• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/139

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

139 Cards in this Set

  • Front
  • Back
LN follicles:
Cortex vs Paracortex (cell contents, function)
Cortex: B cells located here, proliferate here

Paracortex: T Cells; between follicle and medulla; where blood enters
In extreme cell immune response, this region of the LN becomes enlarged.
Paracortex--responsible for LAD
Patients with DiGeorge have a poorly developed _____ of the lymph node.
Paracortex not weel dev'd (low T cell count)
LN:
Cords vs Sinus (cell contents)
In what region are both of these located?
Medulla:
Sinus: macs
Cords: Plasma cells
Sinusoids of spleen:
B vs T Cell locations
PALS--periarterial lymphatic sheet contains T cells

B cells in follicles, white pulp
What cell type is responsible for removing encapsulated bacteria from blood?

Where is this cell located?
Macs in spleen remove encapsulated bacteria
Vaccine requirements for the asplenic.

Why?
Need immunization against encapsulated bacteria--strep pneumo, h flu, n meningitidis, salmonella, klebsiella) need pneumovax, h flu vaccine, meningococcus

Bc no longer have macs to get rid of encaps bacteria
Howell-Jolly Bodies: Asplenic
Splenic infarct (wedge shape/triangle = classic sign of ischemia)
Axillary node
Upper limb, lateral breast
Celiac node
Stomach
Superior mesenteric node
Duodenum, jejunum
Colic node
Sigmoid colon
Inferior mesenteric node
Sigmoid colon
Internal iliac node
Rectum (above pectinate line)
Superficial inguinal node
Anal canal
Scrotum
Superficial thigh
Superficial and deep plexuses (nodes)
Testes
Para-aortic node
Scrotum
Popliteal node
Lateral side; dorsum of foot
Right lymphatic duct
Right arm, right half of head
Thoracic duct
Everything right lymphatic duct doesn't drain (remember Right lymphatic drains Right arm, right half of head)
The thoracic duct drains at the_______.
Junction of left subclavian in internal jugular vein
Thymus:
Cortex vs Medulla (cells and processes)
Cortex has immature T Cells
Corticomedullary junction: where selection occurs
Medulla-->mature T cells; AKA selection
Embryologic origin of thymus.
Thymus comes from epithelium of third branchial pouch
Innate immune system:
Cells involved
Nphils, macs, DCs (APCs for macs), NKCs, complement
Adaptive immune system:
Cells involved
T cells, B cells, circulating Abs
NKCs:
Enzymes used
When are they activated?
Perforins and granzymes to induce apoptosis of virally infected cells

(Only lymphocyte member of innate immunity!)

Activated when receive nonspecific activation signal on target cell and/or absence of MHC I on target cell surface
These cytokines enhance NKC activity.
IL-12, IFN-beta, IFN-alpha

IFN very important for inducing NKCs and cells neighboring infected cells to generate substances that will inhibit viral protein synthesis
This cytokine stimulates T cells.
IL-2
This cytokine stimulates macrophages.
IFN-gamma
This cytokine inhibits T cells and macrophages.
IL-10
This cytokine stimulates B cells.
IL-4, IL-5
Beginning with BM, describe maturation of T cells.

Include CD markers.
BM-->Thymus Cortex (CD4+8+)-->Positive and Negative Selection at corticomedullary jn in thymus(negatively selected cells undergo apoptosis)-->CD4+ or CD8+
CD8+ cells:
Role
Enzymes used
Kills virus-infected cells directly
Neoplastic cells
Donor graft cells

~NKCs

Use perforins (helps deliver granzymes) and granzymes (activates apoptosis)

CD8 binds MHC1
These cells recognize the absence of MHC1.
NKCs
These cells are activated by binding MHC1.
CD8+
What type of cytokine induces a T helper cell to become Th1?
IL-12
This cytokine is elevated in times of viral infection.
IL-12
These cytokines are released by Th1 cells.
IL-2-->stimulates T cells
IFN-gamma-->stimulates macs
IL-10-->inhibits Th1
This cytokine induces formation of Th2 cells.
IL-4 (humoral response--B cell response)
These cytokines are released by Th2 cells.
IL-4, 5-->stimulate B cells
IL-10-->inhibit Th cells; inhibits macs
What is class switching and what cells undergo this?
IgM-->IgG = class switching (for B Cells)
Describe steps necessary to activate CD4+ cell.
MHCII on APC recognizes TCR (T cell receptor) and presents antigen to CD4+

