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Test your basic knowledge |
USMLE Step 1 Immunology
Start Test
Study First
Subjects
:
health-sciences
,
usmle-step-1
Instructions:
Answer 50 questions in 15 minutes.
If you are not ready to take this test, you can
study here
.
Match each statement with the correct term.
Don't refresh. All questions and answers are randomly picked and ordered every time you load a test.
This is a study tool. The 3 wrong answers for each question are randomly chosen from answers to other questions. So, you might find at times the answers obvious, but you will see it re-enforces your understanding as you take the test each time.
1. Only the _______ contribute to the Fc region
T cell activation; no with CD 4 or CD 8
Edema and necrosis in that region
Active; passive - fast but short half life (3 weeks!)
heavy chains
2. In general What are T cells good for?
Anti viral and anti tumor
Antidote for digoxin intoxication
Cytokine IL 10 secreted by Th2
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
3. What are the main symptoms of T cell immunodeficiencies?
Immunosuppression after kidney transplantation
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
isotype
4. What is the late phase reaction of anaphylaxis allergy? what mediates it?
IgG
mesenchymal
secondary
Hours later (instead of minutes); instead of release of preformed mediators - mast cells synthesize PGs and LTs that mediate the late phase reaction (edema - inflammation - decreased airflow)
5. What are the symptoms of serum sickness?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Celiac
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
2 heavy chains and two light chains
6. Monomer in circulation - ___ when secreted
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
dimer
7. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
Negative!
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
MAC (membrane attack complex) Which is activated by C5b - C9 and results in lysis and cytoxicity by creating pores in the target membrane; encapsulated organisms (S. pnuemonia - H.influenzae - B perfussis for example) and other organisms with non pep
...
8. What is a factor that is a predictor for a bad transplantation?
Axillary
Paracortex
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Th cells fail to produce interferon gamma; a lot of IgE
9. What is the pathology in hyperacute transplant rejection?
Delayed type hypersensitivity
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
B - T - and NK cells
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
10. Which are the only two antiinflammatory cytokines?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
TGF beta and IL 10
DM type I and RA
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
11. What does interferon gamma do? What two type of cells does it attack mostly?
Th2; Th1
IgE
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
12. What lymph node drains the lateral side of the dorsum of the foot?
opsonizes
Popliteal
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
IgM or IgG antibodies coat the antigen and result in activation of MAC complex via the classical pathway OR fixed macrophages in the spleen phagoctyose the opsonized (C3b or igG) antigens - ex penicillin reaction; IgM AIHA - anti B IgMs in a group A
13. What does IL 5 do?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Barrel hoop basement membrane fenestrations
Popliteal
14. What are the autoantibodies for myasthenia gravis?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Anti Ach receptor
Steroid responsive nephrotic syndrome
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
15. What is recomb gamma interferon used for?
Immunoflourescent staining of tissue biopsies
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Receiving preformed Antibodies
Chronic granulomatous disease
16. The alternative pathway is the only constutively...
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Daclizumab; prevent ACUTE rejection of renal transplant
Immunoflourescent staining of tissue biopsies
active complement pathway
17. What do mature naive B lymphocytes express?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Activates cytotoxic CD 8 T cells as second signal
Graves
IgM and IgD
18. What lymph node drains the breast?
Axillary
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Macrophages - Dendritic cells - B cells
Pernicious Anemia and Hashimotos
19. Leukocyte adhesion defect presents with...
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
neutrophilia!
Anti topoisomerase
secondary
20. Other than stimulating fever - what else does IL 6 do?
Hours later (instead of minutes); instead of release of preformed mediators - mast cells synthesize PGs and LTs that mediate the late phase reaction (edema - inflammation - decreased airflow)
Stimulate the liver to release acute phase reactants
Anti viral and anti tumor
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
21. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
delayed!
Wiskott Aldrich syndrome
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
IgM and IgA
22. Describe the capsular structure of a lymph node; What are the functions of the LN?
Capsule of lymph node is made up of type III collagen (made by reticulin fibers!) - extension of this collagen extends into the splenic tissue as trabeculae; nonspecific filtration of lymph by Macrophages - Antibody production (via activation) - stor
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Complement activation (active in both)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
23. Which disease is associated with B8?
lowest concentration
Binds to Mtor which (like tacrolimus and cyclosporine just in a different pathway) inhibits IL 2 production and thus t cell proliferation in response to IL 2 producton
Graves
Celiac
24. which B and T cell disorder presents with specifically low IgM?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Previous transfusion; pregnant woman whose fetus had paternal antigens
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Wiskott Aldrich syndrome
25. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
B - T - and NK cells
NK cells
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
26. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Cells that stil have weird parts of their membrane that macrophages usually bite off
High endothelial venules are post capillary cuboidal endothelial cells that contain specific adhesion molecules for lymphocytes with specific binders that allows for lymphocytes to drain out of the vasculature into the lymph node structure (this is h
A B and T cell disorder; X linked recessive; progressive deletion of B and T cells; thrombocytopenic purpura - infections - eczema; high IgE and IgA but low IgM
27. which of the transplant rejections is antibody mediated? why does it occur?
type four
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Some microbial surfaces (only) have mannan binding lectin which activates a protease that cleaves C2 and C4 which combine to make C3. the rest follows the alternative pathway
28. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Alternative splicing of mRNA
1) VJ light chain random creation 2) VDJ (heavy chain) random creation 3) random combination of light with heavy 4) somatic hypermutation (high frequency mutating that occurs on activation) 5) terminal deoxynucleotidyl transferase (TDT) random additi
...
