Flashcards in Immunology Deck (232):
Medulla of lymph node
Medullary cords with closely packed lymphocytes and plasma cells
Contain reticular cells and macros communicate with efferent lymphatics.
Houses T cells. Between cortex between follicles and medulla. High endothelial venules
Which part of lymph node enlarged in immune response?
paracortex. This part is also underdeveloped in digeorge syndrome
stomach drains to
duodenum drains to
superior mesenteric node
sigmoid colon drains to
colic then inferior mesenteric
rectum drains to
internal iliac nodes
anal canal below pectinate drains to
testes drain to
superficial and paraaortic
superficial inguinal node
superficial inguinal node
lateral dorsum of foot drains
right lymphatic duct drains
right arm, right chest, right half of head
thoracic duct drains
everything beisdes what the right lymphatic duct drains
structure of sinusoids of spleen
vascular channels in red pulp with barrel hoop basement membrane
T cells of spleen found in
periarterial lymphatic sheath in white pulp
B cells of spleen found in
follicles on outer edge of white pulp
Macrophages of spleen are especially important for
removing encapsulated bacteria
What are the encapsulated organisms?
Findings in a blood smear after a splenectomy
howell jolly bodies
Cortex of thymus
immature T cells
medulla of thymus
pale with mature T cells
epithelial reticular cells coming together to make hassall's corpuscles
positive selection (MHC restriction) occurs
in the cortex of thymus
negative selection (nonreactive to self) occurs
in the medulla of thymus
MHC I is expressed on all nucleated cells except for
part of MHC1, helps to transport molecule to cell surface
loading of antigen in MHC II
release of invariant chain in acidified endosome
loading of antigen in MHC1
in RER with intracellular peptides
Graves' Diabetes type 1
rheumatoid arthritis, diabetes type 1
when do NK cells kill?
Exposed to a nonspecific activation signal on target or absence of class I MHC
NK activity enhanced by
IL-2, IL-12, IFN beta, IFN a
When an immature T cell enters the thymus, it immediate gets what receptors?
CD4+ CD8+ AND TCR
SIgnal for Helper T cells to become Th1 cells
Signal for helper T cells to become Th2 cells
T Cells expressing TCRs able to bind self MHC survive
T cells expressing TCRs with a high affinity for self antigens= apop
B7 expressed by DC
CD28 expressed by naive T cell
What happens after the primary and costimulatory signal is given by dendritic cell to naive T cell?
Naive T cell expresses IL-2 which binds to IL-2R on itself stimulating the naive T cell to differentiate
What happens after the primary and costimulatory signal is given by Th4 cell to naive B cell?
the helper T cell, after being activated by dendritic cell
-->B cell presents antigen on MHC II to activated T cell
-->TCR recognizes correct antigen and releases IL4 and IL5 which stimulate the B cell to differentiate into IgG, IgE, and IgA
What is the only APC that can activate a naive T cell?
the dendritic cell
Describe the costimulatory signal for B cell activation
CD 40 on B cell
CD40 L on Th cell
Th1 cell secretes
Th2 cell secretes
IL4, 5, 10, 13
Th1 cell activates
Th2 cell activates
IgE production by B cells
Th1 cell inhibited by
IL4 and IL10
Th2 inhibited by
How do macrophages and lymphocytes tickle or stimulate each other?
lymphocytes release IFN-y
macrophages release IL1 and TNF-a
--> they help each other out
Hyper IgM caused by
Defective CD 40 and 40L interaction
Contents of cytotoxic T cells (CD8)
1. perforin: makes holes so can deliver bombs
2. granzyme: serine protease, activates apoptosis
3. granulysin: antimicrobial, induces apoptosis
Treg cells express which cell surface markers
CD3, CD4, and CD25
Treg cells produce
IL10 and TGFbeta
heavy chain makes up which portions of antibody
Fc and Fab
light chain makes up which portion of antibody
CD25 is also known as
alpha chain of IL-2 receptor.
complement binds which part of antibody
medial portion of Fc
macrophage binds which part of antibody
distal to where complement binds, between CH2 and CH3
three components of the Fc region
complement binding at CH2 (IgG and IgM)
Carbohydrage side chains
light chains made up of
heavy chains made up of
stomatic hypermutation occurs after
antigen stimulation of B cell. BUT B cells are "born" with their random VJ/VDJ combinations.
What enzyme is responsible for generating the VD/VDJ recomination?
terminal deoxynucleotidyl transferase
--Adds nucleotides to DNA during recombination
When B cells secrete things other than IgM
Mature B lymphocytes express what on their surface
IgM AND IgD
Which antibody can cross the placenta?
Which antibodies can fix complement?
Only IgG and IgM
which antibody is responsible for delayed response to an antigen?
How does IgA work?
