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Test your basic knowledge |
USMLE Step 1 Immunology
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Subjects
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health-sciences
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usmle-step-1
Instructions:
Answer 50 questions in 15 minutes.
If you are not ready to take this test, you can
study here
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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. ________ regulate the cell mediated response.
Acts as second signal on B cells to induce class switching to IgE and IgG
Chronic granulomatous disease
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
Humoral
2. hat is the presentation of Jobs syndrome or Hyper IgE?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Closed circuit where go directly to veins and open where squeeze out of capillary sinusoids and interact with either PALS or with macrophages in the cords of Billroth (for antigen immune function or for blood cleaning or for both) and squeeze back in
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Type IV
3. What is the general structure of an Ab?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
2 heavy chains and two light chains
Receiving preformed Antibodies
Superficial inguinal
4. What are the three types of APCs?
pentamer
A chemotactic factor for neutrophils
Macrophages - Dendritic cells - B cells
Pernicious Anemia and Hashimotos
5. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
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
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
6. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
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
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Closed circuit where go directly to veins and open where squeeze out of capillary sinusoids and interact with either PALS or with macrophages in the cords of Billroth (for antigen immune function or for blood cleaning or for both) and squeeze back in
MS
7. What is the toxicity of muromonab?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
TLR ad nuclear receptors
RNA segment reassortment
8. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
secondary
heavy chains
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Type II hypersensitivity - complement dependent resulting in phagocytosis of RBCs coated with C3b by fixed macrophages in the spleen; Group O mother has anti A - B - IgG Abs that cross placenta and attach to fetal blood group A or B RBCs
9. What is an example of a parasite showing antigenic variation?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Steroid responsive nephrotic syndrome
IL 3; supports growth and differentiation of bone marrow stem cells
10. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Th cells fail to produce interferon gamma; a lot of IgE
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
mesenchymal
11. What are the cell surface proteins on NK cells?
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
Anti smooth muscle
MHC I - CD16 - CD56
IL 4
12. what secretes IL 4?
Basophils! THey want IG E class switch!
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
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
13. What are the function of B cells?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
B - T - and NK cells
14. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
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
T cell activation; no with CD 4 or CD 8
Its main effect is a defect in Ab opsonization for killing
15. What is the mode of inheritance of Chediak Higashi syndrome? What is the disease d/t? What does it result in? What is the presentation?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
No because no peptide fragment!
Fc
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
16. What is the toxicity of azathioprine?
IL 4 - 5 - 10 - 6
Maculopapular rash (palm - soles - back - neck) - jaundice with bile duct necrosis - hepatosplenomegaly - diarrhea; bone marrow and liver transplants (rich with lymphocytes); SCID patient receiving whole blood transfusion
In the germinal center of secondary follicles (In the paler center)
...
17. What lymph node drains the lateral side of the dorsum of the foot?
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
DM type I and RA
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Popliteal
18. What is the main function of TNF alpha? How does it do this?
IgM and IgA
Type II hypersensitivity - complement dependent resulting in phagocytosis of RBCs coated with C3b by fixed macrophages in the spleen; Group O mother has anti A - B - IgG Abs that cross placenta and attach to fetal blood group A or B RBCs
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
NK cells
19. which cells have more complete tolerance - B or T cells?
T
Maculopapular rash (palm - soles - back - neck) - jaundice with bile duct necrosis - hepatosplenomegaly - diarrhea; bone marrow and liver transplants (rich with lymphocytes); SCID patient receiving whole blood transfusion
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
Negative nitroblue tetrazolium reduction test
20. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Cross link
21. other than mediating shock - what else does TNF alpha do? who releases it mainly?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Its a serine protease that activates apoptosis; NK and CD8
Activates Th1 helper cells; Macrophages
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
22. What is the main function of IL 12? other than macrophages who else can release IL 12?
Previous transfusion; pregnant woman whose fetus had paternal antigens
acute phase reactants
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
All MHC 1/CD8
23. What is chronic mucocutaneous candidiasis d/t?
Antidote for digoxin intoxication
T cell dysfunction
Superficial inguinal
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
24. The secondary follicles have __________; primary follicles are dense
pale central germinal centers
MHC class molecules bind to KIRS or CD94 to prevent killing
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)
25. What are the main Cell surface proteins on T cells?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Cyclosporine - OKT3
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
26. What is serum sickness? give an example.
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
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
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
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
27. what happens in a deficiency of C1 esterase inhibitor? DAF?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Anti smooth muscle
Hereditary angioedema; PNH
28. What does interferon gamma do? What two type of cells does it attack mostly?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Chronic granulomatous disease
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
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
29. What is the pathogenesis of acute transplant rejection? When does it occur?
Activates cytotoxic CD 8 T cells as second signal
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
pentamer
30. From where do cytokines come from?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
All MHC 1/CD8
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Lymphocytes
31. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Negative!
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Receiving preformed Antibodies
32. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
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
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
33. What are the autoantibodies for wegeners granulomatosis?
Increases expression of MHC I and MHC II and also activates NK cells
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
pathogenesis
34. What lymph node drains the sigmoid colon?
Anti alpha subunit 3 of collagen on type IV bm
This means that MHC can not recognize it and thus will not be phagocytosed. The humoral response rescues - IgM is the primary response attack. Since there is no class switching (without MHC activation no CD40 L and interleukins to activate!) then the
Immunosuppression after kidney transplantation
Inferior mesenteric
35. What does IL 2 do?
Remove encapsulated bacateria
Type IV
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Activates cytotoxic CD 8 T cells as second signal
36. What cytokines to Th2 secrete?
IL 4 - 5 - 10 - 6
TNF alpha and IL1
Not thymus - BM
CD56
37. Which disease is associated with B8?
Graves
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
38. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Cytokine IL 10 secreted by Th2
39. What do multimeric antibodies require for assembly?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
A j chain
Maculopapular rash (palm - soles - back - neck) - jaundice with bile duct necrosis - hepatosplenomegaly - diarrhea; bone marrow and liver transplants (rich with lymphocytes); SCID patient receiving whole blood transfusion
The patient could become cyanotic in the OR!
40. what ensure that a memory response is generated?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Immunosuppression after kidney transplantation
If there is class switching and plasma cell production (that is when memory cells are produced)
41. What happens in a deficiency of C3?
Internal iliac
Acts as second signal on B cells to induce class switching to IgE and IgG
Increases expression of MHC I and MHC II and also activates NK cells
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
42. what mediates the type II hypersensitivity? What are the two different methods?
Found in the red pulp; contains the cords of billroth or the splenic parenchyma that have APCs/Macrophages that closely interact with the basement membrane of the vasculature and where RBCs squeeze through into the parenchyma and interact with Macrop
Antibody mediated cytotoxicity; either complement dependent or complement independent
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
MHC II - B7
43. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
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
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
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
44. What happens in a secondary follicle?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
DM type I
cannot cross placenta
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
45. IgM can fix complement but...
T cell precursor
The patient could become cyanotic in the OR!
cannot cross placenta
...
46. What are the autoantibodies for graves?
IL 4
...
Fc
Anti TSh receptor
47. Only the _______ contribute to the Fc region
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
Celiac
...
heavy chains
48. The alternative pathway is the only constutively...
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
active complement pathway
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
49. What is oprelevkin? and What is it used for?
Recom IL 11; thrombocytopenia
Cells that stil have weird parts of their membrane that macrophages usually bite off
Its a serine protease that activates apoptosis; NK and CD8
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
50. What are the autoantibodies for other vasculitides?
Superficial inguinal
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)
pentamer
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear