Immuno Flashcards
(39 cards)
lack of all B cells
bruton x linked agammaglobulinemia
cause of bruton
deficiency in (bruton) Tyrosine Kinase
lack of Pus formation
LAD
infection with catalase + organisms
chronic granulomatous disease
albinism
chediak higashi
deficiency of CD40L on T cells
Hyper-IgM. Class switching defect
MHC are encoded by _______ and found on _________
HLA genes
MHC1: all nucleated cells
MHC2: APC’s
present antigen fragments to T cells and bind TCRs
MHC
Needs release of invariant chain for peptide loading
MHC2
Stating that there is a difference when none exists
Type 1 (alpha) error
alpha (epi) is the probability of ____________
making a Type 1 error (False positive)
what does p
there is less than a 5% chance that the data will show a difference/effect that is not actually there (FP)
T cell development: produced in BM and then travel to thymus: explain Cortex, Medulla
Cortex:
Arrive as double negative (no cd4 or cd8)
–>DNA rearrangement –>become Double Positive. POSITIVE selection = those that bind self MHC can survive. go to medulla
Medulla: now those that bind self too tightly die= NEGATIVE selection
Positive (1st) and Negative selection(2nd) T cell
Cortex…Positive selection: When Double Positive T cells bind self MHC, its a positive thing and they survive
Medulla…Negative selection: Now they are Single Positive. Those that bind self too strongly are killed. So binding self strong is a Negative thing.
TB: Cord factor and sulfatide
Cord Factor: prevents MQ maturation and induces TNF release (which forms granuloma)
Sulfatide: “the tide is too strong for phagolysosome fusion)
Superantigen and Cachexia cytokines:
TNF alpha; IFN gamma; IL-1, IL-6.
Alpha is 1, Gamma is 6.
Whats the link between Fluticasone/Budenoside (Pulm Corticosteroids) and TNF alpha?
These drugs inhibit NF-KB, which is the TF that induces TNF alpha production
Radiation therapy causes what kind of damage?
Free radical formation and double stranded DNA breakage
FAS:
9-5 job would kill me FASt (Fas aka Fas-R = CD95)
If its looking autoimmune, we want to kill it FASt (negative selection–>thymic medulla)
whats difference btwn apopotosis and necrossi (basic)
Necrosis = INFLAMMATION
Apopotosis is NOT inflammatory. Note: Apoptosis requires ATP.
Coagulative vs Liquefactive necrosis
Coag: Ischemia;
–>Proteins Denature, and then Enzymatic Degradation
Liquef: ABSCESSES and Brain infarct
- ->Enzymatic degradation first, then Proteins Denature
- ->Neutrophils release lysosomal enzymes that digest the tissue
Order: remember liquefactive is E-P-L: Enzymes first and then Proteins degraded in Liquefactive.
Whats EPL?
Reminds us that order of degradation is Enzymes and then Proteins in Liquefactive necrosis (vs opp order in coag)
renal zones most susceptible to ischemia (and thus ischemic ATN)
Proximal Tubule and Thick Ascending Limb
PCT and TAL nigga
(Red)Hemorrhagic Infarct: Location
where there is dual blood supply
LUNGS, LIVER, INTESTINE
–>can get Reperfusion injury here
