immunology Flashcards
lymph node Cx
follicles of B cells
primary follicles dense and dormant
secondary follicles pale central germinal center and are active
lymph node medullar
medullary cords and sinuses
lymph node paraCx
T cells
underdeveloped in DiGeorge
mediastinal nodes
drain trachea and esophagus
celiac nodes
drain liver, stomach, spleen, pancreas, upper duodenum
superior mesenteric nodes
lower duodenum, jejunum, ileum, colon to splenic flexure
inferior mesenteric nodes
colon from splenic flexure to upper rectum
internal iliac nodes
drain lower rectum to anal canal above pectinate line, bladder, vagina (middle 1/3), prostate
para-aortic nodes
testes, ovaries, kidneys, uterus
superficial inguinal nodes
anal canal (below pectinate line), skin below umbilicus, scrotum
popliteal nodes
dosolateral foot, post calf
what infections are asplenic pts prone to?
encapsulated SHiNE SKiS: S. pneumoniae H. influenza B N. menigitidis E. coli Salmonella Klebsiella group B Strep
where are T cells in spleen
perarteriolar lymphatic sheath (PALS)
where are B cells in spleen
follicles in white pulp
what is in the marginal zone?
APCs
what do you see in blood of asplenic?
Howell-jolly bodies
target cells
thrombocytosis
lymphocytosis
what is thymus derived from?
3rd pharyngeal pouch
MHCI
HLA-A/B/C expressed on all nucleated cells present endogenously synthesized Ags (viral) to CD8 cells Ag loaded in RER associated w/beta2 micrglobulin
MHCII
HLA-D
expressed on APCs
present exogenously synthesized Ags (bacterial) to CD4 cells
associated w/invariant chain
HLA-A3
hemochromatosis
HLA-B27
seronegative arthropathies PAIR psoriatic arthritis ankylosing spondylitis arthritis of IBD Reactive arthritis (reiter syndrome)
HLA-DQ2/DQ8
celiac disease
HLA-D2D
MS
hay fever
SLE
goodpastures
HLA-DR3
DMI
SLE
graves
hashimotos
DR4
RA (4 walls to a rheum)
DMI
DR5
pernicious anemia -> vit B12 deficiency
hashimotos
what enhances NK cells
IL2, 12
INF-alpha
INF-beta
detect cells w/o MHCI on surface
TH1
secrete INF-y to activate macros and CD8 cells
activated by INF-y and IL-12
inhibited by IL-4 and IL-10
TH2
secretes IL-4, 5, 10, 13
recruits eos, promotes IgE
activated by IL-4
Inhibited by INF-y
Treg
surpress CD4 and CD8
express CD3,4,25, and FOXP3
produce IL10, TGF beta
naive T cell activation
DC presents Ag to T cells in lymph node
B7 (on DC) and CD28 (on Tcell) must interact as well
B cell activation and class switching
B cell presents Ag to activated Th cell
CD40L (on Th) binds CD40R (on B cell)
fab
variable region
fragment
Ag binding
determine idiotype
Fc
Constant Carboxy terminal C' binding Carbohydrate side chains determine isotype (IgM, IgG etc)
IgG
main Ab in secondary response most abundant type in serum fixes C' crosses placenta opsonizes bacteria neutralizes bacterial toxins and viruses
IgA
mucous membranes does NOT fix C' monomer in circulation, dimer when secreted most produced Ab overall in breast milk
IgM
primary response fixes C' does not cross placenta monomer on B cells pentamer when secreted
IgD
unknown fnx
IgE
binds mast cells and basophils
cross links when exposed to allergen - type 1 hypersensitivity rxn
lowest concentration in serum
acute phase reactants that are upregulated
mostly d/t IL-6 CRP Ferritin Fibrinogen Hepcidin Serum amyloid A
downregulated acute phase reactants
albumin transferrin (internalized by macros)
CRP