Prevents attachment of bacteria to mucous membranes
IgA form in circulation?
monomer. dimer when secreted
Which Ig is the antigen receptor of the surface of B cells?
thymus independent antigens
antigens lack a peptide component and cannot be presented by MHC to T cells (ex: LPS or capsular antigen)
-->as a result, NO immunologic memory
-->but antibodies are released
Thymus dependent antigens
There IS a protein component (diptheria) and class switching occurs
Classic complement pathway
IgG or IgM mediated
mediated by Mannose on microbe
Alternative pathway turned on by
PAMP pathogen associated molecular pattern
What starts the alternative pathway?
D converts B into Bb
what starts the lectin pathway?
MBL activates a C1 like complex
--cleaves C2 AND C4
--otherwise, same as classic pathway
What prevents complement activation on self cells?
Decay accelerating factor
C1 esterase inhibitor
complement disorder with hereditary angioedema
C1 esterase inhibitor deficiency
What drug is contraindicated in C1 esterase inhibitor deficiency?
severe pyogenic sinus and respiratory tract infections with increased type III hypersensitivity--type of complement deficiency
C3 deficiency. C3 helps clear immune complexes
Recurrent neisseria bacteremia
Complement mediated lysis of RBCs and PNH
What does IL-1 do to endothelium?
induces adhesion molecule expression
fever and acute phase proteins
Differentiation into Th1 cells
Activates NK cells
Increase MHC I and II expression.
Interferon a and b mechanism
Produce a ribonuclease=degradation of viral mRNA
IFN is defense against
--they all activate NK cells to kill virus infected cells
Cell surface proteins on T cells
CD proteins on Th4
B cell CD proteins
CD19, 20, 21
40, MHCII, B7
Receptor for epstein barr virus
CD14 (binds LPS)
NK cell receptors
CD16 (binds Fc)
CD56 (unique marker)
Superantigens secreted by which bugs?
S aureus (TSST-1)
S pyogenes (exotoxin A)
-->NOTE THAT ALL T CELLS ARE ACTIVATED from cross linking fo TCR to MHC II on APCs
Thelper cells are NOT involved. Massive secretion of TNF alpha
Salmonella antigen variation
neisseria gonorrhea antigen variation
what other bugs have antigen variation?
When do you give passive immunization?
Live vaccines activate a
killed vaccines activate a
examples of killed vaccines
marker of mast cell degranulation
Explain Type II hypersensitivity
IgM/G bind to antigen
--Antibody dependent cell mediated cytotoxicity, NK cells
How to test for type II hypersen
Direct and indirect coombs'
immune complex disease where immune complexes bind and deposit where they fix complement=tissue damage
Intradermal injection induces antibodies and complexes in the skin.
---edema, necrosis, activation of complement
When would you see serum sickness?
5-10 days after exposure
most serum sickness is caused by
Sx: serum sickness
fever, urticaria, arthralgias, protienuria, lymphadenopathy
Test for arthus rxn
Describe process of type IV hypersensitivity
t lymphocytes activate macrophages and secrete lymphokines
Examples of type IV hypersensitivity
graft versus host disease
TB skin test
allergic rhinitis and hay fever
Type I hypersensitivity
Four types of blood transfusion reactions
acute hemolytic transfusion
concern when giving blood transfusion to pt with celiac's
many celiac's pts are deficient in IgA
--must receive blood products that lack IgA
Febrile nonhemolytic transfusion rxn
type II hypersensitivity. Host antibodies against donor HLA antigens
sx of febrile nonhemolytic TR
fever, chills, flushing
Acute hemolytic transfusion rxn
type II hypersensitivity. Intravascular hemolysis or extravascular hemolysis
Sx of acute hemolytic transfusion rxn
fever, hemoglobinemia, jaundice (extravascular)
flank pain, hypotension
Drug induced lupus
antiScl70 (DNA topo I)
primary biliary cirrhosis
Anti Jo-1, Anti-SRP, Anti-Mi2
anti glutamate decarboxylase
microscopic polyangiitis, churg strauss
granulomatosis with polyangiitis
type 1 diabetes
mixed CT disease
No B cells: susceptible to which bacteria?
No complement: susceptible to which bacteria?
No granulocyte: susceptible to which bacteria?
No T cells: susceptible to what bacteria?
No T cells, susceptible to which viruses?
how do you test for type IV hypersensitivity?
candida extract skin test
Does the absence of anti-dsDNA of anti-Smith rule out possibility of SLE?
NO--these are highly specific for ruling in
No T cells
Recurrent giardia infection
No B cells (no IgA)
Recurrent candida and aspergillus
recurrent bacterial infections 6 months after birth
-low B cells
-low Ig (all types)
Bruton's X linked agammaglobulinemia
Cause of bruton' x linked agamma?
Defect in Bruton tyrosine kinase so NO B CELL MATURATION
asymptomatic but recurrent sinopulmonary/GI infections. Also history of celiacs or other autoimmune.