B7 on APC co-stimulates CD28 on T cell

T helper cells will then produce cytokines
Describe steps necessary to activate CD8+ cell.
CD8 activation

Virally infected cells present antigen on MHC1 molecule, TCR recognizes it; CD8 helps

Th1 cells release IL-2 and this binds IL-2 receptor on CD8+ cell (co-stimulation)
Describe steps necessary to activate B cell.
B cell activation
Th2 release IL-4,5,6

CD40L on Th cell binds CD40 on B cell and allow for co-stimulation
Th1 vs Th2 cells:
General roles
Cytokines secreted by them
Cytokines inhibiting them
Th1:
regulates cell-mediated response
Secretes IL-2, IFN-gamma
Activates macs and CD8+ cells
Inhibited by IL-10 from Th2

Th2:
Regulates humoral response
Secretes IL-4, IL-5, IL-10
Helps B cells make Ab (IgE>IgG)
Inhibited by IFN-gamma from Th1 cell
Functions of IL-1,2,3,4,5.
Hot T Bone StEAk

HOT: IL-1 (fever)
T: IL-2 (stimulates T cells)
Bone: IL-3 (stimulates BM)
StEak: IL-4 (IgE production)
SteAk: IL-5 (IgA production)
B cell:
Immunoglobulins
CD Markers
IgM
IgD

CD-19,20,21
Epstein-Barr Virus infects this cell.
CD21+

You drink Beer at the Barr when you're 21.
MHC II is present on these cells.
Macrophages
B cells (can act as presenting cells)
Macropahges:
CD markers
Receptors
CD14, 40, 16

Receptors for Fc and C3b (these are opsonins)
NKCs:
CD markers
Receptors
CD16--binds Fc of IgG

Receptor for MHCI
CD16 is present on this cell.
Macrophages and NKCs
What CD markers protect host cells from complement mediated damage?
WBC, RBC, platelets

Protected by CD55 and CD59
What are the acute phase cytokines?
What cell releases these?
Macrophages release IL-1, IL-6, TNF-alpha

These substances mediate fever and ramp up immune system.
What are the 2 pathways to stimulate macrophages to make acute phase cytokines?
1) strep pyogenes, staph aureus release super ag's: crosslink TCR to MHCII on APCs, causes uncoord'd release of IFN-gamma from Th1 and subsequent release if IL-1,6, and TNF-alpha from macs

2) Endotoxins (LPS of gram neg bact); bind CD14 (endotoxin receptor). doesn't require T helper cells.
CD14:
Role
Binds endotoxins (LPS) and activates macs
This cytokine actives eosinophils.
IL-5
IL-1:
Role
Secreted by
Endogenous pyrogen

Causes fever, acute inflammn

Activates endothelium to express adhesion molecules

Secreted by macs
IL-6:
Role
Secreted by
Endogenous pyrogen
Secreted by Th1 cells and macs
IL-8:
Role
Major chemotactic factor for nphils

"Clean up on aisle 8"-->neutrophils recruited by IL-8 to clear infection
These cytokines recruit neutrophils.
IL-8
LT-B4
C5a
IL-12:
Role
Activates NK and Th1 cells
This cytokine mediates septic shock.
TNF-alpha
TNF-alpha:
Role
Activates endothelium
Causes leukocyte recruitment, vascular leakage
Anti-TNF-alpha drugs:
Examples
Uses
Considerations
Etanercept
Infliximab
Adalimumab

These are all MAbs!

Uses: RA, ankylosing spondylitis

Must check for latent Tb prior to dosing, because will make prone to infection!
Cytokine released by all T cells
Role?
IL-3: Supports growth and diff of BM SC's

~GM-CSF
Cytokines released by Th1 cells.
Role?
IL-2:
Stimulates growth of helper and cytotoxic T cells

IFN gamma: activates macs and Th1 cells; antiviral and antitumor properties
Cytokines released by Th2 cells.
Role?
IL-4: induces diff into Th2 cells. Promotes growth of B cells. Class switching to IgE, IgG

IL-5: Promotes differentiation of B cells. Enhances switching to IgA. Stimulates growth and diff of ephils.