opsonin and fixes Cā
ferritin
binds and sequesters Fe
Fibringoen
coagulation factor
promotes endothelial repair, correlates w/ESR
hepcidin
prevents release of Fe bound by ferritin
leads to Anemia of chronic disease
serum amyloid A
prolonged elevation -> amyloidosis
classic activation of Cā
IgG or IgM mediated
GM makes classic cars
alternative activation of Cā
microbe surface molecules
lectin pathway activation of Cā
mannose of other sugars on microbes surface
C3b
opsonization
3b binds bacteria
C3a, C4a, C5a
anaphylaxis
C5a
neutrophil chemotazis
MAC
C5B-9
Cā inhibitors
decay-accelerating factor (DAF, aka CD55)
C1 esterase inhibitor
C1 esterase inhibitor deficeincy
hereditary angioedema
ACE inhibitors CI
C3 deficiency
increases risk of severe recurrent pyogenic sinus and respiratory tract infections
increased susceptibility to type III hypersensitivity rxns
C5-9 deficiencies
Neisseria
DAF deficiency
aka CD55 or CPI anchored enzyme
Cā mediated lysis of RBCs -> paroxysmal nocturnal hemoglobinuria
C3 nephritic factor Ab
usually stabilizes Cā convertase
w/o it you get too much C3b -> stuck in kidneys -> membranoproliferative glomerulonephritis
serum C3b is low
cytokines secreted by macros
IL-1 IL-6 IL-8 IL-12 TNFalpha
cytokines from all T cells
IL-2
IL-3
cytokines from Th1
INF-y
cytokines from Th2
IL-4
IL-5
IL-10
Hot T-bone stEAK
IL-1 hot (fever) IL-2 stimulates T cells IL-3 stimulates bone marrow IL-4 stimulates IgE IL-5 stimulates IgA IL-6 stimulates aKute phase protein production
IL-8
major chemotactic factor for neutros
IL10
atTENuates immune response
decreases expression of MHC class II and Th1 cytokines
inhibits activated macros and dendritic cells
IL-12
induces differentiation of T cells into Th1
activates NK
INF-y
stimulates macros
activates NK cells
what gives sputum color?
myeloperoxidase
blue-green heme containing pigment
chronic granulomatous disease
at risk fro catalase + species
S. aureus
Aspergillus
etc
INF- alpha and beta
defense against viruses for apoptosis of infected cells
T cell markers
TCR (binds Ag MHC complex)
CD3
CD28 (binds B7 on APC)
Th markers
CD4
CD40L
Cytotoxic T cell markers
CD8
Treg markers
CD4
CD25
B cell markers
Ig CD19, 20, 21 CD40 MCH II B7
macro markers
CD14 CD40 MCH II B7 Fc and C3b Rs
NK cell markers
CD16
CD56
HSC markers
CD34
what organisms can be Tx w/preformed Abs?
To Be Healed Very Rapidly Tetanus toxin Botulinum toxin HBV Varicella Rabies
what is the difference in immune response to live vs killed vaccine
live- cellular and humoral response
killed- humoral only response
type I hypersensitivity rxn
skin test for specific IgE
direct coombs test
detects Abs that have adhered to pts RBCs
indirect coombs test
detects serum Abs that can adhere to other RBCs
Serum sickness
type III- IC
deposit in membranes and fix Cā
usually caused by drugs 5-10 days after exposure
fever, urticaria, arthralgia, proteinuria, lymphadenopathy
arthus rxn
local subacute type III- IC
occurs after subdermal injection
edema, necrosis, activation of Cā
test w/immunoflorescence staining
type IV rxns
T cell mediates transplant rejections TB skin tests Touching- contact dermatitis MS
type II rxns
acute hemolytic transfusion rxn autoimmune hemolytic anemia bullous pemphigoid erythroblastosis fetalis ITP pemphigus vulgaris
type III RXNS
arthus rxn SLE polyarteritis nodosa poststreptococcal glomerulonephritis serum sickness