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138 Cards in this Set

  • Front
  • Back
What are 3 functions of a lymph node?
1) store & proliferate B & T-cells
2) make antibodies
3) place for macrophages to filter through
Where are B-cells localized in a lymph node?
follicle - in the outer cortex, 2ndary follicles are pale with active germinal centers
Lymph node medullary CORDS contain:
plasma cells, lymphocytes
Lymph node medullary SINUSES contain:
macrophages, reticular cells - communicate with efferent lymphatics
Where are the T-cells located in a lymph node?
paracortex, which is between the follicles & medulla - contains High Endothelial Venules where lymphocytes enter the node from the blood
Which part of the lymph node gets huge during, say, a viral infection?
PARACORTEX - where the T-cells are!
A patient with DiGeorge's syndrome is going to have a very poorly developed ___ of his lymph node.
paracortex - deficient T-cells
The thoracic duct drains which parts of the body?
everything except R arm and R half of head (drained by right lymphatic duct)
The spleen consists of scattered nodules of ___ pulp in extensive ___ pulp.
white; red
Where would you find B-cells in the spleen?
germinal centers of white pulp
Where would you find T-cells in the spleen?
Periarterial Lymphatic Sheath (PALS) of the white pulp; also in RED PULP!
What is the function of spleen red pulp?
remove old RBCs from circulation
What is the thymus derived from, embryologically?
epithelium of 3rd branchial pouches (ugh...branchial pouches)
Where are mature T-cells located in the thymus?
medulla - pale, also has Hassal's corpuscles
Where in the thymus do positive & negative T-cell selection occur?
corticomedullary junction
Positive selection of T-cells is where they must demonstrate the ability to bind to ___ in order to keep maturing.
peptide:MHC complex
Negative selection of T-cells is where those that ___ are apoptosed, because otherwise they might be autoreactive.
bind too strongly to self-peptide:MHC complexes
Macrophages secrete IL-___ which induces naive T helper cells to become Th___ cells.
IL-12, Th1
Th1 helper cells secrete ___ & ___ which do what?
gamma-IFN & IL-2: activate macrophages and CD8 T-cells, respectively
Which interleukin induces naive helper T-cells to become Th2 cells?
IL-4 (cell source unknown)
Which interleukins help B-cells make antibody (turn them into plasma cells)?
IL-4, 5
Which line of lymphocytes is responsible for autoimmunity?
Which line of lymphocytes is responsible for hay fever and other type 1 hypersensitivity?
Which line of lymphocytes defends against infection by opsonizing bacteria and neutralizing toxins and viruses?
Which line of lymphocytes defends you against tuberculosis, virus-infected cells, and fungi?
Which line of lymphocytes is responsible for graft rejections?
Which line of lymphocytes is responsible for poison ivy allergies?
Which line of lymphocytes regulates the antibody response, either by helping or suppressing?
All NUCLEATED cells have MHC class ___ proteins.
MHC class I
Which type of MHC do antigen presenting cells have?
both MHC I & II
MHC class I genes: (3)
A, B, C
MHC class II genes (3):
MHC class I proteins consist of ___ polypeptide(s):
1 transmembrane polypeptide: alpha chain + beta-2 microglobulin
Where does MHC I pick up its antigen to present?
RER - presents intracellular antigens like viruses
Where does MHC II pick up its antigen to present?
acidified endosome - picks up extracellular antigens that have been phagocytosed
___ T-cells have CD4 which binds to MHC class ___.
helper; MHC II
Cytotoxic T-cells have CD___ which binds to MHC class ___.
What is the CD3 complex?
proteins associated with T-cell receptor complex that transduce signals to the cell interior after Ag has been recognized
What are the 3 kinds of antigen presenting cells?
1) dendritic cells
2) macrophages
3) B-cells
Steps in T helper cell activation: start with Ag being phagocytosed
1) Ag phagocytosed by APC
2) Ag presented on MHC II
3) CD4 T helper cell binds
4) B7:CD28 costimulate Th cell
5) Th cell makes IL-2 and gamma IFN
How is a Tc cell activated?