29. what cell surface proteins are on all APCs?
acute phase reactants
Activates cytotoxic CD 8 T cells as second signal
Binds to Mtor which (like tacrolimus and cyclosporine just in a different pathway) inhibits IL 2 production and thus t cell proliferation in response to IL 2 producton
MHC II - B7
30. What links the adaptive and innate immunity?
All MHC 1/CD8
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Complement activation (active in both)
If there is class switching and plasma cell production (that is when memory cells are produced)
31. What lymph node drains the upper limb?
Anti Jo -1
A recomb cytokine of IL 2; RCC and metastatic melanoma
Cross link
Axillary
32. What is the treatment of acute transplant rejection?
Binds to Mtor which (like tacrolimus and cyclosporine just in a different pathway) inhibits IL 2 production and thus t cell proliferation in response to IL 2 producton
Cyclosporine - OKT3
Anti Jo -1
Inferior mesenteric
33. Type IV hypersensitivity is i...
Celiac
not Ab mediated
T cell activation; no with CD 4 or CD 8
In any situation where immunologically competent cells are transplanted into immunologically crippled recipient; graft rejects all the cells due to foreign proteins resulting in severe organ dysfunction
34. What is passive immunity?
Local infection/inflammation; infection of the ln itself; metastasis
delayed!
Receiving preformed Antibodies
Anti smooth muscle
35. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
except hyperacute
Type IV
Paracortex
36. Which disease is associated withB B27?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
MS - hay fever - SLE - goodpastures
Influenza; antigenic shift; antigenic drift
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
37. IgM can exist as a _______ also
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
pentamer
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
T
38. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
A chemotactic factor for neutrophils
Daclizumab; prevent ACUTE rejection of renal transplant
pathogenesis
Fab portion
39. What lymph node drains the testes?
Stimulate the liver to release acute phase reactants
Increases expression of MHC I and MHC II and also activates NK cells
Give a vaccine with a peptide comp from it that the cell mediated immunity otherwise cant get to! like h.influenzae vaccine. then class switching and memory response can occur
Para aortic
40. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Popliteal
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
41. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
If there is class switching and plasma cell production (that is when memory cells are produced)
Steroid responsive nephrotic syndrome
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
42. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Anti Ach receptor
...
Antihistone
IL 3; supports growth and differentiation of bone marrow stem cells
43. can igG cross the placenta?
Superficial inguinal
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
neutrophilia!
Yes
44. What bugs can actually infect the lymph node itself?
CROSS LINK Beta region on TCR of CD4 cells to the MHC class II on APCs this results in uncoordinated release of Interferon gamma from CD4 Th1 cells and subsequent release of IL1 - IL6 and TNF alpha from Macrophages --> toxic shock syndrome; s. pyogen
Daclizumab; prevent ACUTE rejection of renal transplant
The interstitial tissue of a lymph node is structured into the cortex on the outside Which is densely cellular which transitions into the paracortex Which is less dense and then the medulla Which is least dense. The cells that inhabit these tissues a
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
45. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Defect in LFA 1 integrin (CD 18) protein on phagocytes (neutrophils!); recurrent bacterial infections - severe gingivitis - poor wound healing - absent pus formation - and delayed separation of the umbilicus; neutrophilia
MHC class molecules bind to KIRS or CD94 to prevent killing
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Its main effect is a defect in Ab opsonization for killing
46. How does the alternative pathway lead to MAC activation?
No! That is why they are different from T cells - they can recognize antigens in free solution; if a bug has a peptide fragment that a mature naive B cell recognizes it will bind to it and cause activation - it then gets activated into a plasma cell!
Soluble C3 spontaneously hydrolyzes spontaneously to C3b and opsonizes microbial and host cell surfaces and accumulates on surfaces; C3b activates C5 convertase which leads to MAC activation
Type III hypersensitivity where an exogenous antigen results in a systemic antigen antibody complex disease (takes around 5 days after exposure for the Abs to develop); immune complexes then fix in tissue and activate complement resulting in tissue d
Defect in LFA 1 integrin (CD 18) protein on phagocytes (neutrophils!); recurrent bacterial infections - severe gingivitis - poor wound healing - absent pus formation - and delayed separation of the umbilicus; neutrophilia
47. what will NK cells do to cells covered in IgG Ab? why?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Antihistone
Hemochromatosis
Kill them because they have CD16 on them that recognize the FcG portion
48. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
High endothelial venules are post capillary cuboidal endothelial cells that contain specific adhesion molecules for lymphocytes with specific binders that allows for lymphocytes to drain out of the vasculature into the lymph node structure (this is h
IL 3; supports growth and differentiation of bone marrow stem cells
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
pentamer
49. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Glycoproteins; HLA
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
...
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
50. Name the three opsonins
Immunoflourescent staining of tissue biopsies
CRP - C3b - IgM
Stimulate the liver to release acute phase reactants
IgE; by activating eosinophils