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139 Cards in this Set

  • Front
  • Back
lymph drainage in body
rt lymphatic duct drains rt arm and rt half of head

thoracic duct drains everything else
follicle
-where in LN is it?
-desc
-in cortex of LN
(LN cortex contains follicle (B cells) & paracortex (T cells))

-site of B cell proliferation
-in outer cortex, primary follicles are dormant & dense
-secondary follicles are active & pale in their germinal centers
medulla
consists of:

*medullary cords=closely packed lymphocytes and plasma clels

*medullary sinuses
-communicate with efferent lymphatics
-contain reticular cells and macrophages
paracortex

-when is it enlarged?
-when is it small?
-houses T cells
-region of cortex b/w cortex and medulla
-conains high endothelial venules thru which T and B cells enter blood
==>thus paracortex becomes very enlarged during extreme cellular immmune response

-not well developed in DiGeorge syndrome
sinusoids of spleen
-desc
-where in spleen?

-where find T cells
-where find B cells
-long vascular channels within red pulp of spleen
-fenestrated "barrel hoop" BM
-macrophages nearby

T cells in:
*PALS (Periarterial lymphatic sheath)
*red pulp

B cells in follicles (white pulp)
thymus
-T cells derive from what embryonic tissue?
-cortex contains ?
-medulla contains ?

-what is positive and negative selection?
-where do positive and negative selection occur?
-site of T cell differentiation and maturation
-encapsulated

-arises from 3rd brachial pouch
-lymphocytes (T) are of mesenchymal origin

-cortex is dense w/immature T cells

-medulla is pale & contains:
*mature T cells
*epithelial reticular cells
*Hassall's corpuscles

-positive selection (MHC restriction) & negative selection (non-reactive to self) occur @ corticomedullary jxn
Th1 cells produce
IL2
IFN-gamma
activate macs & cytotoxic T cells
Th2 cells producd
IL-2
IL-4
IL-5
help B cells make Ig (IgE>IgG)
innate immunity:
what actors are involved?
neutrophils
macs
dendritic cells
complement
adaptive immunity:
what actors are involved?
T cells
B cells
circulating Ig
MHC encoded by what genes?
MHC (Major Histocompatibility Complex) coded by HLA (Human Leukocyte Antigen) genes
MHC I vs. MHC II
-why important
-encoded by what genes
-expressed on what cells
-where is Ag loaded
MHC I:
*mediates viral immunity

-encoded by HLA-A, B, and C
-pairs with B2 microglobulin
-expressed on all nucleated cells
-Ag is loaded in RER of mostly intracellular peptides


MHC II:
*main determinants of organ rejection
-encoded by HLA-DP, DQ, DR
-expressed only on APC's
-Ag loaded in an acidified endosome
what are the main determinants of organ rejection
MHC II's
APC cells--ex's
Macs
B cells
Dendritic cells
what do Cytotoxic T cells bind?
Cytotoxic T cells have CD8, which bind MHCI mcs on virus-infected cells
cell w/CD8+ is called what?
cell w/CD4+ is called what?
cytotoxic T cell=cell w/CD8+
helper T cell=cell w/CD4+
what CD's do B cells have?
CD 19, 20
CD3 complex
cluster of polypeptides assoc w/TCR

imp in signal transduction
Ig:
Fab vs. Fc segment
Fab=
"a"ntigen "b"inding segment
-composed of heavy and light chains

Fc=
(composed only of heavy chains)
"c"omplement-binding region (IgG+IgM only)
"c"onstant
"c"arboxy terminal
"c"arbohydrate side chains
opsonization
=phagocytosis of bacteria

(Ig covers the pathogen==>promotes phagocytosis)
neutralization
Ig covers the pathogen==>prevents bacterial adherence to cell
Ig's role in complement
Ig covers the bacteria==>more likely to activate complement
==>enhances opsonization (phagocytosis) of bacteria and lysis
what generates antibody diversity
1. random recombination of VDJ (heavy chain) or VJ (light chain) segments

2. combination of light and heavy chains

3. somatic hypermutation

4. add'n of nucleotides to DNA during "genetic recombination" by terminal deoxynucleotidyl transferase
Ig isotypes: most common to least common
G > A > M > D > E
what Ig's do most mature B cells express?
Ig M and D

They can switch to G, A, or E via isotype switching
IgG fxns
-MC Ig (G>A>M>D>E)