1) recognizes protein presented on MHC I
2) IL-2 from Th cell activates Tc cell to kill virus-infected cell
An antigen presenting cell has which half of the B7:CD28 costimultory signal?
Which part of the antibody fixes complement?
constant part of the heavy chain, of IgG and IgM only
What are 4 characteristics of the Fc portion of an antibody?
1) constant
2) complement binding (IgG, M)
3) carboxy terminal
4) carbohydrate side chains
Which part of the antibody binds antigen?
variable regions of light and heavy chains (Fab fragment)
What are 3 things that antibodies do to bacteria?
1) opsonization to promote phagocytosis
2) neutralization to prevent their adherence to cells
3) complement activation to enhance opsonization & lysis
What are 4 ways to generate antibody diversity?
1) random recombination of VJ (light chain) or VDJ (heavy chain) genes
2) random recombination of heavy chains w/light chains
3) somatic hypermutation (only in B-cells)
4) addition of nucleotides to DNA during genetic recombination by terminal deoxynucleotidyl transferase
What is somatic hypermutation?
nucleotide substitutions into immunoglobulin light and heavy chain genes --> some variant immunoglobulins produced may bind the antigen better
Mature B-cells express ___ and ___ on their surface.
IgM, IgD
What is the process where mature B-cells turn into plasma cells and secrete immunoglobulins other than IgM and IgD?
isotype switching
What is IgG and what does it do?
1) main Ab in 2ndary response
2) most abundant Ig
3) crosses placenta
4) fixes complement (Fc frag)
5) opsonizes bacteria
6) neutralizes toxins & viruses
Which immunoglobulin prevents bacterial attachment to mucous membranes?
secretory IgA (picks up the secretory component from epithelial cells before secretion)
Which immunoglobulin is produced in the primary response to an antigen?
IgM - fixes complement, monomer or pentamer
Which immunoglobulin is found in LOWEST concentration in the serum?
What is IgE responsible for?
type 1 hypersensitivity - induce release of mediators from mast cells & basophils in response to allergen binding (recall: IgE crosslinking and cell degranulation)
What is an isotype?
Ig epitope common to a single class of Ig, like IgG, IgA... (there are 5 classes, each determined by its heavy chain)
What is an allotype?
the encoded proteins of alleles, which are different forms of a gene
What is the cytokine that is:
- secreted by macrophages
- causes fever
- stimulates T-cells, B-cells, PMN, fibroblasts, epithelial cells
IL-1 (hot)
Which cytokine is secreted by Th1 cells that activates Tc cells as well as Th cells?
IL-2 (T-cells)
Which cytokine has a function similar to that of GM-CSF, which is to stimulate bone marrow stem cell growth and differentiation?
This cytokine stimulates B-cells to class switch to IgE and IgG.
Which interleukin enhances B-cell class switching to IgA?
Which cytokine stimulates production and activation of eosinophils?
IL-6 is produced by _____ and stimulates production of _____.
Th cells & macrophages; acute phase reactants
Which interleukin is a major neutrophil chemoattractant?
Which cytokine stimulates Th2 cells and inhibits Th1 cells?
IL-10 - made by Th2 cells
Which cytokine activates NK cells and Th1 cells? Which cells make it?
IL-12; made by macrophages and B-cells
Which cytokine activates macrophages?
gamma-IFN (made by Th1 cells in addition to IL-2)
TNFa is made by ___ and acts to:
1) IL-2 receptor synthesis by Th cells
2) B-cell proliferation
3) attracts neutrophils
4) stimulates DCs to go to LN
Cell surface proteins on Th cells: (5)
1) CD4
2) TCR
3) CD3
4) CD28
5) CD40L
Cell surface proteins on Tc cells: (3)
1) CD8
2) TCR
3) CD3
What kind of cell expresses the following on its surface: IgM, B7, CD19, CD20, CD40, MHC II
What cell surface proteins does a macrophage express?
MHC II, CD14 (both of which are receptors for Fc and C3b)
What do NK cells express on the surface?
MHC I, CD16, CD56 (major marker)
How is complement activated in the classic pathway?
