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96 Cards in this Set
- Front
- Back
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primary follicles in the lymph node
secondary follicles in the lymph node |
primary: dense and dormant
secondary: pale and active |
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Where is high endothelial venule located in the lymph node
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paracortex
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Where are T cells in the lymph node
Where are B cells in the lymph node |
T cells: paracortex
B cells: follicle |
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In what dz is the paracortex not well developed
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DiGeorge syndrome
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what is the primary lymph node drainage site for the lateral side of the dorsum of the foot
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popliteal
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what is the primary lymph node drainage site for the rectum (lower part), anal canal above the pectinate line
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internal iliac
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what is the primary lymph node drainage site for the anal canal below the pectinate line
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superficial inguinal
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what does the right lymphatic duct drain
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right arm and right half of head; Right lymphatic duct drains into R subclavian vein
(thoracic duct drains everything else; thoracic duct drains into L brachiocephalic vein) |
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what is the main antibody in secondary (delayed) response to Ag
What is the antibody in primary (immediate) response to Ag |
IgG delayed
IgM immediate |
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immature B lymphocytes express what on their surfaces
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IgM, CD19, CD20, CD21 (receptor for EBV), CD40, MHC II, B7
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what are thymus-independent Ag
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no peptide component, so can't be presented to MHC, like LPS
stim release of IgM only and no immunologic memory results |
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What Ig crosses the placenta?
What Ig is seceted? |
IgG
IgA |
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What do IL-1, -2, -3, -4, -5 do
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Hot T-Bone stEAk
IL-1: fever IL-2: stim T-cells IL-3: stim Bone marrow IL-4: stims IgE IL-5: stims IgA |
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what cytokine stims production and activation of eosinophils
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IL-5
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1. What secretes IL-8 and what does IL-8 do?
2. What secretes TNF-alpha and what is its fxn? |
IL-8: secreted by macrophages; major chemotactic factor for neutrophils
TNF-alpha: seceted by macrophages; mediates septic shock, causes leukocyte recruitment and vascular leak |
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What cell surface protein is a receptor for EBV (on what cell?)
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CD21
on B cells |
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CD21 is a receptor for what virus
what cell is CD21 on |
EBV
on B cells |
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What cell surface protein on NK cells bind Fc of IgG
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CD16
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against what bacteria does the MAC of complement defend
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gram-negative
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what are the two primary opsonins in bacterial defense
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C3b and IgG
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What 2 things help prevent complement activation on self-cells
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DAF (decay-accelerating factor) and C1 esterase
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what complement components are involved in viral neutralization
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C1-4
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what complement components are involved in opsonization, binding bacteria
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C3b
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what complement components are involved in anaphylaxis
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C3a and C5a
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what complement deficiency leads to hereditary angioedema
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C1 esterase
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what does a deficiency in C3 cause
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severe, recurrent pyogenic sinus and respiratory tract infections
increased susceptiblity to Type 3 hypersensitivity rxns |
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What complement deficiency causes a Neisseria bacteremia
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C5-8
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What does a deficiency in DAF cause
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complement-mediated lysis of RBCs and PNH
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What is PNH
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paroxysmal noctural hemoglobinuria
complement-induced hemolysis, red urine, thrombosis (accentuated at night) |
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What is the mechanism of action of Inteferon (alpha, beta, gamma)
