Test your basic knowledge |

USMLE Step 1 Immunology

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. Which HLA's are included in MHC I? MHC II?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
TGF beta and IL 10
A - B - C; all the D's
IgM and IgG

2. which antibody is involved in the primary response or immediate response to an antigen?
isotype
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
IgM
CD21 on B cells (although there is T cell lymphocytosis in EBV)

3. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Daclizumab; prevent ACUTE rejection of renal transplant
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
opsonizes
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

4. What are the autoantibodies for hashimotos?
A chemotactic factor for neutrophils
pathogenesis
Negative nitroblue tetrazolium reduction test
Antimicrosomal and antithyroglobulin

5. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Antidote for digoxin intoxication
Anti TSh receptor
Internal iliac
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

6. What lymph node drains the thigh?
T cell activation; no with CD 4 or CD 8
Anti glutamate carboxylase and anti insulin
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Superficial inguinal

7. are Th cells involved in trapping of antigens of endotoxin/LPS?
The patient could become cyanotic in the OR!
Acts as second signal on B cells to induce class switching to IgE and IgG
For some reason a mature naive B lymphocyte got away from tolerance and the result was a production an Ab on its surface with an Fab region that recognized the alpha 3 collagen subunit on the BM as non self. It then gets activated by a Th2 cell (enti
No because no peptide fragment!

8. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Histamine; post capillary venules - vasodilation
T
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Rheumatic arthritis

9. What is the cause of thymic aplasia? What is its presentation? What are the labs?
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
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
IL 1 and IL 6
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

10. when can graft versus host disease? What is the result?
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
Superficial inguinal
...
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

11. What are the two signals required for B cell class switching? Which is the second signal?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
MHC I - CD16 - CD56

12. What are howell jolly bodies?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Internal iliac
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Edema and necrosis in that region

13. What is serum sickness? give an example.
Anti alpha subunit 3 of collagen on type IV bm
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
Complement activation (active in both)
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

14. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
All MHC 1/CD8
Negative selection
Remove encapsulated bacateria
A chemotactic factor for neutrophils

15. what happens in a deficiency of C1 esterase inhibitor? DAF?
Hereditary angioedema; PNH
Activates Th1 helper cells; Macrophages
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Negative!

16. What are the T cell functions?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
In the germinal center of secondary follicles (In the paler center)
Popliteal
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

17. How is sirolimus different from tacrolimus?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
IL 5

18. what results in symptoms of shock in an acute hemolytic transfusion reaction?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
IgM and IgA
Into cortex and medulla; cortex is where immature T lymphocytes enter - at the corticomedullar junction is where positive and negative selection occur; and at the medulla is where the mature T lymphs - reticulin cells and hassalls corpuscles are (dea

19. What is the general structure of an Ab?
cannot cross placenta
Pernicious Anemia and Hashimotos
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
2 heavy chains and two light chains

20. What is the pathogenesis of HyperIgE syndrome? What are the labs?
IL 1 and IL 6
Anti TSh receptor
Its main effect is a defect in Ab opsonization for killing
Th cells fail to produce interferon gamma; a lot of IgE

21. Complements are...
acute phase reactants
In the germinal center of secondary follicles (In the paler center)
Anti U1 RNP (ribonucleoprotein)
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

22. What does IL 4 do?
Acts as second signal on B cells to induce class switching to IgE and IgG
Superficial inguinal
Antidote for digoxin intoxication
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

23. Which MHC presents intracellular peptides? how so?
Activates Th1 helper cells; Macrophages
MHC I; from RER with help of the B2 microglobulin
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

24. IgE has the ___________ in the serum
lowest concentration
Axillary
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Anti topoisomerase

25. What is the main cytokine released by T cells? What does it do
Its main effect is a defect in Ab opsonization for killing
IL 3; supports growth and differentiation of bone marrow stem cells
Paracortex; viral infection
Fc

26. Which disease is associated with B8?
Sinusitis - otitis media - pneumonia
IgG
Graves
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

27. What is passive immunity?
Antidote for digoxin intoxication
CD56
Receiving preformed Antibodies
Barrel hoop basement membrane fenestrations

28. What does interferon gamma do to be antiviral?
False! B cell class switching requires a second signal
2 heavy chains and two light chains
The red pulp of the spleen its where the vasculature channels go through and interact with the parenchyma of the spleen (has macrophages) which empty in the sinuses; they are both encapsulated (with trabeculae) secondary lymphoid organs that trap ant
Increases expression of MHC I and MHC II and also activates NK cells

29. What are the autoantibodies for myasthenia gravis?
Anti Ach receptor
Anti U1 RNP (ribonucleoprotein)
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
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

30. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
IgG
...
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

31. The two heavy chains of an antibody contribute to the...
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
Daclizumab; prevent ACUTE rejection of renal transplant
Sinusitis - otitis media - pneumonia
Fab portion

32. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
Fc
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
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

33. The secondary follicles have __________; primary follicles are dense
Anti Ach receptor
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
mesenchymal
pale central germinal centers

34. where do NK cells develop?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Anti viral and anti tumor
Not thymus - BM

35. Which diseases are associated with DR5?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
T cell dysfunction
TGF beta and IL 10
Pernicious Anemia and Hashimotos

36. can igG cross the placenta?
Negative nitroblue tetrazolium reduction test
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
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Yes

37. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
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
Negative!
Anti Jo -1
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

38. Monomer in circulation - ___ when secreted
CRP - C3b - IgM
Anemias (esp due to renal failure)
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
dimer

39. What is colostrum?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Increases expression of MHC I and MHC II and also activates NK cells
The igA found in breast milk
IgAs in mothers breast milk!

40. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
Negative selection
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Anti mitochondrial
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

41. What are the main symptoms of T cell immunodeficiencies?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
If there is class switching and plasma cell production (that is when memory cells are produced)
IgM and IgA

42. What are the autoantibodies for Mixed connective tissue disease?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
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
Anti Jo -1
Anti U1 RNP (ribonucleoprotein)

43. what cell surface proteins are on all APCs?
MHC II - B7
Recom IL 11; thrombocytopenia
not Ab mediated
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

44. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
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
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
pathogenesis
Stimulate the liver to release acute phase reactants

45. other than eat and bite RBCs what else do Macrophages of spleen do>
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Remove encapsulated bacateria
C5a
T cell activation; no with CD 4 or CD 8

46. What are the cell surface proteins on NK cells?
MHC I - CD16 - CD56
T cell and antibody mediated vascular damage due to MHC non self being recognized as self by self lymphocytes and resulting in attack of the foreign antigens it presents (all of them); months to years after; no :(
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
CRP - C3b - IgM

47. To what portion of the Antibody do the complements bind?
Brain - eyes - placenta/fetus - testicles; because they can have an antigen in there and not get attacked by immune system because dont have contact with immune system via blood and lymph; if an infection occurs such that trauma results in exposure t
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Fc
Previous transfusion; pregnant woman whose fetus had paternal antigens

48. What are the labs in brutons agammaglobulinemia?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
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)
Superficial inguinal
Viral neutralization of igM and IgG!

49. What is oprelevkin? and What is it used for?
Recom IL 11; thrombocytopenia
Celiac
Anti Jo -1
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

50. What are the cell surface proteins for Macrophages? which two are for opsonins?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
For some reason a mature naive B lymphocyte got away from tolerance and the result was a production an Ab on its surface with an Fab region that recognized the alpha 3 collagen subunit on the BM as non self. It then gets activated by a Th2 cell (enti
MS - hay fever - SLE - goodpastures
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)

Test your basic knowledge |

USMLE Step 1 Immunology

Communication skills, Self help skills, Self improvement skills, Productivity skills, Writing skills, Business skills, Thinking skills & More...

502 Pages | Only $12 | PDF / EPub, Kindle Ready

Top Scores

Link to This Test

Related Subjects