*fix complement
*cross placenta
*secondary antibody response
*opsonizes bacteria
*neutralizes bacterial toxins and viruses (coats their surface so they cannot adhere to tissue)
IgM fxns
-primary response to Ag
-fix complement but does not cross placenta
-all mature B cells express IgM (and IgD) but can switch to Ig G, A, or E via isotype switching
-monomer or pentamer (huge!)
IgA fxns
"secretory Ig": picks up secretory component from epithelial cells before secretion
-found in secretions (ie breast milk)
-prevents bacterial and viral adherence to mucosal surfaces
-does not fix complement (only IgM and IgG fix complement)
Goljan: most potent activator of complement system
IgM
IgE fxns
-Type 1 hypersensitivity:
IgE exposed to Ag
==>IgE induces release of mediators from mast cells and B cells

*mediates immunity to worms

-lowest concentration of the Ig's
which Ig mediates immunity to worms
Ig E
isotype
-desc
-what determines it
isotype=IgG, IgA, IgM, IgD, or IgE

Ig epitope common to a single class of Ig (determined by heavy chain)
what determines whether an Ig is IgG, IgA, IgM, etc
the heavy chain
allotype of Ig
=polymorphism

Ig epitope that differs b/w different members of same species
("allo"=different members of same species, eg allograft)
idiotype of Ig
-specific for a given Ag

-Ig epitope determined by Ag-binding site
helper T cells-

cell surface proteins
TCR
CD3
CD4
CD28
CD40L
cytotoxic T cells-

cell surface proteins
TCR
CD3
CD8
B cells-

cell surface proteins
IgM
B7
MHCII

CD19
CD20
CD40
Macrophages-

cell surface proteins
MHCII
CD14
Receptors for Fc
Receptors for C3b
NK cells-

cell surface proteins
receptors for MHCI

CD16
CD56
all cells except mature RBC's have what cell surface protein?
MHCI
what stimulates dendritic cells to migrate to lymph nodes?
TNF-alpha
TNF-alpha
-secreted by what
-fxns
-secreted by macs

*B cell proliferation
*IL-2 receptor synthesis by Th cells
*attracts & + neutrophils
*stimulates dendritic cell to migrate to LN
IL-6
-secreted by what
-fxns
-secreted by Th & macs

*production of acute phase reactants
*production of Ig
IL-8
-secreted by what
-fxns
-secreted by Th

*neutrophil chemotactic factor
IFN-gamma
-secreted by what
-fxns
-secreted by Th
-stimulates macs
interferons
-desc
-MOA

fxns of:
-alpha-IFN
-beta-IFN
-gamma-IFN
=interfons "interfere" w/viral synthesis
-induce production of 2nd protein that inhibits viral protein synthesis by degrading viral mRNA (but not host mRNA)

-place uninfercted cells in anti-viral state

-alpha-IFN & beta-IFN (-) viral protein syntehesis

-gamma-IFN (IFN-gamma) incr MHC I & II expression and antigen presentation in all cells

-activates NK cells to kill virus-infected cells
active vs. passive immunity
active immunity--you contracted the dz yourself and mkae your own Ig (takes awhile but then you have memory cells for life)

passive immunity-you are given Ig from another person to Tx dz they were just exposed to; rapid onset but fast offset
*Ig administered (passive) for ppl exposed to Tetanus, Botulinum, HepB, and Rabies:
*mneum: "To Be Healed Rapidly"
which pathogen has 2 flagellar variants?
Salmonella (think of a salmon with its 2 flagella flapping as it swins)
relapsing fever
Borrelia
which pathogen has programmed antigenic rearrangement?
trypanosomes (parasisite)
which bacteria uses a pilus protein?
Neisseria
anergy
-self-reactive T cells (bad!) become non-reactive without co-stimulatory mcs

-B cells also become anergic, but tolerance is less complete than in T cells
Arthus Rxn
type of Type III hypersens.

