Immuno2 0519FA Flashcards
what Igs do mature B cells express on surface?
IgM, IgD
how do B cells make the other Ig?
differentiate by isotype switching (gene rearrangement via cytokines and CD40 L) into PLASMA CELLS that secrete IgA, G, E.
IgM structure
monomer on B cell.
PENTAMER in tissue.
how does IgM shape help it function?
pentamer shape allows it to efficiently trap free Ags out of tissue while humoral response evolves
function of IgM
produced in primary/immediate response to Ag.
fixes complement but does not cross placenta.
IgD
unclear fx.
found on surface of many B cells and in serum.
IgA function
prevent attachment of bacteria and viruses to MUCOUS MEMBRANES.
does NOT fix complement.
IgA structure
monomer in circ.
dimer when secreted.
by what method does IgA cross epithelial cells?
transcytosis - pick up secretory component from epith cells before secretion.
where is IgA found?
secretions (tears, saliva, mucus).
breast milk/colostrum.
IgG function
main Ab in secondary/delayed response to Ag.
fixes complement.
crosses placenta.
opsonizes bacteria.
neutralizes bact toxins and viruses.
what cells does IgE bind?
mast cells and basophils - cross-links when exposed to allergen, mediating type I hypersensitivity through release of inflamm mediators (histamine)
which Ig is most abundant in blood?
IgG
which Ig provides passive immunity to infants?
IgG - CAN CROSS PLACENTA
Which Ig is in lowest conc in serum?
IgE
how does IgE also mediate immunity to worms?
activate eosinophils
what Ig is released in response to thymus-independent Ags?
(Ags lacking peptide component; cannot be presented by MHC to T cells)
IgM ONLY.
no immunologic memory.
what occurs when thymus-DEpendent Ags bind?
(Ags contain protein component)
B cells directly interact with Th cells (CD40-CD40), which release IL-4,5,6,10. cytokines induce class switching and immunologic memory in B cells.
complement is part of what kind of immunity?
innate (+ inflammation)
membrane attack complex (MAC) of complement defends against?
gram neg bacteria
what activates CLASSIC pathway of complement?
IgG or IgM
“GM makes CLASSIC cars”
what activates ALTERNATIVE pathway of complement
microbe surface molecules
function of C1, 2, 3, 4
viral neutralization
function of C3b
opsonization
function of C3a, C5a
anaphylaxis
function of C5a
neutrophil chemotaxis
function of C5b-9
cytolysis by MAC
what are the primary OPSONINS in bact defense?
C3b and IgG
*C3b also helps clear immune complexes
what are the INHIBITORS of complement?
- decay-accelerating factor (DAF)
- C1 esterase inhibitor
–help prevent complement activation on self cells
C1 esterase inhibitor deficiency
HEREDITARY ANGIOEDEMA.
decreased C4 bc it is broken down by C1 esterase.
what is contraindicated in C1 esterase inhibitor deficiency?
ACE inhibitors
C3 deficiency
severe recurrent pyogenic sinus and resp tract infx.
increased susceptibility to type III hypersens.
C5-9 deficiencies
recurrent Neisseria bacteremia
DAF (GPI anchored enzyme) deficiency
complement-mediated lysis of RBCs
and paroxysmal nocturnal hemoglobinuria.
TYPE I hypersensitivity
ANAPHYLAXIS AND ATOPIC:
free Ag cross-links IgE on presensitized mast cells and basophils, triggering release of vasoactive amines that act at postcapillary venules.
onset of TYPE I hypersensitivity
rxn develops RAPIDLY after Ag exposure due to PREFORMED Ab.
*first contact with Ag is ASYMPTOMATIC. class switch to IgE. IgE binds receptors on cells, ready for re-exposure.
test for TYPE I hypersensitivity
scratch test.
radioimmunosorbent assay.
TYPE II hypersensitivity
ANTIBODY-MEDIATED:
IgM, IgG bind fixed Ag on enemy cell, leading to lysis by complement (MAC) or phagocytosis
mechanisms of TYPE II hypersensitivity
- opsonize cells or activate complement.
- Ab recruit neutrophils and macrophages to incite tissue damage.
