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Test your basic knowledge |
USMLE Step 1 Immunology
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health-sciences
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usmle-step-1
Instructions:
Answer 50 questions in 15 minutes.
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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. Type IV hypersensitivity is i...
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
not Ab mediated
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
2. How is sirolimus different from tacrolimus?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Superficial inguinal
Antibody mediated cytotoxicity; either complement dependent or complement independent
3. which interleukin receptor is required for NK development? activation?
Anti topoisomerase
IL 15; IL 12 - interferon Beta and interferon alpha
Defect in B cell maturation; idiopathic - presents at older age and normal number of B cells and hyperplastic germinal centers because B cells can be activated but can not produce Abs
C5a
4. where are complements produced?
Liver! (they are proteins circulating in the blood)
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
5. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Axillary
Rheumatic arthritis
C5a
Macrophages - Dendritic cells - B cells
6. what will NK cells do to cells covered in IgG Ab? why?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
An antigen encounter (presented by APC for Th2) with Th2 will result in it to go to the cortical section and help with B cell activation; Cytotoxic T cell will enter vasculature/efferent lymph to go kill; B cell will wait for Th2 for activation and t
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Kill them because they have CD16 on them that recognize the FcG portion
7. What is the defect in hyper IgM syndrome? What are the lab results?
Cyclosporine - OKT3
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
DM type I and RA
An acidified endosome with the antigen fuses with the MHC which causes the release of the invariant chain Which is sitting in spot of antigen and stabilizing the MHC II
8. What are the three types of lymphocytes?
Paracortex
Digeorge syndrome - 22q11 deletion resulting in failure to develop 3rd and 4th pharyngeal pouches; cardiac and great vessel congenital defects - tetany from hypocalcemia - recurrent viral/fungal infections from T cell deficiency; hypoPTH - hypoCa - a
B - T - and NK cells
RNA segment reassortment
9. which of the transplant rejections is antibody mediated? why does it occur?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
NK cells
TLR ad nuclear receptors
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
10. ________ regulate the cell mediated response.
Humoral
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Immunosuppression after kidney transplantation
isotype
11. What cytokines to Th2 secrete?
TGF beta and IL 10
MHC I - CD16 - CD56
IL 4 - 5 - 10 - 6
Histamine; post capillary venules - vasodilation
12. What are the autoantibodies for primary biliary cirrhosis?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
False! B cell class switching requires a second signal
MHC II - B7
Anti mitochondrial
13. where do somatic hypermutation and class switching occur?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
...
mesenchymal
In the germinal center of secondary follicles (In the paler center)
14. What is the pathogenesis of a candida skin test?
Delayed type hypersensitivity
Antidesmoglein
Anemias (esp due to renal failure)
Defect in B cell maturation; idiopathic - presents at older age and normal number of B cells and hyperplastic germinal centers because B cells can be activated but can not produce Abs
15. What does interferon gamma do to be antiviral?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Th2; Th1
Increases expression of MHC I and MHC II and also activates NK cells
Inferior mesenteric
16. What lymph node drains the upper limb?
IgM and IgG
not Ab mediated
Axillary
pathogenesis
17. What is muromonab - CD3 (OKT3)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Lymphocytes
It is a localized type III hypersensitivity reaction to an external antigen; localized instead of systemic; ?; intradermal injection of the antigen results in antibody production and antigen antibody complexes deposit in the skin
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
18. What are the two signals required for B cell class switching? Which is the second signal?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
neutrophilia!
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
19. What are the two signals required for Th1 cells? what happens after then activated?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
...
20. What is an example of a parasite showing antigenic variation?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
21. what cell surface marker is used for NK cells as it is unique to them?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
CD56
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
22. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
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
It is a localized type III hypersensitivity reaction to an external antigen; localized instead of systemic; ?; intradermal injection of the antigen results in antibody production and antigen antibody complexes deposit in the skin