IL-10: Modulates inflamm response. Inhibits activated T cells and Th1. Activates Th2.
This cytokine is released by regulatory T cells.
IL-10
Interferon:
Mechanism
alpha and beta: inhibit viral protein synthesis

gamma: inc'd MHCI and II expression and Ag presentation in all cells

Activates NK cells to kill virus-infected cells
IFN-alpha:
Clinical use
HBV
HCV
Kaposi's
Leukemia
Malignant melanoma
IFN-beta:
Clinical use
MS
IFN-gamma:
Clinical use
Chronic granulomatous disease
Aldesleukin:
Clinical use
AKA IL-2
Renal cell carcinoma
Metastatic melanoma
EPO:
Clinical use
Anemias; esp in renal failure or pts undergoing chemotx
Filgrastim:
Clinical use
(gra stim-->granulocyte stimuln) AKA granulocyte CSF

BM recovery (after chemo)
Sagramostim:
Clinical use
Granulocyte macrophage colony stim factor

BM recovery (after chemo)
This cytokine is similar to GM-CSF in its effects.
IL-3 (Bone of Hot T Bone mnemonic)
Oprelvekin:
Clinical use
IL-11; use in thrombocytopenia
Thrombopoietin:
Clinical use
Thrombocytopenia
HLA genes that encode MHC II.
HLA DR
HLA DQ
HLA DP

Doctor walks into DQ to get a Dr Pepper
CD marker displayed only by helper T cells.
CD4
CD marker displayed only by cytotoxic T cells.
CD8
CD marker displayed on all T cells.
CD3
CD marker displayed by B cells.
CD19,20,21
CD marker displayed by all NKCs.
CD16 (binds IgG)
CD marker that inhibits C9 binding.
CD55, 59
CD marker that acts as endotoxin receptor.
CD14 (on macs)
This cytokine promotes B cell growth and differentiation.
IL-4,5
This cytokine is produced by Th1 cells.
IL2, IFNgamma
This cytokine is produced by Th2 cells.
IL-10
This cytokine is involved in growth and activation of eosinophils.
IL-5
This cytokine inhibits macrophage activation.
IL-10
Pyrogens secreted by monocytes and macrophages.
IL1,6; TNF alpha
This cytokine inhibits Th1 cell production.
IL-10
This cytokine inhibits Th2 cell production.
IFN-gamma
This cytokine mediates inflammation.
IL-1,6, TNF alpha
This cytokine enhances synthesis of IgE and IgG.
IL-4
This cytokine enhances synthesis of IgA.
IL-5
This cytokine is released by virally infected cells.
IFN-alpha, beta
This cytokine supports growth and differentiation of BM SCs.
IL-3
This cytokine supports T cell proliferation, differentiation, and activation.
IL-2
Bond that holds antibodies together.
Disulfide bonds holds Ab together; connect heavy chain to light chain, light chain to light chain, etc.
Fab region of antibody:
Function
Comprising regions
Antigen-binding
Determines idiotype--unique Ag binding pocket; only 1 antigenic specificity expressed per B cell (B Cells produce Abs!)

Composed of 2 light chain and 2 heavy chain regions
Fc region of antibody:
Function
Comprising regions
Constant
Carboxy terminal
Complement binding
Carbohydrate side chains
Determines isotype (IgM, IgD, etc)

2 heavy chains!
List 5 types of heavy chains and corresponding immunoglobulins.
Mu--IgM
Delta--IgD
Gamma--IgG
Alpha--IgA
Epsilon--IgE
List types of light chains
Ratio?
Lambda
Kappa

No functional difference between these 2!