(serum sickness (ImCo) is more common than Arthus Rxn)

Arthus Rxn=
-inject Ag into skin
-Ig bind Ag
-Ag-Ig complexes deposit in skin
==>activate complement
==>edema, necrosis
Type IV hypersensitivity
=Delayed T cell mediated hypersens.

mneum: "4 T's"
-T cells (Th1)
-TB skin tests
-Touching (i.e. poison ivy)
-Transplant rejxn
hemolytic anemia is mediated by which type of hypersensitivity
Type II (Ig against RBC)
MG is mediated by which type of hypersensitivity
Type II (Ig against Ach-R)
erythroblastosis fetalis is mediated by which type of hypersensitivity
Type II (Ig against Rh+ in baby)
Rheumatic fever is mediated by which type of hypersensitivity
Type II (Ig against receptor)
the pathogenesis of which derm problem involves hypersensitivity
bullous pemphigoid=Type II hypersen
Rh arthritis is mediated by which type of hypersensitivity
Type III (ImCo)

There is IgM that is Anti-IgG
==>IgM-IgG complexes settle on joints
polyarteritis nodosum is mediated by which type of hypersensitivity
type III

(P-ANCA)
post-strep glomerulonephritis is mediated by which type of hypersensitivity
type III
Arthus rxn is mediated by which type of hypersensitivity
Type III
hypersensitivity pneumonitis is mediated by which type of hypersensitivity
type III
Type I DM is mediated by which type of hypersensitivity
Type IV
MS is mediated by which type of hypersensitivity
Type IV
Guillain Barre is mediated by which type of hypersensitivity
Type IV
GVHD is mediated by which type of hypersensitivity
Type IV
Hashimoto's thyroiditis is mediated by which type of hypersensitivity
Type IV (First aid p. 194)
contact dermatitis is mediated by which type of hypersensitivity
Type IV
what chronic dz's are mediated by Type IV hypersensitivity
Type I DM
Hashimoto's thyroiditis
MS
Guillain-Barre
DiGeorge Syndrome
-desc
-genetics (deletion)
"T"hymic & para"T"hyroid aplasia (b/c aplasia of 3rd & 4th pharyngeal pouches)
==>deficient "T" cells
==>recurrent viral and fungal infxns

-"T"etany d/t hypocalcemia
-congenital defect of heart and great vessels
*22q11 deletion
22q11 deletion is assoc with what dz
DiGeorge
Bruton's agammaglobulinemia
-desc
-pg
"B"'s:

"B"rutons=
deficient "B" cells=
"B"acterial infxns
"B"oys (X-linked)

-X-linked recessive defect in V(H) (heavy chain) gene segments to undergo gene arrangment
==>defective tyrosine kinase gene which is required for maturation of pre-B cells to mature B cells
==>arrest B cell development in pre-B cell stage
==>low levels of all Ig
SCID
-desc
-et
SCID=Severe Combined Immunodeficiency Dz

-deficient B and T cells==>recurrent:

Bacterial
Viral
Fungal
Protozoal

infxns

many possible causes:
-ADA deficiency ("SCID ADA TL"; ADA=Adenosine Deaminase)
-defective IL-2 receptors
-failure to synthesize MHCII
IL-12 deficiency:

how present
present w/multiple mycobacterial infxns

IL-12 activates Th1 cells & NK cells and Th1 cells;

Th1 cells are required to kill Mycobacteria, i.e. in Mycobacteria tuberculosis:

-MƏ (APC’s with MHC II) present Ag to CD4+ Th cells

-MƏ release:
*IL-1→activates Th1, fever
*IL-12→(+) Th1 formation

Th1 cells release:
*IL-2
→(+) Th1 proliferation (positive feedback)
→Activates monocytes→MƏ

*IFN-γ→(+) MƏ to kill tb

Lipids from killed tubercle bacillus→caseous nec
Activated MƏ fuse→multinucleated giant cells
hyper-IgM syndrome
-et
-desc
-presentation
-caused by defect in CD40L ligand on Th cells
==>cannot class switch (interaxn b/w CD40L on Th cells & CD40 on B cells is req for isotype switching)
==>high levels of IgM, low levels of IgA, IgG, IgE

-present w/severe pyogenic URT and LRT infxns early in life (pyogenic infxn= bacteria that produces pus/abscesses, i.e. SA)
Wiskott-Aldrich syndrome
-inheritance pattern
-desc
-serum levels
-Sx
-X-linked (wiSKOTT (~Scott)=boy=X-linked)

*Imagine a boy named SKOTT with these Sx (recurrent infxns & bleeds to death)

(some info from HY CB p. 154)

1. Thrombocytopenia
==>purpura
==>bleeding = MCCoD
(prolonged bleeding at umbilical stump or after circumcision)

2. inab to mount IgM response against capsular polysaccharide of bacteria:

H flu
Strep
N men

(these bugs have polysacchide capsules; thus these are the same bugs that infect ppl with sickle cell anemia & asplenic pts)


[mneum: "WIPE" ("IPE"=triad of Sx)

