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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. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
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
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Superior mesenteric
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

2. where are complements produced?
Previous transfusion; pregnant woman whose fetus had paternal antigens
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Liver! (they are proteins circulating in the blood)
Antidesmoglein

3. What is the presentation of common variable immunodef? and What are the labs?
CD56
Can be acquired in 20s -30s; increased risk of autoimmune disease - lymphoma - Sp infections; normal number of B cells and no plasma cells and immunoglobulin
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
...

4. The alternative pathway is the only constutively...
Superficial inguinal
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
active complement pathway
Inferior mesenteric

5. Which are the only two antiinflammatory cytokines?
Fc
CRP - C3b - IgM
TGF beta and IL 10
Paracortex

6. where do somatic hypermutation and class switching occur?
Chronic granulomatous disease
In the germinal center of secondary follicles (In the paler center)
Pernicious Anemia and Hashimotos
CRP - C3b - IgM

7. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
TNF alpha and IL1
Alternative splicing of mRNA
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

8. what cell surface marker is used for NK cells as it is unique to them?
Anti IF
CD56
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Basophils! THey want IG E class switch!

9. What are some catalase positive organisms?
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
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
S. aureus - E. Coli - aspergillus
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

10. What are the function of B cells?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Cross link
Steroid responsive nephrotic syndrome

11. What is the most common selective Ig deficiency? What is the presentation?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
cannot cross placenta
Acts as second signal on B cells to induce class switching to IgE and IgG
B - T - and NK cells

12. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
Histamine; post capillary venules - vasodilation
A chemotactic factor for neutrophils
Daclizumab; prevent ACUTE rejection of renal transplant
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

13. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Anti glutamate carboxylase and anti insulin
All MHC 1/CD8
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

14. What is filgrastim and sargramostim? and What is it used for?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Antimicrosomal and antithyroglobulin

15. What does IL 10 do? who is secreted by?
Acts as second signal on B cells to induce class switching to IgE and IgG
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
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

16. where do NK cells develop?
Not thymus - BM
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
CRP - C3b - IgM
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

17. What are the autoantibodies for polymyositis and dermatomyositis?
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
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Anti Jo -1
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

18. IgG...
opsonizes
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

19. Which diseases are associated with DR5?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Pernicious Anemia and Hashimotos
Popliteal

20. which of the hypersensitivity reactions is not Ab mediated?
No because no peptide fragment!
Anti TSh receptor
2 heavy chains and two light chains
Type IV

21. Describe the Mannose Lectin pathway
Anti Jo -1
TNF alpha and IL1
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
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

22. give an example of how influenza does a major antigenic shift.
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
RNA segment reassortment
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Liver! (they are proteins circulating in the blood)

23. What is the marginal zone of the spleen? what happens there?
Antibody mediated cytotoxicity; either complement dependent or complement independent
B - T - and NK cells
lowest concentration
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

24. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
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
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
cannot cross placenta
CD56

25. Leukocyte adhesion defect presents with...
neutrophilia!
opsonizes
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
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

26. The Fc region is found on the...
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
carboxy terminal
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
not Ab mediated

27. The secondary follicles have __________; primary follicles are dense
pale central germinal centers
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
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
Popliteal

28. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Liver! (they are proteins circulating in the blood)
neutrophilia!
Bind FcG for antibody dependent cellular cytotoxicity
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

29. 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
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
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
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

30. What is the general structure of an Ab?
Liver! (they are proteins circulating in the blood)
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
2 heavy chains and two light chains
Th cells fail to produce interferon gamma; a lot of IgE

31. which cells have more complete tolerance - B or T cells?
T
Anti smooth muscle
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

32. What are the autoantibodies for type I diabetes mellitus?
Anti glutamate carboxylase and anti insulin
secondary
Hereditary angioedema; PNH
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

33. What are the major functions of Antibodies?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
S. aureus - E. Coli - aspergillus
Its main effect is a defect in Ab opsonization for killing
type four

34. What does IL 4 do?
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
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Rheumatic arthritis
Acts as second signal on B cells to induce class switching to IgE and IgG

35. To what disease do the autoantibodies to IgG (rheumatoid factor)?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Sinusitis - otitis media - pneumonia
pentamer
Rheumatic arthritis

36. What cytokines to Th2 secrete?
IL 4 - 5 - 10 - 6
MHC I - CD16 - CD56
T cell activation; no with CD 4 or CD 8
No because no peptide fragment!

37. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
except hyperacute
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Th2; Th1
Increases expression of MHC I and MHC II and also activates NK cells

38. Complements are...
Paracortex; viral infection
acute phase reactants
Bind FcG for antibody dependent cellular cytotoxicity
Superior mesenteric

39. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Alternative splicing of mRNA
IgA
SP infections
Interferon gamma and IL 2

40. What is the pathology seen in chronic transplant rejection?
Th2; Th1
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Remove encapsulated bacateria
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

41. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
The igA found in breast milk
Hereditary angioedema; PNH
Popliteal
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

42. For which toxins are preformed antibodies (passive) given?
Activate macrophages
Tetanus - Botulinum - HBV - Rabies
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
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

43. What is the toxicity of muromonab?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Steroid responsive nephrotic syndrome
IL 4 - 5 - 10 - 6
not Ab mediated

44. What is the receptor for EBV? On what cells is that located?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Lymphocytes
Recom IL 11; thrombocytopenia
CD21 on B cells (although there is T cell lymphocytosis in EBV)

45. What is recomb gamma interferon used for?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Sinusitis - otitis media - pneumonia
Chronic granulomatous disease
neutrophilia!

46. What lymph node drains the upper limb?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Axillary
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Anti Jo -1

47. How is the antigen loaded onto a MHC II?
type four
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
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
isotype

48. What is the cause of thymic aplasia? What is its presentation? What are the labs?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
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
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

49. What does interferon gamma do? What two type of cells does it attack mostly?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
A j chain

50. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
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
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
IgA
IgG