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USMLE Step 1 Immunology

Subjects : health-sciences, 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...
delayed!
TLR ad nuclear receptors
Anti U1 RNP (ribonucleoprotein)
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

2. What are some sinopulmonary infections?
IgG
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Sinusitis - otitis media - pneumonia
Internal iliac

3. What are the autoantibodies for autoimmune hepatitis?
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
Anti smooth muscle
Previous transfusion; pregnant woman whose fetus had paternal antigens
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

4. What are the T cell functions?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
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
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
IgG

5. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
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
Cytokine IL 10 secreted by Th2
MHC II - B7
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

6. What is immune complex disease? give an example.
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
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
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

7. What is the main function of interferons?
Anti topoisomerase
Anemias (esp due to renal failure)
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

8. give an example of how influenza does a major antigenic shift.
MHC I; from RER with help of the B2 microglobulin
Anti IF
RNA segment reassortment
Antimicrosomal and antithyroglobulin

9. What do mature naive B lymphocytes express?
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
By transcytosis
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
IgM and IgD

10. The pathogenesis of contact dermatitis is ________ hypersensitivity
type four
Active; passive - fast but short half life (3 weeks!)
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
lowest concentration

11. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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 :(
Severe pyogenic infections early in life

12. How is i Th1 helper cell inhibited?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
When you select for which MHC it will have; take out the lymphs that self react
Cytokine IL 10 secreted by Th2
mesenchymal

13. What is the white pulp of the spleen?
IgG
Anti Jo -1
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Acts as second signal on B cells to induce class switching to IgE and IgG

14. Which disease is associated with DR7?
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
except hyperacute
Steroid responsive nephrotic syndrome
Thrombocytopenia

15. What is the pathology of acute transplant rejection? is it reversible?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Cells that stil have weird parts of their membrane that macrophages usually bite off
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

16. What are target cells?
IL 4 - 5 - 10 - 6
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
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
Cells that stil have weird parts of their membrane that macrophages usually bite off

17. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
Anti Ach receptor
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

18. What are the autoantibodies for Mixed connective tissue disease?
Anti U1 RNP (ribonucleoprotein)
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
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
Influenza; antigenic shift; antigenic drift

19. Which type of selection of thymic development provides central tolerance?
Negative selection
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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
MHC I - CD16 - CD56

20. What are the autoantibodies for myasthenia gravis?
Sinusitis - otitis media - pneumonia
encapsulated
Anti Ach receptor
type four

21. Which is the main antibody that provides passive immunity to infants?
Para aortic
Kill them because they have CD16 on them that recognize the FcG portion
IgG
Secretory component

22. What is the cause of thymic aplasia? What is its presentation? What are the labs?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
When you select for which MHC it will have; take out the lymphs that self react
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
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

23. What does interferon gamma do? What two type of cells does it attack mostly?
Antidesmoglein
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
IgG
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

24. in which immunodef order do you see a lot of pus? no pus?
Interferon gamma; Th1
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

25. What is hereditary angioedema? What are the C3 levels?
Macrophages - Dendritic cells - B cells
TGF beta and IL 10
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
Steroid responsive nephrotic syndrome

26. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Immunoflourescent staining of tissue biopsies
RNA segment reassortment
Anemias (esp due to renal failure)
Cross link

27. What is thrombopoietin used for?
Thrombocytopenia
not Ab mediated
Celiac
If there is class switching and plasma cell production (that is when memory cells are produced)

28. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Superficial inguinal
Fab portion
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Rheumatic arthritis

29. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
IgG
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
Alternative splicing of mRNA
IgG

30. What is the defect in hyper IgM syndrome? What are the lab results?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Anemias (esp due to renal failure)
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
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

31. What cytokines to Th2 secrete?
Secretory component
Basophils! THey want IG E class switch!
IL 4 - 5 - 10 - 6
...

32. What are the autoantibodies for sjorgens syndrome?
Anti SS- A (anti RO) and Anti SS- B
Cyclosporine - OKT3
T cell activation; no with CD 4 or CD 8
Internal iliac

33. What happens in a deficiency of C3?
Cyclosporine - OKT3
Anemias (esp due to renal failure)
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

34. What are the two signals required for Th1 cells? what happens after then activated?
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!
Histamine; post capillary venules - vasodilation
Internal iliac

35. which B and T cell disorder presents with specifically low IgM?
NK cells
IgG
Wiskott Aldrich syndrome
Cyclosporine - OKT3

36. Which antibody mediates immunity to worms? how?
IgE; by activating eosinophils
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
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

37. What does IL 2 do?
Superior mesenteric
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
Activates cytotoxic CD 8 T cells as second signal
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

38. What are the two signals to kill for NK cells?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Anti smooth muscle
All MHC 1/CD8
TNF alpha and IL1

39. is IgM an opsonizer?
Negative!
Anti viral and anti tumor
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

40. What are the main Cell surface proteins on T cells?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Pernicious Anemia and Hashimotos
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 :(
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

41. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
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
Bind FcG for antibody dependent cellular cytotoxicity

42. 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?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Axillary
Not thymus - BM
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

43. IgG...
Anti glutamate carboxylase and anti insulin
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
opsonizes
Sinusitis - otitis media - pneumonia

44. The alternative pathway is the only constutively...
Thrombocytopenia
active complement pathway
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
IL 4 - 5 - 10 - 6

45. In general What are T cells good for?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Immunoflourescent staining of tissue biopsies
Anti viral and anti tumor
Previous transfusion; pregnant woman whose fetus had paternal antigens

46. What is the common variable immunodeficiency ? How is it different from Brutons?
DM type I
IgM
Alternative splicing of mRNA
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

47. What are the autoantibodies for systemic sclerosis?
Anti topoisomerase
A j chain
active complement pathway
MHC I - CD16 - CD56

48. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
B - T - and NK cells
Th cells fail to produce interferon gamma; a lot of IgE
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
except hyperacute

49. What is passive immunity?
Steroid responsive nephrotic syndrome
IgE
Receiving preformed Antibodies
Antibody mediated cytotoxicity; either complement dependent or complement independent

50. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
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
IgM and IgA
pathogenesis
IgE