Should have 2 kappa per 1 lambda

If have multiple myeloma, this ratio will be thrown off based on type of Ab creating.
IgG structure:
Heavy and light chains
2 gamma heavy chains
2 either lambda or 2 kappa regions (light chains)
Terminal deoxynucleotidyl transferase:
Role
Adds nucleotides to DNA during VJ (light chain) or VDJ (heavy chain) rearrangement
What initiates VDJ recombination?
Recombination activating gene complex RAG 1 and RAG2 recognize RSSs and initiate VDJ recombination

Results break in dsDNA at Recombination Signal Sequences (RSS) that flank V, D, and J regions
Mutations in RAG genes
Inability to initiate VDJ rearrangement and results in arrest of B and T cells development

B and T cells can't express unique Ag receptors (Antibodies)
Half-life of IgG
21 days--passive immunization requires monthly inoculation
Main antibody in secondary response to antigen.
IgA (delayed response = secondary response)
Main antibody in primary response to antigen.
IgM (immediate response = primary response)
Immunoglobulin associated with allergies because it's bound by mast cells and basophils.
IgE
Immunoglobulin that comprises 75% of total immunoglobulin pool.
IgG
Immunoglobulin present in large quantities on membrane of B cells.
IgD, IgM
Immunoglobulin that crosses the placenta and confers immunity to neonates.
IgG
Immunoglobulin that can occur as dimer.
IgA
Immunoglobulin largely confined to intravascular pool.
IgM (early Ab)
Immunoglobulin distributed evenly between intravascular and extravascular pools.
IgG
Immunoglobulin in mucoserous secretions such as saliva, colostrum, milk, genitourinary secretions.
IgA
Immunoglobulin that can occur as pentamer.
IgM
Thymus independent Ag's vs Thymus dependent antigens:
General
Examples
Thymus independent: no peptide component; MHC can't bind anything, ex: LPS on gram neg bact

Results in release of IgM, don't form memory

Thymus dep Ag's:
ex: vaccines, will create memory

Allows for class-switching: IgM-->IgG
Release of IL-4,5,6
What stimulates alternative pathway of complement?
Microbial (LPS)
Classic PW:
What stimulates it?
Complement factor involved?
Ag-Ab complexes


C1 = first copmlement involved
C1 esterase inhibits cleavage of C1 (prevents cascade)
Complement factors associated with anaphylaxis.
Why?
C3a, C5a: Anaphylaxis
C3a-->**mast cells, basophils-->histamine
-->edema, vasc perm-->BP drops bc fluid is trapped in swelling

Tx w/epi
Complement factor associated with neutrophil chemotaxis.
C5a: nphil chemotaxis
Complement factors associated with membrane attack complex.
C5b-9: makes membrane attack complex
C1 esterase:
Role
Effect of deficiency
C1 esterase inhibits cleavage of C1 and prevents classic PW activation

Deficiency leads to hereditary angioedema (results in elevations of bradykinin)
Deficiency of this complement factor results in recurrent pyogenic sinus and respiratory tract infections.
C3

Recurrent infections withstrep pneumo, h flu

Inc'd susceptibility to type III hypersens rxns (esp GN)
Deficiency of this complement factor results in neisseria bacteremia.
Deficiency of C5-C8--

(gonococcal and meningococcal bacteremia)

These are involved in MAC (membrane attack complex)
Deficiency of this results in lysis of RBCs and paroxysmal nocturnal hemoglobinuria.
Deficiency of Decay Accelerating factor (CD55)
Paroxysmal nocturnal hemoglobinuria:
Presentation
Dx
Tx
Hemosiderinuria-->iron deficiency anemia
Chronic intravascular hemolysis
Thrombosis

Dx with Ham's test--RBCs lyse at low pH

Tx:
Iron
Warfarin (too many platelets)
BM transplant (bc due to
Which vaccines result in rapid immunity after exposure to the bug?
To Be Healed Rapidly:
Give pre-formed Ab's and vaccine for:
Tetanus
Botulinum
HBV
Rabies

Also RSV (respiratory syncytial virus for premature babies in winter months)
What is anergy?
Self-reactive T cells become nonreactive without co-stimulatory molecule (tolerance to self)
List granulomatous diseases
Tb (only one that is caseating)
Fungal infections (histo, blasto)
Syphilis (gummas)
Leprosy
Cat scratch fever
Sarcoid
Crohn's
Berylliosis
Listeria
Foreign bodies
Wegner's granulomatosus
Chronic granulomatous disease
This bacteria results in cat scratch fever.
Bartonella henselae