W=Wiscott Aldrich
I=recurrent pyogenic Infxns
P=thrombocytic Purpura
E=Eczema]
Job's syndrome
-pathogenesis
-presentation
Th1 cells fail to produce IFN-gamma
==>no activation of macs
==>neutrophils fail to respond to chemotactic stimuli

Presentation:
-"cold" (noninflamed) Staph aureus infxns
-eczema
-coarse facies
-high IgE levels
-retained primary teeth
leukocyte adhesion
-pathogenesis
-presentation
-defect in LFA-1 adhesion proteins on phagocytes
-presents with:
*pyogenic and fungal infxns
*delayed separation of umbilicus
Chediak-Higashi syndrome
AR;

defect in microtubular functioning and lysosomal emptying of phagocytic cells

Presentation:
-recurrent Staph and Strep infxns
-partial albinism
-peripheral neuropathy
chronic granulomatous dz
-desc
-inheritance pattern
[RR Path p. 16]

-X-rec

lack NADPH oxidase
==>reduced production of superoxide radical
==>no respiratory burst (resp burst requires superoxide radical & H2O2)
==>neutrophils cannot phagocytose things

Present:
lots of infxns, esp
-Staph
-E coli
-Aspergillus

Dx confirmed w/negative nitroblue tetrazolium dye reduction test (test is negative b/c no respiratory burst (resp burst requires superoxide radical & H2O2))
chronic mucocutaneous Candidiasis
-et
T-cell dysfxn specifically regarding Candida
==>skin and mucous membrane candidiasis
selective IgA deficiency
-desc
-et
==>problems w/secretions and mucous membranes (that's what "secretory IgA" affects)
*sinus and lung infxns
*milk allergies, diarrhea


-d/t problems w/class switching (can't switch from IgM==>IgA)
ataxia-telangiectasias

-inheritance pattern
-et
-Sx
-assoc w ?
-AR

defect in DNA repair enzymes
==>cerebellar prob (ataxia)
==>spider angiomas (telangiectasias)

*associated IgA deficiency
common variable immunodeficiency
-nl # circulating B cells, but...

decr #plasma cells==>decr Ig
ANA
SLE
anti-ds DNA
specific for SLE
anti-Smith
specific for SLE
anti-histone Ig
drug-induced SLE
anti-IgG Ig
=Rh factor

Rh arthritis
anti-neutrophil Ig
-ex
-suggests what
eg. C-ANCA, P-ANCA

-suggests vasculitis
C-ANCA
vasculitis

(Wegener's granulomatosis)
P-ANCA
vasculitis
anti-centromere Ig
Scleroderma (CREST) [not diffuse]
anti-Scl-70
scleroderma (diffuse) [not CREST]
anti-mitochondrial Ig
primary biliary cirrhosis
anti-microsomal Ig
Hashimoto's thyroiditis
antigliadin Ig
celiac dz (=celiac sprue)
anti-basement membrane Ig
Goodpasteur's
anti-epithelial cell Ig
pemphigus vulgaris
anti-Jo-1 Ig
polymyositis (=progressive symmetric proximal mm wkness d/t CD8+ destruction of myofibers)

dermatomyositis (~polymyositis but shawl-face skin rash and incr risk of malignancy)
which dz's assoc w/

HLA B27
"PAIR"

Psoriasis
Ankylosis spondyliasis
IBD
Reiter's syndrome

Notice how "AIR" were all in that one MSK lecture we had
which dz's assoc w/

HLA B8
Grave's dz
celiac sprue
which dz's assoc w/ DR2
Note: these are all types of hypersensitivity:

Hay fever (Type I)
Goodpasteur's (Type II)
SLE (Type III)
MS (Type IV)
which dz's assoc w/DR3?
Type I DM (assoc w/DR 3 & 4)
which dz's assoc w/DR4
Type I DM (assoc w/DR 3 & 4)
RA
which dz's assoc w/DR5
pernicious anemia==>B12 def
Hashimoto's thyroiditis
which dz's assoc w/DR7
steroid-responsive nephrotic syndrome
hyperacute rejection
-time frame
-desc
-within minutes
-preformed anti-donor Ig
acute rejection
-time frame
-desc
-reversible?
-within weeks
-Type 4 (delayed) hypersensitivity: Tc cells react against foreign MHCs