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place uninfected cells in an antiviral state
1. alpha and beta inhibit viral protein synthesis by inducing production of a ribonuclease that degrades viral mRNA, not host mRNA 2. gamma-interferon increases MHC I and II expression and Ag presentation in all cells 3. Activate NK cells to kill virus-infected cells |
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What are examples of passive immunity
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preformed Ab given after exposure to :
Tetanus toxin, Botulinum toxin, HBV, or Rabies virus (To Be Healed Rapidly) |
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What are examples of passive immunity
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preformed Ab given after exposure to :
Tetanus toxin, Botulinum toxin, HBV, or Rabies virus (To Be Healed Rapidly) also IgA in breast milk |
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How do T cells become anergic
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Self-reactive T-cells become nonreactive w/o costimulatory molecule
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What are granulomatous dz
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TB, Fungal infections (like Histo)
Syphilis, Leprosy Cat scratch fever, Sarcoidosis Crohn's dz, Berylliosis |
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what disorder is assoc w/ anti-smooth muscle auto-Ab
w/anti-glutamate decarboxylase w anti-SS-A (anti-Ro) and anti SS-B (anti-La) |
autoimmune hepatitis
Type 1 DM Sjogren's syndome |
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what disorder is assoc w/antimicrosomal, anti-TG auto-Ab
w/anti-desmoglein w/ anti-jo-1 |
Hashimoto's thyroiditis
Pemphigus vulgaris Polymyositis, dermatomyositis |
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what disorder is assoc w/antimitochondrial auto-Ab
w/anti-histone w/ anti-IgG |
PBC
Drug-induced lupus Reumatoid arthritis (rheumatoid factor; against Fc portion of IgG) |
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what disorder is assoc w/anti-dsDNA, anti-Smith auto-Ab
w/ anti-U1 RNP (ribonucleoprotein) w/ anticentromere w/ anti-Scl-70 (anti-DNA topoiosmerase I) |
specific for SLE
Mixed CT dz Scleroderma (CREST) Scleroderma (diffuse) |
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what is the defect in Hyper IgM syndrome
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defective CD40Ligand on T helper cell = inability to class switch
get severe pyogenic infections in early life |
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what is clinical presentation in Hyper-IgE syndrome
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Job's syndrome: failure to produced IFN-gamma by Th1 cells --> inability of neutrophils to respond to chemotactic stimuli
coarse Facies, cold (noninflamed) staph Abscesses, retained primary Teeth, increased IgE, Dermatologic probs (eczema) FATED |
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what disease presents as disseminted mycobacterial infections, and a decrease in IFN-gamma
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IL-12 receptor deficiency
decreased Th1 response --> decreased IFN-gamma in lab |
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what is the clinical presentation of Wiskott-Aldrich syndrome
what are the lab findings what is the defect |
Triad: TIE: Thrombocytopenia purpura, Infections, Eczema
Labs: decreased IgM!, increased IgE, IgA Defect: X-linked recessive, progressive deletion of B and T cells |
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what is the clinical presentation of Ataxia-Telangiectasia
What is the defect |
Triad: cerebellar defects (ataxia), spider angiomas (telangiectasia), IgA deficiency (sinopulmonary infection)
defect: DNA repair enzymes (mutated ATM gene) |
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what is the clinical presentation in Leukocyte adhesion deficiency (LAD) Type 1
what is the defect what are the lab findings |
Recurrent bacterial infections, absent pus formation!, delayed separation of umbilicus!
Defect: in LFA-1 integrin (CD18) protein on phagocytes Labs: Neutrophilia |
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what is the clinical presentation of Chediak-Higashi syndrome
What is the defect |
Recurrent pyogenic infections by staph and strep, partial albinism, peripheral neuropathy
Defect: auto recessive, defect in microtubular function w/decrease in phagocytosis |
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what are catalase-positive organisms
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S. aureus, E. coli, Aspergillus
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what are the major Sx of graft-versus-host disease
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maculopapular rash, jaundice, hepatosplenomegaly, and diarrhea
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What are the different defects in Severe combined immunodeficiency (SCID)
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1. Defective IL-2 receptor (most common, X-linked)
2. Adenosine deaminase deficiency (knocks out both T and B cells) 3. failure to synthesize MHC II antigens (lack CD4+ cells) |
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what drugs are used to trx acute transplant rejection
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cyclosporine, OKT3
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Name 4 disorders due to B-cell dysfunction.
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1. Bruton's (X-linked) agammaglobulinemia: defect in BTK --> blocks B-cell differentiation/maturation
2. Hyper-IgM syndrome: defective CD40L on Th cells --> inability to class switch 3. IgA deficiency: defect in isotype switching 4. Common variable immunodeficiency (CVID): defect in B-cell maturation; many causes |
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Name 4 disorders due to T-cell dysfunction.
