innate cells migrating to infection sites?
rolling adhesion, tight binding, diapedesis, migration
how do macrophages act on pathogens?
they reorganise their actin cytoskeleton to engulf bacteria digested in the cell
what are pseudopodia?
macrophage extentions that engulf apoptotic cells
describe the characteristics of macrophages
developed in tissues from precursors
active phagocytic cells
activated by inflammation
long lived
where is the antigen concentrated when arriving via lymph?
lymph nodes
describe the humoral adaptive immune response
antibody (from B cells) mediated extracellular attack
describe the cell mediated adaptive immune response
T cell coordinated intracellular attack
where do B cells mature?
bone marrow
what are B cell receptors?
an antibody (surface immunoglobulin)
what are the 5 stages of the adaptive immune response?
antigen recognition, lymphocyte activation, antigen elimination, contraction (homeostasis), memory
explain the structure of an antibody
bivalent monomer: 4 polypeptide chains (2 light, 2 heavy)
antigen binding fragment (Fab)
crystalline fragment (Fc) - binds cells/complement
what are the 6 functions of antibodies?
agglunitation
opsonisation
neutralisation
cytotoxicity
inflammation
complement activation
(ICONAC)
explain agglutination
enhances phagocytosis and reduces number of infectious units to be dealt with
explain opsonisation
coating of antigen with antibody to enhance phagocytosis
explain antibody neutralisation
blocks adhestion of bacteria and viruses to mucosa
blocks active site of toxin
explain antibody-dependant cell-mediated cytotoxicity
antibodies attached to target cell
non specific immune system cells come and destroy it
explain antibody inflammation
cell disruption by complement, which attracts phagocytic/defensive immune cells
what do helper T cells do in cell mediated immunity?
help B cells
help cytotoxic T cells
direct innate responses
explain the structure and subdivision of T cells in relation to CD(number)’s
T cell receptor on surface, CD3 identifies cells
further subdivided by expression of one of 2 surface molecules: CD4 or CD8
what do CD4 T helper cells do?
recognised antigen presented in MHC 2 on antigen-presenting cells surface and ‘help’ them
what do CD8 cytotoxic T cells do?
recognise antigen presented in MHC 1 on many cell types and can be induced to kill
name 3 signals T cells need for activation
antigen presented in context of MHC
surface molecule costimulation
soluble molecules (cytokines)
how do T cells ‘help’ B cells?
antigen recognition -> T cell effector molecule expression -> B cell activation and proliferation -> differenciation to resting memory cells and antibody-secreting plasma cells
what are the 2 functions of helper T lymphocytes?
help the antigen-driven maturation of B and T cells
facilitate/magnify the interaction between APCs and immunocompetent lymphocytes
what are the steps of the helper T lymphocyte mechanism?
helper T lymphocyte (Th) interacts through antigen-specific and antigen-independant mechanisms -> undergoes differenciation -> mature Th interacts with plasma or T-effector cells
what 3 things may cause inflammation?
physical/chemical damage
infectious agent
antigen challenge
what are the 3 aims of inflammation?
expel foreign infection
prevent metastasis
structural and functional repair
what are the 5 clinical features of inflammation?
redness (rubor) - vasodilation
heat (calor) - vasodilation and fever
swelling (tumour) - ECM fluid
pain (dolor) - pain mediators (bradykinin/serotonin)
function loss (functio laesa) - inhibited limb movement
how does inflammation promote healing of damage?
mobilises effector cells and molecules to site
creates environment suitable for repair
explain the negatives of inflammation
can become out of proportion with threat
more damage than trauma would’ve caused (loss of organ/tissue function)
what is the outcome of sterilising immunity?
recovery
what is the outcome of non-sterilising immunity?
chronic infection
what is the outcome of immune failure?
death
what key defenses are necessary in mycobacterium tubercullosis?
cell mediated immunity
macrophages controlling cell
T cell production of interferon gamma
cytokines
what does M.tb cause?
apical destruction
when does M.tb grow best?
high oxygen levels
what will lungs affected by M.tb contain?
granulomas, caseous necrosis, lymphocytes, epitheloid cells
explain how tb spreads in cavitary tb
cavities open into bronchi allowing M.tb spread through coughing
how has M.tb adapted to survive phagocytosis?
alters phagocyte and coats it with coronin and inhibits its ability to bind to a lysosome
neutralises phagosomal acidification
name the interleukins involved in the M.tb immune response
Interleukin 12 and 18
what is unusual about HIVs life cycle?
its a retrovirus (genome reverse transcribed and integrated into host genome)
what cells keep HIV ‘in check’?
cytotoxic CD8 T cells
what relationship do CD8 response and viral set point have?
greater CD8 response results in lower viral set point
what antibody initially defends against HIV?
free gp-41 specific non-neutralising IgM
what are the symptoms of dengue fever?
fever, rash, mild headache
what damage can severe dengue fever do?
plasma leakage
multi organ impairment
haemmorhage
what 2 antibodies accumulate during the dengue fever immune response?
initially IgM then IgG
explain the difference in secondary dengue infections from the same/different serotypes
same serotype - increased protective immunity
different serotype - increased chance of severity
name some examples of type 1 hypersensetivity
hay fever, food allergies, pet allergies, insect bites
what cells cause type 1 hypersensetivity?
