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. So antibodies are the effectors for the humoral response. List some of their functions.
IgM and IgA
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
DM type I and RA
Fc

2. What are the autoantibodies for goodpastures syndrome?
neutrophilia!
SP infections
Anti alpha subunit 3 of collagen on type IV bm
Superior mesenteric

3. What is the toxicity of azathioprine?
C5a
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
A j chain
...

4. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

5. What are the main symptoms of T cell immunodeficiencies?
Anti alpha subunit 3 of collagen on type IV bm
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
MHC II - B7
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

6. What is the presentation of hyperIgM syndrome?
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
IgE
Superficial inguinal
Severe pyogenic infections early in life

7. other than eat and bite RBCs what else do Macrophages of spleen do>
Remove encapsulated bacateria
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
T
Active; passive - fast but short half life (3 weeks!)

8. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
IL 4 - 5 - 10 - 6
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
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
Anti viral and anti tumor

9. What is chronic mucocutaneous candidiasis d/t?
Negative nitroblue tetrazolium reduction test
Celiac
Cross link
T cell dysfunction

10. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
IgG
Immunosuppression after kidney transplantation
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
pathogenesis

11. What does IL 2 do?
A j chain
Activates cytotoxic CD 8 T cells as second signal
Yes
Basophils! THey want IG E class switch!

12. Which is the main antibody that provides passive immunity to infants?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
IgG
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
IgAs in mothers breast milk!

13. 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
Local infection/inflammation; infection of the ln itself; metastasis
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
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

14. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Pernicious Anemia and Hashimotos
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Previous transfusion; pregnant woman whose fetus had paternal antigens
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

15. What are the major functions of Antibodies?
Macrophages - Dendritic cells - B cells
lowest concentration
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

16. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
Complement activation (active in both)
Active; passive - fast but short half life (3 weeks!)
Sinusitis - otitis media - pneumonia
TNF alpha and IL1

17. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Type IV
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
MS
IgG

18. Leukocyte adhesion defect presents with...
neutrophilia!
Anti topoisomerase
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
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

19. Which antibodies can be multimeric?
Active; passive - fast but short half life (3 weeks!)
IgM and IgA
cannot cross placenta
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

20. What is the main function of interferons?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Kill them because they have CD16 on them that recognize the FcG portion
False! B cell class switching requires a second signal

21. What lymph node drains the breast?
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
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
Axillary
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

22. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
RNA segment reassortment
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
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
Negative nitroblue tetrazolium reduction test

23. Type IV hypersensitivity is i...
Active; passive - fast but short half life (3 weeks!)
cannot cross placenta
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
not Ab mediated

24. What are the autoantibodies for pernicious anemia?
Anti IF
B - T - and NK cells
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Liver! (they are proteins circulating in the blood)

25. What are the autoantibodies for graves?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Anti TSh receptor

26. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
IgM and IgA
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
CRP - C3b - IgM

27. What are MHC's necessary for? By themselves?
B - T - and NK cells
T cell activation; no with CD 4 or CD 8
Negative!
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

28. What are the three types of APCs?
A recomb cytokine of IL 2; RCC and metastatic melanoma
...
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Macrophages - Dendritic cells - B cells

29. What is the general structure of an Ab?
2 heavy chains and two light chains
T cell activation; no with CD 4 or CD 8
Immunoflourescent staining of tissue biopsies
MS

30. What type of fenestrations are found in the red pulp of the spleen?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
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
Barrel hoop basement membrane fenestrations

31. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Internal iliac
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
acute phase reactants
Its main effect is a defect in Ab opsonization for killing

32. Which helper T cells' development is induced by IL 4? IL 12?
Anti alpha subunit 3 of collagen on type IV bm
Th2; Th1
Severe pyogenic infections early in life
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

33. What is the receptor for EBV? On what cells is that located?
Lymphocytes
CD56
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
CD21 on B cells (although there is T cell lymphocytosis in EBV)

34. what prevents NK cells from killing normal cells if their default is to kill?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
MHC class molecules bind to KIRS or CD94 to prevent killing
Antidote for digoxin intoxication
Anti Ach receptor

35. ________ regulate the cell mediated response.
Antibody mediated cytotoxicity; either complement dependent or complement independent
CD21 on B cells (although there is T cell lymphocytosis in EBV)
...
Humoral

36. What is passive immunity?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
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
Receiving preformed Antibodies
Axillary

37. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Para aortic
Graves
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

38. What is the toxicity of muromonab?
Anti viral and anti tumor
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Fc

39. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Negative selection
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
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 :(
neutrophilia!

40. What are the two signals required for Th1 cells? what happens after then activated?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Cyclosporine - OKT3
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
B - T - and NK cells

41. What is the presentation of Brutons agammaglobulinemia?
except hyperacute
Edema and necrosis in that region
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

42. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Paracortex; viral infection
Histamine; post capillary venules - vasodilation
IgG

43. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Paracortex; viral infection
Negative nitroblue tetrazolium reduction test
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

44. In general What are T cells good for?
The patient could become cyanotic in the OR!
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Anti viral and anti tumor

45. What do multimeric antibodies require for assembly?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
A j chain
IgG
Anti alpha subunit 3 of collagen on type IV bm

46. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
delayed!
CRP - C3b - IgM
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
Glycoproteins; HLA

47. What lymph node drains the sigmoid colon?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Inferior mesenteric

48. What are the autoantibodies for systemic sclerosis?
A recomb cytokine of IL 2; RCC and metastatic melanoma
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
Anti topoisomerase
All MHC 1/CD8

49. Monomer in circulation - ___ when secreted
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
DM type I and RA
dimer
CD56

50. what mediates the type II hypersensitivity? What are the two different methods?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Local infection/inflammation; infection of the ln itself; metastasis
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
Activate macrophages