Selective IgA deficiency.
what do pts with selective IgA deficiency test false positive for?
beta HcG. cuz of heterophile antibody
what is a heterophile antibody?
induced antibody that is characterized by broad reactivity with antibodies of other animal species
pt in 20's and 30s suddenly present with lymphoma and sinupulmonary infections. Normal B cell number but decreased plasma cells and immunoglobulin
Cause of CVID
defect in B cell maturation
pts with CVID increased risk of
pt has tetany, recurrent viral/fungal infections
lab findings in Digeorge
absent thymic shadow
--low T cells
cause of DiGeorge
22q11 =failure of 3rd and 4th branchial pouches to form
(also cause of tetraology of fallot and persistent truncus arteriosus! cool!)
disseminated mycobacterial infections
IL-12 receptor deficiency
lab findings in IL12 receptor deficiency
primary teeth retained
Hyper IgE (Job's syndrome)
Cause of hyper IgE (Job's)
Th1 cells fail to produce IFN-y
--neutrophils fail to go where they need to go
--will have lots of Th2 cells
candida infections of skin and mucous membranes
Chronic mucocutaneous candidiasis
--caused by T cell dysfunction
Failure to thrive, chronic diarrhea
--recurrent fungal, viral, bacterial infections
XRay and lymph node biopsy findings in SCID
Absence of thymic shadow
No germinal centers in lymph nodes
No B cells
--Decreased Tcell recombinant excision circles
--decreased T cells on flow cytometry
cause of SCID
1. Defective IL2 (most common)
2. Adenosine deaminase deficiency
Ataxia, spider angiomas, and IgA deficiency
Cause of ataxia telangiectasia
Defects in ATM gene: codes for DNA repair enzymes
Lab findings in Ataxia telangiectasia
Severe pyogenic infections early in life
Cause of hyperIgM
defective CD40L cannot class switch
wiskott aldrich syndrome
Cause of wiskott aldrich
WAS gene defective. T cells unable to reorganize actin cytoskeleton
inheritance of wiskott aldrich
Lab findings of wiskott aldrich
Increased IgE, IgA
Recurrent bacterial infections, no pus, and delayed separation of umbilical cord
leukocyte adhesion deficiency
Cause of Leukocyte adhesion deficiency
Defect in LFA-1 integrin (CD-18)
lab findings in leukocyte adhesion deficiency
recurrent pyogenic infections by staph and strep
PARTIAL albinism and peripheral neuropathy
Cause of chediak higashi
Defect in lysosomal trafficking regulator gene (LYST). Microtubule dysfunction in phagosome-lysosome fusion
inheritance of chediak higashi
giant granules in neutrophils
lab findings in chediak higashi
abnormal dihydrorhodamine flow cytometry test
chronic granulomatous disease
susceptibility to catalase positive organisms (S aureus, E coli, aspergillus)
chronic granulomatous disease
cause: Chronic granulomatous disease
lack of NADPH oxidase. Cannot make reactive oxygen species in neutrophils
Susceptible to BOTh catalase positive and negative orgs
myeloperoxidase deficiency. Cannot turn H2O2 into an O2 radical...EVEN though H2O2 is provided by catalase negative organisms!
From identical twin
acute rejection time frame
chronic rejection time frame
months to years
hyper acute rejection: type of hypersensitivity rxn?
Type II. preformed antibodies in transplant recipient attack donor cells (blood mismatch)
occlusion of graft vessels causing ischemia and necrosis
vasculitis of graft vessels with dense intertitial lymphocytic infiltrate
Fibrosis of graft tissue and blood vessels
mechanism of acute rejection
-CTL react against foreign MHC
which rejection is NOT reversible?
macropapular rash, jaundice, hepatosplenomegaly and diarrhea in a transplant pt
which types of transplants most susceptible to GVH disease?
bone marrow and liver transplants (rich in lymphocytes)
blocks diff and activation of T cells
--No IL2 and IL2R
tox of cyclosporine
Binds FK binding protein, inhibiting calcineurin
tox of tacrolimus (FK506)
same as cyclosporin, but NO gingival hyperplasia and NO hirsuitism
Sirolimus (rapamycin) mechanism
Inhibits mTOR and T cell proliferation
Use of sirolimus
tranplant and drug eluting stent
hyperlipidemia, thrombocytopenia, leukopenia
precursor of 6 MP
--interferes with synthesis of nucleic acids
--toxic to lymphocytes
--GN and hemolytic anemia
Muromonab-CD3 (OKT3) mech
Binds CD3 and blocks T cell signal
Tox of muromonab
cytokine release syndrome, hypersensitivity
Anti-IgE for sever asthma
renal failure anemia
alpha IFN use:
Hep B, C
chronic granulomatous disease
Recovery of bone marrow
HER 2 antibody