IgE and mast cells
what happens to mast cells during type 1 hypersensetivity?
degranulation releasing histamine and prostoglandins
which antibodies target type 2 and 3 hypersensetivity?
IgM and IgG
what cells are involved in type 4 hypersensetivity?
CD8 cytotoxic T cells
CD4 T cells
what is the difference between organ specific and non-organ specific autoimmune diseases?
organ specific - attack on self-antigens of given organ damaging its structure and function
non-specific - widespread self-antigens are attacked damaging blood vessels/nuclei etc.
define autoimmunity
misdirected immune response, attacks our own bodies as opposed to pathogens
what is the pathway to autoimmunity?
genetic factors or infection/environmental exposure -> immune regulation -> autoimmunity
name 4 organ-specific autoimmune disorders
type 1 diabetes
goodpastures syndrome
MS
graves disease
name 3 systemic autoimmune diseases
rheumatoid arthritis
sclerodema
lupus
what happens during graves disease?
non-regulated auto-antibodies bind to thyroid stimulating hormones (TSH) causing hyperthyroidism
what occurs during transplant rejection?
T cells activated against donor transplantation antigens (CD4 and CD8)
stimulation in peripheral lymphoid tissues
antibody production, complement activation
what are the 4 types of transplant rejections?
hyperacute - existing antibodies in hosts blood
acute cellular - T cells destroy graft parenchyma
acute humoral - antibodies damage graft vasculature
chronic - associated with parenchymal fluids
what is primary immunodeficiency?
congenital, resulting from genetic defects
what is secondary immunodeficiency?
acquired - result of other diseases or conditions
name 3 secondary immunodeficiency diseases
HIV
malnutrition
immunosuppression
name 3 examples of primary immunodeficiency diseases
allergies
autoimmunity
abnormal lymphocyte
how do B cell deficiencies present?
reduced/absent follicles and germinal centres in lymphoid organs
reduced Ig serum levels
how do T cell deficiencies present?
reduced T cell zones in lymphoid organs
reduced DTH reactions to common antigens
name 3 combined immunodeficiencies and what causes them
TB+ SCID - common gamma chain deficiency
TB- SCID - adenosine deaminase deficiency
less profound - CD40L deficiency
describe the characteristics of X-linked SCID
‘bubble boy’ disease
mutations in cytokine receptors IL-2Ry chain
T cells/NK cells fail, B cells normal but no help for efficient antibody responses
what does ADA-SCID deplete?
T/B/NK cells, basal expression in all cells, enhanced by thymocytes
explain the characteristics and causes of alopecia
FoxN1 deficiency, hair and epithelial thymus fail to develop -> ineffective thymus -> no T cells
B cells normal but no help
what 3 common antibodies are deficient in FoxN1 deficiency?
brutons tyrosine kinase
CD40L
IgA
what occurs in humoral/B cell defects?
lack of antibody
recurrent sepsis
bacterial infections in airways
GI failure
explain what an IgA deficiency could cause
an IL deficiency - cytokines need to mature lymphocyte into mature IgA plasma cell
what are 3 common phagocyte defects?
neutrophil function
respiratory burst (CGD)
mendelian susceptibility to mycobacterial disease (MSMD)
which IL is involved in familial mediterranean fever (FMF)?
IL-1
name the 4 things occuring in immune regulatory failure
loss of central and peripheral tolerance
molecular mimicry
innapropriate activation
explain the pathogenesis of autoimmune diseases
susceptible genes causes a failure in self-tolerance resulting in a persistance of functional self-reactive lymphocytes
in the event of an environmental trigger (infection/injury) these self-reactive lymphocytes will activate causing immune responses against self-tissues
explain immune mediated inflammatory response
chronic diseases with prominent inflammation caused by failure in tolerance or regulation
results from immune responses target self antigens or microbial antigens
may be caused by T-cells or antibodies
may be systemic or organ specific
name 2 autoimmune diseases that contain T cell specific auto-antigens which produces an anti-host response
graves - T cells to thyroid follicular epithelial cells
myasthenia gravis - T cells to ACl receptor
