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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 characterizes an arthus reaction?
Edema and necrosis in that region
IgM
Lymphocytes
Anti alpha subunit 3 of collagen on type IV bm

2. What does IL 4 do?
Acts as second signal on B cells to induce class switching to IgE and IgG
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
Para aortic

3. How does igA cross the epithelium?
By transcytosis
active complement pathway
pentamer
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

4. What is the clinical use for azathioprine?
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
Macrophages - Dendritic cells - B cells
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
...

5. What are the autoantibodies for other vasculitides?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Antidote for digoxin intoxication

6. which B and T cell disorder presents with specifically low IgM?
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
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
IgM and IgG
Wiskott Aldrich syndrome

7. How does complement link innate and adaptive?
Negative!
IgE; by activating eosinophils
In the germinal center of secondary follicles (In the paler center)
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

8. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Rheumatic arthritis
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Superficial inguinal
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

9. In thymic development - What is the positive selection? negative selections?
Not thymus - BM
IgG
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
When you select for which MHC it will have; take out the lymphs that self react

10. What is the late phase reaction of anaphylaxis allergy? what mediates it?
RNA segment reassortment
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)
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Humoral

11. What is an example of a parasite showing antigenic variation?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
IgM and IgG
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

12. To what disease do the autoantibodies to IgG (rheumatoid factor)?
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
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Rheumatic arthritis

13. What is Aldesleukin? What is it used for
pale central germinal centers
A recomb cytokine of IL 2; RCC and metastatic melanoma
Cyclosporine - OKT3
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)

14. what happens in a deficiency of C1 esterase inhibitor? DAF?
The igA found in breast milk
...
Hereditary angioedema; PNH
isotype

15. What are the autoantibodies for polymyositis and dermatomyositis?
A chemotactic factor for neutrophils
Anti Jo -1
IgG
Antihistone

16. What is the toxicity of azathioprine?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
...
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

17. describe the pathogenesis of delayed type IV hypersensitivity
MHC I - CD16 - CD56
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
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 cells react to the angtigen and activate leukocyted (macrophage acitivation)

18. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Delayed type hypersensitivity
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
A recomb cytokine of IL 2; RCC and metastatic melanoma

19. What lymph node drains the rectum (above the pectinate line)?
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
Internal iliac
Wiskott Aldrich syndrome
Negative!

20. which interleukin receptor is required for NK development? activation?
IL 3; supports growth and differentiation of bone marrow stem cells
IL 15; IL 12 - interferon Beta and interferon alpha
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Superficial inguinal

21. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
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
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

22. What is the main function of interferons?
T cell dysfunction
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
All MHC 1/CD8
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

23. What cytokines to Th2 secrete?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
The igA found in breast milk
MHC class molecules bind to KIRS or CD94 to prevent killing
IL 4 - 5 - 10 - 6

24. What is the pathogenesis of a hypersensitivity reaction?
First a B cell gets sensitized to an allergen - after sensitization - it gets induce by Th2 secreting IL4 to class switch from IgM to IgE - next time blood stream is exposed to allergen these antigens cross like IgEs on mast cells and result in chemi
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
MS
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

25. What is the main cytokine that activates eosinophils?
IL 5
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
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
IgE; by activating eosinophils

26. Which diseases are associated with DR2?
T
Kill them because they have CD16 on them that recognize the FcG portion
MS - hay fever - SLE - goodpastures
MHC class molecules bind to KIRS or CD94 to prevent killing

27. Give an example of someone who could get hyperacute transplant rejection.
Previous transfusion; pregnant woman whose fetus had paternal antigens
Antidote for digoxin intoxication
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
DM type I

28. can igG cross the placenta?
Yes
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

29. what bacteria are a splenectomy patient most susceptible to? why?
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
MHC I - CD16 - CD56
Not thymus - BM
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

30. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
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
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
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

31. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Superficial inguinal
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

32. What are C1 - C2 - C3 - C4 important for?
Viral neutralization of igM and IgG!
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
MHC I; from RER with help of the B2 microglobulin

33. What is colostrum?
Humoral
Antihistone
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
The igA found in breast milk

34. What does granulysin do?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Cells that stil have weird parts of their membrane that macrophages usually bite off
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
MS

35. How does the alternative pathway lead to MAC activation?
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
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
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Local infection/inflammation; infection of the ln itself; metastasis

36. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Local infection/inflammation; infection of the ln itself; metastasis
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Antimicrosomal and antithyroglobulin
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

37. What are the autoantibodies for Celiac disease?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Barrel hoop basement membrane fenestrations
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

38. is IgM an opsonizer?
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
Negative!
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

39. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Alternative splicing of mRNA
Secretory component
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
The patient could become cyanotic in the OR!

40. 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
Popliteal
IL 4
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

41. Describe the complement independent Type II hypersenstivity reaction. Give an example.
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Anti SS- A (anti RO) and Anti SS- B
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

42. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
In the germinal center of secondary follicles (In the paler center)

43. What is the autoantibody for SLE that is nonspecific? Specific?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Macrophages - Dendritic cells - B cells
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

44. For which toxins are preformed antibodies (passive) given?
Tetanus - Botulinum - HBV - Rabies
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Yes
Fc

45. Which is the main antibody that provides passive immunity to infants?
IgG
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
No because no peptide fragment!
Glycoproteins; HLA

46. What is thrombopoietin used for?
Wiskott Aldrich syndrome
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Thrombocytopenia
Basophils! THey want IG E class switch!

47. What are the autoantibodies for autoimmune hepatitis?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Anti smooth muscle
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Superficial inguinal

48. What is digoxin immune Fab used for?
Fab portion
Severe pyogenic infections early in life
Antidote for digoxin intoxication
Axillary

49. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Sinusitis - otitis media - pneumonia
Thrombocytopenia
except hyperacute
Edema and necrosis in that region

50. other than mediating shock - what else does TNF alpha do? who releases it mainly?
encapsulated
Macrophages - Dendritic cells - B cells
Activates Th1 helper cells; Macrophages
Receiving preformed Antibodies