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
2 heavy chains and two light chains
23. What is the presentation of Brutons agammaglobulinemia?
CRP - C3b - IgM
Antihistone
IgG
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
24. What does IL 4 do?
Acts as second signal on B cells to induce class switching to IgE and IgG
Remove encapsulated bacateria
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
In IgE AIHA- it results in MAC attack (remember IgE is not an opsonin!) - in IgG AIHA C3b (and IgG) opsonization results in phagocytosis by fixed macrophages in the spleen
25. which of the hypersensitivity reactions is not Ab mediated?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Liver! (they are proteins circulating in the blood)
Immunoflourescent staining of tissue biopsies
Type IV
26. What are the major functions of Antibodies?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Previous transfusion; pregnant woman whose fetus had paternal antigens
IL 4
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
27. describe the pathogenesis of delayed type IV hypersensitivity
Activates cytotoxic CD 8 T cells as second signal
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
28. What is recomb gamma interferon used for?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Chronic granulomatous disease
First a B cell gets sensitized to an allergen - after sensitization - it gets induce by Th2 secreting IL4 to class switch from IgM to IgE - next time blood stream is exposed to allergen these antigens cross like IgEs on mast cells and result in chemi
The igA found in breast milk
29. What are the autoantibodies for drug induced lupus?
TNF alpha and IL1
Antihistone
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
DM type I and RA
30. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Thrombocytopenia
TNF alpha and IL1
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Paracortex; viral infection
31. What is the main function of IL 8?
Negative nitroblue tetrazolium reduction test
Basophils! THey want IG E class switch!
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
A chemotactic factor for neutrophils
32. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
Superficial inguinal
Activate macrophages
They directly stimulate Macrophages by binding CD14; also the alternative complement pathway binds to these host surfaces and induces MAC complex; also TLRs exist for endotoxins; also IgM though not an opsonin can act as a pentamer and trap the antig
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
33. What is the main cytokine that activates eosinophils?
IL 5
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
34. What does CD16 on NK cells do?
Bind FcG for antibody dependent cellular cytotoxicity
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
Popliteal
Th2; Th1
35. Which HLA's are included in MHC I? MHC II?
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36. What are the two signals to kill for NK cells?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
S. aureus - E. Coli - aspergillus
active complement pathway
37. What are the autoantibodies for graves?
IL 5
All MHC 1/CD8
Active; passive - fast but short half life (3 weeks!)
Anti TSh receptor
38. What are the three types of APCs?
Macrophages - Dendritic cells - B cells
No because no peptide fragment!
Steroid responsive nephrotic syndrome
MHC class molecules bind to KIRS or CD94 to prevent killing
39. What are the autoantibodies for type I diabetes mellitus?
CRP - C3b - IgM
Severe pyogenic infections early in life
Anti glutamate carboxylase and anti insulin
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
40. What does it mean if there are igM in the serum at birth?
not Ab mediated
IL 3; supports growth and differentiation of bone marrow stem cells
Chronic granulomatous disease
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
41. What do multimeric antibodies require for assembly?
Basophils! THey want IG E class switch!
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
acute phase reactants
A j chain
42. Describe complement dependent Type II hypersensitivity. Give an example.
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
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
TLR ad nuclear receptors
43. other than eat and bite RBCs what else do Macrophages of spleen do>
Chronic granulomatous disease
CRP - C3b - IgM
Remove encapsulated bacateria
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
44. What is the autoantibody for SLE that is nonspecific? Specific?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
In the germinal center of secondary follicles (In the paler center)
45. What is recomb alpha interferon used for?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Popliteal
Superficial inguinal
Paracortex
46. What is the cause of thymic aplasia? What is its presentation? What are the labs?
pale central germinal centers
Digeorge syndrome - 22q11 deletion resulting in failure to develop 3rd and 4th pharyngeal pouches; cardiac and great vessel congenital defects - tetany from hypocalcemia - recurrent viral/fungal infections from T cell deficiency; hypoPTH - hypoCa - a
Antihistone
neutrophilia!
47. What does IL 10 do? who is secreted by?
Acts as second signal on B cells to induce class switching to IgE and IgG
dimer
Aut. Dominant; C1 esterase inhibitor deficiency resulting in continued C1 which results in increased C2 and C4 cleavage products which have anaphyltoxic activity and result in swelling of face and oropharynx
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
48. What are target cells?
IgAs in mothers breast milk!
Celiac
Cells that stil have weird parts of their membrane that macrophages usually bite off
N. meningitidis - H. influenzae - S. pneumonia - Salmonella d/t lack of C3b opsonization for MAC d/t lack of complement activation d/t lack of IgM; MAC is needed by encapsulated avoid by humoral and cell mediated through their capsule
49. Name two endogenous pyrogens
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
IL 1 and IL 6
Bind FcG for antibody dependent cellular cytotoxicity
IgE; by activating eosinophils
50. What lymph node drains the thigh?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Anti Jo -1
Superficial inguinal
Lymphocytes
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