IgM, IgG (bind complement with their constant heavy chain portions)
How is complement activated in the alternate pathway?
by molecules on the surface of microbes, especially ENDOTOXIN!!!
Complement defends the host against infection by what kind of bacteria?
gram negative
C1, 2, 3, 4 do what?
neutralize viruses
C3b does what?
opsonization (recall: macrophages have Fc and CD14 surface proteins which are receptors for C3b), also clears immune complexes from serum!
What complements are responsible for anaphylaxis?
C3a, C5a (C5a is also neutrophil chemoattractant, like IL-8 and LTB4)
Which complements mediate cytolysis by forming MAC?
C5b, 6, 7, 8, 9
What happens if you don't have C1 esterase inhibitor?
hereditary angioedema from overactive complement
What happens if you don't have C3?
severe recurrent pyogenic sinus and respiratory tract infections
Deficiency of C6-C8 causes bacteremia by which species?
Deficiency of Decay Accelerating Factor causes:
paroxysmal nocturnal hemoglobinuria
What do interferons do to uninfected cells when there is a viral infection going on?
puts them in an anti-viral state; activate NK cells to kill virus-infected cells
How do gamma interferons help in a viral infected state?
increase MHC I & II expression, upregulate antigen presentation in all cells
What kind of immunity is getting antibodies premade by another host?
passive - rapid onset immunity but short lived
What kind of immunity is induced after personal exposure to foreign antigens?
active - slow onset but memory forming (long lasting)
Exposure to what 4 toxins call for passive immunity for quick action?
- rabies
- tetanus
- botulinum
Which protozoan has antigen variation?
Which bacteria can have antigen variation?
- Salmonella (flagella)
- Borrelia (relapsing fever)
- N.gonorrhea (pilus)
Which virus is famous for antigenic variation by shifting or drifting?
influenza virus
What happens to T-cells that bind to self molecules but don't have a costimulatory signal?
anergy - become nonreactive
Anaphylaxis, asthma, hives, local wheal and flare are all examples of what kind of hypersensitivity?
type 1 - antigen crosslinks IgE on presensitized mast cells & basophils --> release vasoactive amines like histamine
How does type 2 hypersensitivity work?
IgM, IgG bind to antigen on cell; can --> lysis or phagocytosis
(examples: autoimmune hemolytic anemia, Rh disease, Goodpasture's, rheumatic fever, Grave's, bullous pemphigoid, myasthenia gravis, ITP)
What are the 3 components of type 3 hypersensitivity?
antigen: antibody: complement
attracts neutrophils which release enzymes and cause tissue damage (PAN, SLE, RA, immune complex glomerulonephritis)
Describe what happens in serum sickness:
1) inject forein proteins
2) make Abs against them
3) Ag:Ab complexes deposit in membranes (systemic)
4) fix complement --> tissue damage
How does serum sickness manifest clinically?
5-10 days after antigen exposure, patient will present with fever, urticaria, arthralgia, proteinuria, lymphadenopathy
What is the Arthus reaction?
intradermal injection of foreign Ag --> Ag:Ab complexes in skin with LOCAL inflammation & necrosis, edema, complement activation (example: farmer's lung)
Wot is type 4 hypersensitivity? (I'm so bored...)
SENSITIZED T-cells bind antigen and release cytokines that activate macrophages --> transplant rejection, positive PPD skin test, contact dermatitis
Bruton's agammaglobulinemia =
XR defect in tyrosine kinase gene, low B-cells and ALL immunoglobulins! Recurrent bacterial infections after 6 mo of age when Mom's IgG wears out
DiGeorge's syndrome =
failed development of 3rd & 4th pharyngeal pouches --> no thymus (so no T-cells) or parathyroids, tetany, recurrent viral & fungal infections, 22q11 del, congenital heart defects (truncus, tetralogy)
low B & T-cells, defect in stem cell differentiation, recurrent bacterial, viral, fungal, protozoal infections (many causes like ADA deficiency, defective IL-2 receptors, no MHC II antigens)
Disseminated mycobacterial infections. Due to low activation of:
Th1 cells (IL-12 receptor deficiency)
Super high levels of IgM and very low levels of IgG, IgA, IgE suggest:
hyper-IgM syndrome where defective CD40L on Th cells leads to inability to help B-cells class switch
Elevated IgA, normal IgE, and low IgM levels along with recurrent pyogenic infections, thrombocytopenic purpura, and eczema suggest:
Wiskott-Aldrich syndrome (XR), can't mount IgM response to encapsulated bacteria (polysaccharide antigen)!
Job's syndrome =
Th1 cells don't make gamma-IFN so can't activate macrophages --> no TNFa to attract neutrophils --> recurrent staph abscesses, eczema, coarse facies, retained primary teeth (odd), and HIGH IgE!
Leukocyte adhesion deficiency syndrome =
defective LFA-1 adhesion proteins on phagocytes (early severe pyogenic & fungal infections, delayed separation of umbilicus)
What do you suspect in a patient who gets recurrent infections by staph & strep, is partially albino, and has peripheral neuropathies?
Chediak-Higashi (AR) - microtubule dysfunction --> impaired phagocytosis and melanin distribution
Some who gets a lot of infections with S.aureus, E.coli, and aspergillus, and a negative nitroblue tetrazolium dye reduction test has:
chronic granulomatous disease - NADPH oxidase deficiency
Chronic mucocutaneous candidiasis =
T-cell dysfunction specifically against Candida albicans
Selective immunoglobulin deficiency =
usually selective IgA deficiency due to defect in class switching (get sinus and lung infections, milk allergies, diarrhea)
Ataxia-telangiectasia =
defect in DNA repair against x-rays, presents with progressive cerebellar ataxia and spider angiomas, associated with IgA deficiency
anti-dsDNA, anti-Smith antibodies =
anti-histone antibodies =
drug-induced lupus
anti-IgG antibodies =
rheumatoid arthritis (anti-IgG is rheumatoid factor)
anti-centromere antibodies =
CREST scleroderma
(calcinosis, Raynaud's, esophageal dysmotility, sclerodactyly, telangiectasia, limited skin involvement to face and fingers)
anti-scl-70 antibodies =
diffuse scleroderma
(widespread skin involvement, rapid progression, early organ involvement)
anti-mitochondrial antibodies =
primary biliary cirrhosis
(intrahepatic, obstructive jaundice, steatorrhea, pruritus, xanthoma, high ALP)
anti-epithelial cell antibodies =
pemphigus vulgaris
anti-microsomal antibodies =
Hashimoto's thyroiditis
anti-thyroglobulin antibodies =
Hashimoto's thyroiditis
anti-Jo-1 antibodies =
1) dermatomyositis (skin rash, inc. risk malignancy, progressive proximal muscle weakness)
2) polymyositis (progressive proximal muscle weakness)
anti-U1RNP antibodies =
mixed connective tissue disease (FA p319)
anti-gliaden antibodies =
celiac sprue
anti-basement membrane antibodies (collage type 4)
HLA B27 =
psoriasis, ankylosing spondylitis, IBD, Reiter's syndrome
HLA B8 =
Grave's, celiac sprue
multiple sclerosis, hay fever, SLE, Goodpasture's
diabetes mellitus type 1 (and lupus?)
diabetes mellitus type 1, rheumatoid arthritis
Hashimoto's thyroiditis, pernicious anemia --> B12 deficiency
steroid-responsive nephrotic syndrome
Presence of preformed, anti-donor antibodies leads to which type of transplant rejection?
hyperacute - occurs w/in minutes after transplant
Tc cells reacting to foreign MHCs is what kind of transplant rejection?
acute rejection - weeks after transplant, reversible with immunosuppressants like cyclosporin & OKT3
Describe a chronic transplant rejection:
occurs months to years later, irreversible, antibody-mediated vascular damage (fibrinoid necrosis)
Explain graft vs. host disease:
immunocompetent T-cells grafted along with the transplanted tissue starts attacking "foreign" proteins --> severe organ dysfunction, maculopapular rash, jaundice, hepatosplenomegaly, diarrhea