*REVERSIBLE w/immunosuppressants like cyclosporine and OKT3
chronic rejection
-time frame
-desc
-reversible?
-months-years
-antibody-mediated vascular damage (damage to bv)
-irreversible
GVHD
-immunocompetent graft reacts against immunosuppressed host
==>severe organ dysfxn==>
*macropapular rash
*jaundice
*hepatosplenomegaly
*severe diarrhea
"cytotoxic hypersensitivity"
Type 2 hypersensitivity
some ex's of encapsulated bacteria (contain capsule)

-what is purpose of capsule
-how test for an encapsulated bacteria
note: all of these cause pneumonica/meningitis:

Step pneumo
H flu
Klebsiella pneumoniae
N men

*polysaccharide capsule protects against phagocytosis

*test for encapsulated bact w/Quellung rxn: when reactant added, capsule swells ("sweLLUNG" with "QueLLUNG")
what is an antiphagocytic virulence factor?
polysaccharide capsule
dipicolinic acid
dipicolinic acid==>thus spore-forming bacteria, eg:

Bacillus cereus/anthracis
Clostridia (botulinum/tetani/diff/perf)
Staph aureus
-virulence factor
-desc
-virulence factor=Protein A,
which binds Fc-IgG==>prevents complement activation

causes:
1. inflammatory dz
*skin infxn
*organ abscesses
*pneumonia

2. toxin-mediated:
*TSST-1=superantigen (superantigens bind MHCII-TCR
==>polyclonal T-cell activation)
*exfoliative toxin==>scalded skin syndrome (mneum: usu exfoliation is good for your skin, but it's way too much in SA)
*entertoxin==>GI prob via preformed toxins
rheumatic fever
-sequelae of GAS pharyngitis (not GAS impetigo)

"rheumatic" fever gives you:
-arthritis (just like "rheumatoid" arthritis--remember Jerry in MSK lab)
-heart problem

mneum: no "rheum" for SPECCulation:

S=Subcutaneous nodules
P=Polyarthritis
E=Erythema marginatum
C=Carditis
C=Chorea
Strep pyogenes
=GAS

1. Pyogenic:
*pharyngitis
*cellulitis
*impetigo

2. Toxigenic
*scarlet fever
*TSS

-Ig to M protein enhances host defenses against GAS
-ASO titer detects recent GAS infxn

*Sequelae are immunologic:
mneum: "PH"aryngitis gives you glomerulonePHritis and rheumatic PHever

pharyngitis/impetigo==>glomerulonephritis

pharyngitis only==>rheumatic fever

-sequelae of GAS pharyngitis (not GAS impetigo)

"rheumatic" fever gives you:
-arthritis (just like "rheumatoid" arthritis--remember Jerry in MSK lab)
-heart problem

mneum: no "rheum" for SPECCulation:

S=Subcutaneous nodules
P=Polyarthritis
E=Erythema marginatum
C=Carditis
C=Chorea
scarlet fever--what bug
GAS
TSS--what bug
SA or GAS
M protein
GAS

Ig to M protein enhances host defense ag GAS
ASO titer
detects recent GAS infxn
MCC meningitis
Strep pneumo
MCC otitis media in kids
Strep pneumo
MCC pneumonica
Strep pneumo
MCC sinusitis
Strep pneumo
Strep pneumo
MCC of "MOPS":

Meningitis
Otitis media in kids
Pneumonia
Sinusitis
*encapsulated
*IgA protease

*"rusty" sputum
*sepsis in sickle cell anemia
*splenectomy
what bug causes "rusty" sputum
Strep pneumo
what bact causes sepsis in sickle cell anemia
Strep pneumo
what bact assoc w/splenectomy
Strep pneumo
IgA protease
Strep pneumo or
Enterococcus faecalis
=enterococci (enterococci=
Enterococcus faecalis or
Enterococcus faecium)

[enterococcus=intestine
faecalis=feces]

-cause UTI and subacute endocarditis
-grow in 6.5% NacCl
-Lancefield Group D (Enterococci and nonenterococcoal Group D strep)
-Pen-G resistant
enterococci
-refers to what bact`
Enterococcus faecalis or
Enterococcus faecium

[enterococcus=intestine
faecalis=feces]

-cause UTI and subacute endocarditis
-grow in 6.5% NacCl
-Lancefield Group D (Enterococci and nonenterococcoal Group D strep)
-Pen-G resistant
Lancefield group D
=enterococci (Enterococcus faecalis or
Enterococcus faecium)

or nonenterococcal Group D strep
prosthetic devices and catheters
Staph epidermidis
Strep viridians
-part of nl oral flora
-cause dental caries and subacute endocarditis