- bind to normal cellular receptors and interfere with functioning.
test for TYPE II hypersensitivity
direct and indirect Coombs
TYPE III hypersensitivity
IMMUNE COMPLEX:
Ag-Ab (IgG) complexes activate complement, which attracts neutrophils that release lysosomal enzymes
serum sickness
TYPE III hypersensitivity. Abs to foreign proteins are produced (takes 5 days). IC form and are deposited in membranes, where they fix complement to cause tissue damage.
presentation of serum sickness
often caused by DRUGS. fever. urticaria. arthralgias. proteinuria. lymphadenopathy.
5-10 days after Ag exposure.
Arthus reaction
local subacute reaction in which INTRADERMAL INJECTION of Ag induces Abs, forming IC in skin. complement is activated.
presentation of Arthus reaction
edema.
necrosis.
which is more common, serum sickness or Arthus reaction?
serum sickness
test for TYPE III hypersensitivity
immunofluorescent staining
TYPE IV hypersensitivity
DELAYED (CELL-MEDIATED):
sensitized T lymphocytes encounter Ag and release lymphokines to activate MACROPHAGES.
4T’s of TYPE IV hypersensitivity
T lymphocytes.
Transplant rejection.
TB skin test.
Touching (contact dermatitis).
test for TYPE IV hypersensitivity
patch test
ex: PPD
which is the only hypersensitivity that does NOT involve Abs?
TYPE IV hypersensitivity
TYPE I hypersensitivity disorders
Anaphylaxis: bee sting, food/drug allergies.
Allergic and atopic disorders: rhinitis, hay fever, eczema, hives, asthma.
TYPE II hypersensitivity presentation
tends to be specific to tissue or site where Ag is found
TYPE III hypersensitivity presentation
can be assoc with vasculitis and systemic manifestations
TYPE III hypersensitivity disorders
other than serum sickness and Arthus rxn
SLE. rheumatoid arthritis. polyarteritis nodosum. PSGN. hypersensitivity pneumonitis.
blood transfusion rxn: allergic rxn
type I hypersensitivity.
against plasma proteins in transfused blood.
presentation of allergic rxn to blood transfusion
urticaria.
pruritus.
wheezing.
fever.
treat w/ antihistamines.
blood transfusion rxn: anaphylactic rxn
severe rxn.
IgA-deficient pts must receive blood products without IgA.
presentation of anaphylactic rxn to blood transfusion
dyspnea. bronchospasm. hypotension. resp arrest. shock.
blood transfusion rxn: febrile nonhemolytic transfusion rxn (FNHTR)
type II hypersensitivity rxn.
host Ab against donor HLA Ags and leukocytes.
presentation of FNHTR
fever.
headache.
chills.
flushing.
blood transfusion rxn: acute hemolytic transfusion rxn (HTR)
type II hypersens rxn.
intravasc hemolysis: ABO incompatibility.
extravasc hemolysis: host Ab rxn against foreign Ag on donor RBCs.
presentation of acute HTR
fever. hypotension. tachypnea. tachycardia. flank pain. hemoglobinemia (intra). jaundice (extra).
bacterial infx in T cell deficiency
sepsis
bacterial infx in B cell deficiency
encapsulated organisms: S.pneumoniae. H.Influenzae type B. Neisseria meningitidis. Salmonella. Klebsiella pneumoniae. group B Strep.
“SHiN SKiS”
bacterial infx in granulocyte deficiency
BUrkholderia cepacia.
Nocardia.
Staphylococcus.
Serratia.
“no GRAiN for the BUNSS”
bacterial infx in complement deficiency (C5-9)
Neisseria
viral infx in T cell deficiency
CMV.
EBV.
VZV.
chronic infx w/ resp and GI viruses.
viral infx in B cell deficiency
enteroviral encephalitis.
poliovirus (live vaccine contraindicated).
fungal/parasitic infx in T cell deficiency
candida.
PCP.
fungal/parasitic infx in B cell deficiency
GI giardiasis (due to no IgA)
fungal/parasitic infx in granulocyte deficiency
candida.
aspergillus.
B cell deficiencies tend to produce?
recurrent bacterial infxs
T cell deficiencies tend to produce?
fungal and viral infxs
