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. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
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
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Negative!

2. What does granzyme do? who secretes it?
Activates Th1 helper cells; Macrophages
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
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
Its a serine protease that activates apoptosis; NK and CD8

3. Describe complement dependent Type II hypersensitivity. Give an example.
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
isotype
Th cells fail to produce interferon gamma; a lot of IgE
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

4. What are the autoantibodies for drug induced lupus?
Chronic granulomatous disease
Antihistone
Anti smooth muscle
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

5. What are the autoantibodies for type I diabetes mellitus?
Tetanus - Botulinum - HBV - Rabies
Macrophages - Dendritic cells - B cells
Anti glutamate carboxylase and anti insulin
IgG

6. Monomer in circulation - ___ when secreted
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
Inferior mesenteric
dimer
...

7. What is the white pulp of the spleen?
TLR ad nuclear receptors
Alternative splicing of mRNA
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
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

8. which cytokine inhibits TH2 cells? secreted by who?
Inferior mesenteric
Anti SS- A (anti RO) and Anti SS- B
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
Interferon gamma; Th1

9. What is the pathology of acute transplant rejection? is it reversible?
Interferon gamma and IL 2
IgG
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
IL 4

10. In thymic development - What is the positive selection? negative selections?
When you select for which MHC it will have; take out the lymphs that self react
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Carbohydrate
...

11. What is Aldesleukin? What is it used for
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
acute phase reactants
A recomb cytokine of IL 2; RCC and metastatic melanoma

12. Give an example of someone who could get hyperacute transplant rejection.
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Chronic granulomatous disease
Previous transfusion; pregnant woman whose fetus had paternal antigens
Fc

13. What does it mean if there are igM in the serum at birth?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Local infection/inflammation; infection of the ln itself; metastasis
...
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

14. What is passive immunity?
Popliteal
Receiving preformed Antibodies
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)
pale central germinal centers

15. What is the presentation of hyperIgM syndrome?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Anti IF
CRP - C3b - IgM
Severe pyogenic infections early in life

16. which type of immunity is slow but long lasting? as opposed to...
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Anemias (esp due to renal failure)
Active; passive - fast but short half life (3 weeks!)

17. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
Its a serine protease that activates apoptosis; NK and CD8
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
TNF alpha and IL1
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

18. What is a factor that is a predictor for a bad transplantation?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
type four
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

19. What is the common variable immunodeficiency ? How is it different from Brutons?
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
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
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
TGF beta and IL 10

20. What are the two signals required for Th1 cells? what happens after then activated?
Hereditary angioedema; PNH
lowest concentration
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
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

21. Which is the most abundant antibody in blood?
IgG
Chronic granulomatous disease
Axillary
TGF beta and IL 10

22. Describe the complement independent Type II hypersenstivity reaction. Give an example.
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Inferior mesenteric
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Tetanus - Botulinum - HBV - Rabies

23. What are the T cell functions?
...
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
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

24. What does IgA pick up from epithelial cells before being secreted?
mesenchymal
Secretory component
neutrophilia!
...

25. which interleukin receptor is required for NK development? activation?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
IL 15; IL 12 - interferon Beta and interferon alpha
IgM and IgD
Inferior mesenteric

26. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Internal iliac
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
Type IV

27. What are the mediators that mast cells release?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Carbohydrate
Active; passive - fast but short half life (3 weeks!)
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

28. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Acts as second signal on B cells to induce class switching to IgE and IgG
IgE; by activating eosinophils
Delayed type hypersensitivity
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

29. What are the labs in brutons agammaglobulinemia?
type four
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Stimulate the liver to release acute phase reactants
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

30. Name the three opsonins
MS - hay fever - SLE - goodpastures
CRP - C3b - IgM
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)
Activate macrophages

31. What are the autoantibodies for hashimotos?
Immunoflourescent staining of tissue biopsies
Antimicrosomal and antithyroglobulin
S. aureus - E. Coli - aspergillus
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

32. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Internal iliac
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
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

33. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Activate macrophages
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Activates Th1 helper cells; Macrophages
not Ab mediated

34. Describe the Mannose Lectin pathway
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
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
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

35. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Anemias (esp due to renal failure)
Its main effect is a defect in Ab opsonization for killing
Activates Th1 helper cells; Macrophages

36. __________ are a part of the innate system.
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
B - T - and NK cells
NK cells
Anti Jo -1

37. What are the autoantibodies for pernicious anemia?
When you select for which MHC it will have; take out the lymphs that self react
Barrel hoop basement membrane fenestrations
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Anti IF

38. What are the function of B cells?
Severe pyogenic infections early in life
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

39. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
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
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

40. can igG cross the placenta?
TGF beta and IL 10
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Yes
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

41. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of 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
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
dimer
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

42. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
False! B cell class switching requires a second signal
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Paracortex; viral infection
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

43. What is epo used for?
Anemias (esp due to renal failure)
No! That is why they are different from T cells - they can recognize antigens in free solution; if a bug has a peptide fragment that a mature naive B cell recognizes it will bind to it and cause activation - it then gets activated into a plasma cell!
pale central germinal centers
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

44. What is the clinical use for sirolimus? what should you combine it with?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
encapsulated
Antihistone
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

45. How does igA cross the epithelium?
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
Receiving preformed Antibodies
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
By transcytosis

46. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Type IV
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
T cell precursor
Daclizumab; prevent ACUTE rejection of renal transplant

47. What are some catalase positive organisms?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
IgM and IgG
S. aureus - E. Coli - aspergillus
NK cells

48. Which antibody mediates immunity to worms? how?
Chronic granulomatous disease
In the germinal center of secondary follicles (In the paler center)
IgE; by activating eosinophils
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

49. What are the cell surface proteins on NK cells?
MHC I - CD16 - CD56
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
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Inferior mesenteric

50. What lymph node drains the thigh?
Superficial inguinal
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
Hemochromatosis
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells