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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.
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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. What lymph node drains the testes?
Th cells fail to produce interferon gamma; a lot of IgE
Para aortic
pale central germinal centers
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

2. 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)
Hemochromatosis
Anemias (esp due to renal failure)
Influenza; antigenic shift; antigenic drift

3. Which disease is associated withB B27?
active complement pathway
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

4. What does Interferon alpha and beta do? how?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
acute phase reactants
MHC I; from RER with help of the B2 microglobulin

5. What is the main cytokine released by T cells? What does it do
IL 3; supports growth and differentiation of bone marrow stem cells
IL 5
MHC I - CD16 - CD56
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

6. What is anergy? why does this occur?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
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
Antimicrosomal and antithyroglobulin

7. What is the main function of interferons?
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
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Daclizumab; prevent ACUTE rejection of renal transplant
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

8. What is chronic mucocutaneous candidiasis d/t?
Superficial inguinal
T cell dysfunction
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
pentamer

9. other than C3a - what other complement acts as an anaphyloxin?
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
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Anti topoisomerase
C5a

10. What cytokines to Th2 secrete?
IL 4 - 5 - 10 - 6
Anti Jo -1
False! B cell class switching requires a second signal
MHC II - B7

11. What is the receptor for EBV? On what cells is that located?
T
IgM and IgG
...
CD21 on B cells (although there is T cell lymphocytosis in EBV)

12. Only the _______ contribute to the Fc region
Severe pyogenic infections early in life
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
heavy chains

13. what bacteria are a splenectomy patient most susceptible to? why?
IgG
pale central germinal centers
S. aureus - E. Coli - aspergillus
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

14. What is the late phase reaction of anaphylaxis allergy? what mediates it?
Antidesmoglein
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)
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Histamine; post capillary venules - vasodilation

15. What is the main function of IL 8?
isotype
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
neutrophilia!
A chemotactic factor for neutrophils

16. How does the alternative pathway lead to MAC activation?
Hemochromatosis
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
TGF beta and IL 10
carboxy terminal

17. where do NK cells develop?
CRP - C3b - IgM
...
Not thymus - BM
lowest concentration

18. Type IV hypersensitivity is i...
Anti glutamate carboxylase and anti insulin
not Ab mediated
Active; passive - fast but short half life (3 weeks!)
If there is class switching and plasma cell production (that is when memory cells are produced)

19. To what portion of the Antibody do the complements bind?
Activates cytotoxic CD 8 T cells as second signal
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
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
Fc

20. What links the adaptive and innate immunity?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
IgM and IgG
Complement activation (active in both)
T cell activation; no with CD 4 or CD 8

21. How do you test for chronic granulomatous disease?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Daclizumab; prevent ACUTE rejection of renal transplant
Popliteal
Negative nitroblue tetrazolium reduction test

22. Which diseases are associated with DR5?
Anti smooth muscle
Pernicious Anemia and Hashimotos
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Basophils! THey want IG E class switch!

23. Which type of selection of thymic development provides central tolerance?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Kill them because they have CD16 on them that recognize the FcG portion
Negative selection
Activates Th1 helper cells; Macrophages

24. What is the common variable immunodeficiency ? How is it different from Brutons?
TNF alpha and IL1
Interferon gamma; Th1
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
Edema and necrosis in that region

25. What lymph node drains the anal canal (below the pectinate line)?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Antimicrosomal and antithyroglobulin
pale central germinal centers
Superficial inguinal

26. What is a factor that is a predictor for a bad transplantation?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

27. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
pathogenesis
Rheumatic arthritis
CD21 on B cells (although there is T cell lymphocytosis in EBV)

28. what cell surface marker is used for NK cells as it is unique to them?
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
CD56
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Immunosuppression after kidney transplantation

29. What are some catalase positive organisms?
Superior mesenteric
heavy chains
S. aureus - E. Coli - aspergillus
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

30. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Fc
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
Paracortex; viral infection
Acts as second signal on B cells to induce class switching to IgE and IgG

31. What is the clinical use of Muromonab?
RNA segment reassortment
A j chain
Immunosuppression after kidney transplantation
Not thymus - BM

32. What are the autoantibodies for systemic sclerosis?
pathogenesis
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
...
Anti topoisomerase

33. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Anti Jo -1
T cell precursor
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
...

34. What cytokines are released by Th1 cells?
Interferon gamma and IL 2
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
Stimulate the liver to release acute phase reactants
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

35. What kinds of receptors activate innate immunity?
Pernicious Anemia and Hashimotos
TLR ad nuclear receptors
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

36. What are the three types of lymphocytes?
Immunosuppression after kidney transplantation
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Remove encapsulated bacateria
B - T - and NK cells

37. What is filgrastim and sargramostim? and What is it used for?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
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
DM type I
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

38. What are the main symptoms of T cell immunodeficiencies?
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
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Axillary
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

39. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
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
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
pale central germinal centers
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

40. What is the cause of thymic aplasia? What is its presentation? What are the labs?
Remove encapsulated bacateria
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
except hyperacute
Paracortex

41. which antibodies can bind complement?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
pentamer
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
IgM and IgG

42. What can cause a lymph node enlargement?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Local infection/inflammation; infection of the ln itself; metastasis
...
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

43. Which is the main antibody in the delayed or secondary response to an antigen?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
IgG

44. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
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
...
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

45. A lymph node is a ________ lymphoid organ.
...
Antibody mediated cytotoxicity; either complement dependent or complement independent
secondary
active complement pathway

46. What are the main symptoms of B cell immunodeficiencies?
Anti SS- A (anti RO) and Anti SS- B
SP infections
Superior mesenteric
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

47. How is sirolimus different from tacrolimus?
A j chain
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Popliteal

48. Describe the Mannose Lectin pathway
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
except hyperacute
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
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

49. Which diseases are associated with DR4?
DM type I and RA
...
Anti viral and anti tumor
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

50. what mediates the type II hypersensitivity? What are the two different methods?
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
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Antibody mediated cytotoxicity; either complement dependent or complement independent
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction