IMM Flashcards
Innate immunity description
Natural, inborn
1st line: physical barriers
2nd line: monophagocyte system, complement, cytokines
How does inflammation start
PRR binding –> cellular activation –> phagocytosis –> cytokine release –> inflammation
Acute phase reactant description
IL-6 stimulants can be measured (fibrinogen, C3, CRP, haptoglobin)
Neutrophils
First to site of injury, phagocytosis, free vs marginate, main cell in pus
Eosinophils
Defense against parasites and fungi
NK cells
Uses PRR or ADCC (Fc receptors), perforin + granzymes
No memory, short lifespan
Adaptive immunity description
Acquired, highly specific, memory, long duration
Th1
CD4+
Produces IL-2
Protection against intracellular pathogens
Initiates clonal expansion of CD8+ cells
Th2
CD4+ Produces IL-4, 5, 10, 13 Protection against extracellular pathogens Regulates B cell class switching Activated by B cells
Treg
Produces IL-10
Maintains tolerance to self antigens
Th17
Mediates delayed type hypersensitivity reactions
Inhibits Treg, promotes autoimmune reactions
Cytotoxic T cells
CD8+
Perforin + granzymes
Destroys intracellular pathogens + cancer cells
T cell dependent activation
2 simultaneous signals, MHC II + CD4+
Most common
B cell isotype switch upon activation
T cell independent activation
2 simultaneous signals, PAMP
Inefficient, no memory
Plasma cells
No surface Ig
Short lifespan in circulation
Long lifespan in bone marrow
MHC I is located on
All nucleated cells
MHC II is located on
APCs only
IL-1
Pyogenic, initiates acute phase response
IL-2
Growth and proliferation of T and B cells
IL-4
Promotes Th2 differentiation
IL-5
B cell differentiation
IL-6
Liver to make APR
IL-8
Neutrophil chemotaxis
IL-10
Calming cytokine released by Treg, suppresses Th2
TNFa
Principle mediator of acute phase response
SCID
No T or B cells
Bare lymphocyte
Defects in MHC expression
Wiscott Aldrich
Intrinsic platelet defect
DiGeorge syndrome
Thymus not developed
B cell deficiencies
Recurrent bacterial infections
T cell deficiencies
Severe viral infections
Intravascular hemolysis
Decreased haptoglobin
Hemoglobinemia, hemoglobinurea
Increased LDH
Scihistiocytes
Extravascular hemolysis
Spherocytes
Increased ubil
Increased LDH
Decreased Hct
Mechanisms of complement
Opsonization (90% of the time)
Cell lysis
Complement cascade phases
Recognition phase
Activation phase: generation of C3 convertase
MAC phase
Classical pathway recognition phase
Generation of C1qrs complex, activation on C2 and C4
Calcium dependent
Classical pathway activation phase
C4b2a acting on C3 (amplification loop)
Lectin pathway
Activated with carbohydrate and MBL
Alternative pathway
Continuous hydrolysis of H2O
CR1
Transports opsonized immune complexes to fixed tissue macrophages
CR2
Binds iC3b, receptor for EBV
CR3
Binds iC3b
Innocent bystander effect
Once C5678 is formed, C9 binding occurs spontaneously
DAF CD55
Inhibits production of C3 convertase
C1 esterase inhibitor
Inhibits activation phase
Factor H
Dissociates C3bBb from cell surface
Factor I
Cofactor with factor H
Protectin CD59
Inhibits C9 from binding
C1 esterase inhibitor deficiency
Hereditary angioedema, uncontrolled action of C1 on C4 or C2 causing swelling
C3 nephritic factor
Continuous complement activation, binds and stabilizes C3bBb, autoantibody found in mesangioglomerulonephritis
PNH
Lack of GPI linked proteins (no DAF)
Decreased C1q,r,s C4
Large amount of immune complex deposits (SLE, arthritis, Alzheimer)
C2 deficiency
Most common in Caucasians, usually not serious
C3 deficiency
Repeat infections
Properdin deficiency
X linked, increased susceptibility to Neisseria infections
Septic shock
Extensive intravascular activation of complement by bacterial endotoxin (increased anaphylatoxins)
Deficiency of C’ receptors
Similar to C3 deficiency (repeated infections)
In affected infants: delayed separation of umbilical cord, recurrent ulcerating infections, abnormal paper thin scar formation
