Immunology Flashcards
Functions (4) of complements and respective mediators
- Inflammation (C3a, C5a)
- Opsonization (C3b)
- Lysis (C5b, 6~9)
- Immune complex removal (C1,4,2,3b)
3 activation pathways of complements
- Classical
- Lectin
- Alternative
Which bacteria is related to C5~9 deficiency?
Neisseria
What disease is associated with C1/4/2 deficiency?
immune complex disease
MHC-I vs MHC-II
MHC-I:
A,B,C [all nucleated cells]
present to CD8+ T cells
MHC-II:
DP,DQ,DR [antigen-presenting cells]
present to CD4+ T cells
Functions of antibodies (6)
toxin neutralization
complement activation
agglutination
opsonization
mast cell degranulation
antibody-mediated cell-mediated cytotoxicity
Which antibody isotype can cross placenta?
IgG
Which antibody isotype is a: pentamer? dimer?
IgM
IgA
Compare T-dependent and independent pathways of B cell activation
T-dependent:
✓ isotype switching to IgA & IgG
✓ memory
Key processes for B cell maturation (3)
Gene rearrangement
Affinity maturation (somatic hypermutation & clonal selection)
Isotype switching
Which site of thymus does positive and negative selection of T cells occur?
cortex
medulla
3 key signals for activation of T cells
MHC-TCR signal
Co-stimulatory signal (CD28 + CD80/86)
IL-2
Cytokines released by Th1,2, Treg
Th1: IFN-γ, IL-2
Th2: IL-4,5,13
Treg: IL-10, TGF-β
What is central tolerance and peripheral tolerance in immunology?
autoreactive immature lymphocytes are identified and removed in primary lymphoid organs (i.e. negative selection)
protection against autoreactive mature lymphocytes in peripheral tissues by Treg cells or deprivation of activation signals
Pathogenesis of Hyper IgM syndrome
CD40L / CD40 deficiency –> impaired T-dependent B cell activation –> ↑ IgM
Genes for agammaglobulinaemia
BTK / BLINK
Pathogenesis of chronic granulomatous disease
mutation in one subunit of NADPH oxidase complex –> phagocytes susceptible to catalase-positive pathogens –> phagocytes with live phagocytosed pathogens –> granuloma
Pathogenesis of leukocyte adhesion deficiency
adhesion molecules deficiency –> ⨉ entry of neutrophils into infected tissues –> unresolved infection with no pus formation
(↑ ↑ neutrophils)
3 forms of allograft rejection and time
hyperacute (mins ~ 1w)
acute (days ~ 6m)
chronic (months ~ years)
Where do pre-formed anti-donor HLA Ab come from? (3) How to prevent the resulting rejection?
multiple blood transfusions (e.g. long-term dialysis)
multiple pregnancies
previous allograft rejection
Cross-matching
2 exceptions for ABO group typing in allograft transplant
graft that do not express ABO Ag (cornea, heart valve, HSCs…)
young infant recipient (low Ab level)
For HLA typing, which type are required in organ transplant and HSCT?
organ transplant: A,B,DR
HSCT: all 6
Exception for cross-matching in allograft transplant (why? (2))
liver graft
(large size, good regeneration ability)
How to revert acute allograft rejection episode? (2)
high-dose IV steroid
anti T-cell Ab
Immunosuppression regimen in transplantation
- Induction:
- anti-T cell Ab
- Long-term prevention:
a. corticosteroid
b. cytotoxic drug
c. T-cell activation inhibitor
3 phase of immune surveillance
elimination, equilibrium, escape
What is CAR T-cell therapy? What is its major side effect?
T cells that express chimeric antigen receptor to kill tumour cells
cytokine release syndrome
Which immune cell is applied in tumour vaccines?
dendritic cells
2 ways to solve immune checkpoints activation to treat cancer
anti-PDL1 antibody / anti-PD1 antibody
anti-CTLA4 antibody
–> preserve activation of anti-tumour T cells
2 portions of CAR in CAT T cell therapy
Extracellular portion (variable domain of Ab)
Cytoplasmic portion (T-cell signalling domain)
Side effects of immunosuppression in transplantation
↑ infection
↑ incidence of malignancy and toxicity
cyclosporine: HT, nephrotoxicity, hepatotoxicity
steroid S/E