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1. Thymic aplasia (DiGeorge syndrome): failure to develop 3rd/4th phayrngeal pouch due to 22q11 deletion
2. IL-12 receptor deficiency: on Th1 cells 3. Hyper-IgE syndrome (Job's syndrome): Th1 fail to produce IFN-gamma 4. chronic mucocutneous candidiasis: T-cell dysfunction |
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Name 3 disorders due to B and T cell dysfucntion.
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1. Severe combined immunodeficiency (SCID): most commonly defective IL-2 receptor
2. Ataxia-talengiectasia: defective DNA repair enzyme; ATM gene 3. Wiskott-Aldrich syndrome: progressive deletion of B and T cells |
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Name 3 disorders due to phagocyte dysfunction
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1. Leukocyte adhesion deficiency (type 1): defect LFA-1 integrin (CD18) protein on phagocytes
2. Chediak-Higashi syndrome: defect in microtubular function with decreased phagocytosis 3. Chronic granulomatous disease: lack of NADPH oxidase |
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What is the defect in Bruton's agammaglobulinemia?
presentation? |
X-linked recessive.
Defect in BTK (tyrosine kinase gene) --> blocks B-cell differentiation/maturaiton recurrent bacterial infections after 6 months (decreased IgG) due to opsonization defect |
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What are presentations in IgA deficiency?
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sinus and lung infections
milk allergies and diarrhea Anaphylaxis on exposure to blood products with IgA |
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How do you differentiate b/t common variable immunodeficiency (CVID) and Bruton's agammaglobulinemia based on lab findings?
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CVID: normal # of B cells but low plasma cells and Ig's
Bruton's normal pro-B but low B cells and Ig of all classes |
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22q11 deletion leads to what defects? disease?
presentation? |
failure to develop 3rd/4th pharyngeal pouches
DiGeorge syndrome (thymic aplasia and parathyroid aplasia) tetany (hypocalcemia) recurrent viral/fungal infection congenital heart and great vessel defect |
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what immune deficiency is caused by lack of NADPH oxidase?
presentation? Lab finding? |
chronic granulomatous disease
increases susceptibility to catalase-positive organisms (e.g. S. aureus, E coli, and Aspergillus) Negative Nitroblue tetrazolium dye reduction test |
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what has a "barrel hoop" fenestrated basement membrane
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the spleen
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where are T cells and B cells found in the spleen
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T cells: PALS (periarterial lymphatic sheath) and the red pulp
B cells: follicles w/in white pulp |
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what is the process that happens in splenic dysfunction
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decreased IgM -> decreased complement activation -> decreased C3b opsonization -> increased susceptiblity to encapsulated orgs
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What organisms are encapsulated and why is that significant
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Klebsiella, Salmonella, S. pneumoniae, H. influenzae, N. meningitidis
increased susceptibility in splenic dysfunction |
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What 3 things are seen post-splenectomy
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Howell-Jolly bodies (nuclear remnants), Target cells, Thrombocytosis
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cortex of thymus
medulla of thymus |
cortex: dense w/immature T cells
medulla: pale w/mature T cells |
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where do positive and negative selection of T cells take place
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in thymus at corticomedullary junction
cortex: positive selection (MHC restriction) Medulla: negative selection (non reactive to self) |
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Hassall's corpuscles
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in medulla of thymus
they are dead epithelial reticular cells arranged in eosionphilic concentric circles |
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What cytokines do Th1 cells make
what cytokines are they inhibited by |
IL-2, IFN-gamma
activate macrophages and CD8 T-cells inhibited by IL-10 (made from Th2) |
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MHC I vs MHC II?
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MHC I: HLA-A, B, C
expressed on almost all nucleated cells. Antigen is loaded in RER of mostly intracellular peptides mediates viral immunity pairs with beta2-microglobulin MHC II: HLA-DR, -DP, -DQ expressed only on APCs antigen is loaded following reelase of invariant chain in acidified endosome |
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What cytokines do Th2 cells make
what cytokines are they inhibited by |
IL-4, IL-5, IL-10
help B cells make antibody (IgE > IgG) inhibited by IFN-gamma (by Th1) |
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What dz are associated w/HLA B27
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Psoriasis, Anklyosing spondylitis, IBD, Reiter's syndrome
(PAIR) |
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What HLA subtypes are associated with the following diseases?
DM type 1 Reumatoid arthritis Hashimoto's Grave's |
DM type 1: DR3, DR4
RA: DR4 Hashimoto's: DR5 Grave's: B8 |
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What is the only lymphocyte member of the innate immune system
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NK cells
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When are NK cells induced to kill
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when exposed to a non-specific activation signal on a target cell+/or an absence of class I MHC on target cell surface
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what cytokine are macrophages activated by and what do the release?
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activated by IFN-gamma
Release IL-1 and TNF-alpha |
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what are the APCs
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macrophages, dendritic cells, B cells
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what cytokines do macrophages release and what do they do
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IL-1, TNF-alpha
stimulate T-cells (CD4) IL-8: chemotactic to neutrophils |
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What are the superantigens
How do they work |
S. aureus and S. pyogenes
cross-link the B-region of the TCR to the MHC Class 2 on the APCs -> uncoordinated release of IFN-gamma release from Th1 cell and macrophage release of IL-6, IL-1, TNF-alpha |
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How do endotoxins/LPS work
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from gram-negative bacteria
directly stimulate macrophages by binding to endotoxin receptor CD14; T-cells are NOT involved |
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costimulatory signal
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for Th activation; Signal 2
interaction b/w B7 on APC and CD28 on Th cells |
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How are Tc cells activated
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endogenously synthesized (viral or self) proteins presented on MHC I and recognized by TCR on Tc cell (Signal 1)
Signal 2: IL-2 from Th cells activated Tc cell |
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How is B cell class switching activated
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Signal 1: IL-4, IL-5, IL-6 from Th2 cell
Signal 2: CD40 R activated on B cell by binding CD40 ligand on Th cell |
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What part of the antibody determines idiotype
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Fab fragment
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where does complement bind in IgG and IgM
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Fc portion (Ch2 specifically)
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What part of the Ab determines the isotype
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Fc region
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Name 2 immunosuppresants that blocks secretion of IL-2 by Th1 cells.
Name a immunosuppresant that directly block IL-2 |
Cyclosporine
Tacrolimus (FK506) Daclizumab: monoclonal antibody that has high affinity for IL-2 |
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Which immunosuppresant binds to CD3 and blocks T cell signal transduction?
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Muromonab-CD3 (OKT3)
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What is the MOA of sirlimus (rapamycin)?
Clinical indication? |
binds to mTOR --> inhibit proliferation of T cell in response to IL-2
indicated for immunosuppression after kidney transplantation in combo with cyclosporine and corticosteroids |
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Name 2 immunosuppressants taht block synthesis of nucleic acid.
Elaborate on MOA |
Azatioprine: antimetabolite precursor of 6-mercaptopurine --> toxic to proliferating T cells
Mycophenolate mofetil: inhibit de novo guanine synthesis |
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Toxicity of Azatioprine?
What drug can enhance the toxic effect of this drug? |
Bone marrow suppression.
Active metabolite mercaptopurine is metabolized by xanthine oxidase, thus toxic effects may be increased by ALLOPURINOL |
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Cyclosporine
MOA? toxicity? |
binds to cyclophiline --> inhibit calcineurin --> prevent production of IL-2 and its receptors
viral infection and lymphoma nephrotoxicity (prevent with mannitol) |
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Tacrolimus (FK506)
MOA? Toxicity? |
binds to FK-binding protein --> inhibit secretion of IL-2 and other cytokines
nephrotoxicity, peripheral neuropathy, HTN, pleural effusion, hyperglycemia |
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Filgrastim, sargramostim
What are they? indication? |
Granulocyte colony stimulating factor
recovery of bone marrow |
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alpha interferon
indication? |
Hep B, C
Kaposi's sarcoma Leukemias malignant melanoma |
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Beta interferon
Indication? |
multiple sclerosis
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game interferon
indication? |
chronic granulomatous disease
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Oprelvekin (IL-11)
indication? |
thrombocytopenia
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