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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. Which is the main antibody that provides passive immunity to infants?
Severe pyogenic infections early in life
Receiving preformed Antibodies
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
IgG

2. Give three examples of bacteria that use antigenic variation and how.
Internal iliac
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
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Type IV

3. What is filgrastim and sargramostim? and What is it used for?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
C5a
Anti topoisomerase

4. What is the most common example of passive immunity?
Hereditary angioedema; PNH
IL 1 and IL 6
CD56
IgAs in mothers breast milk!

5. A lymph node is a ________ lymphoid organ.
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Antimicrosomal and antithyroglobulin
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
secondary

6. To what portion of the Antibody do the complements bind?
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
Fc
IL 1 and IL 6
neutrophilia!

7. The two heavy chains of an antibody contribute to the...
Fab portion
delayed!
T cell dysfunction
Macrophages - Dendritic cells - B cells

8. can igG cross the placenta?
Yes
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
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

9. What is the late phase reaction of anaphylaxis allergy? what mediates it?
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
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)
Daclizumab; prevent ACUTE rejection of renal transplant
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

10. Which are the only two antiinflammatory cytokines?
T cell dysfunction
TGF beta and IL 10
except hyperacute
IL 1 and IL 6

11. What is chronic mucocutaneous candidiasis d/t?
Chronic granulomatous disease
T cell dysfunction
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
CD21 on B cells (although there is T cell lymphocytosis in EBV)

12. For which toxins are preformed antibodies (passive) given?
TLR ad nuclear receptors
Tetanus - Botulinum - HBV - Rabies
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

13. What is the general structure of an Ab?
Remove encapsulated bacateria
When you select for which MHC it will have; take out the lymphs that self react
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
2 heavy chains and two light chains

14. Which MHC presents intracellular peptides? how so?
Anti IF
carboxy terminal
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
MHC I; from RER with help of the B2 microglobulin

15. describe the classic complement pathway.
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Superficial inguinal
Influenza; antigenic shift; antigenic drift
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

16. From where do cytokines come from?
Th cells fail to produce interferon gamma; a lot of IgE
IgE; by activating eosinophils
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Lymphocytes

17. What are the autoantibodies for polymyositis and dermatomyositis?
Anti Jo -1
secondary
Activate macrophages
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

18. What do mature naive B lymphocytes express?
Negative!
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
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
IgM and IgD

19. What are the autoantibodies for autoimmune hepatitis?
Paracortex; viral infection
Recom IL 11; thrombocytopenia
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
Anti smooth muscle

20. What lymph node drains the lateral side of the dorsum of the foot?
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
Superficial inguinal
By transcytosis
Popliteal

21. which immunodeficiency presents with delayed separation of the umbilicus? ataxia? telangiectasia?albinism? anaphylaxis on exposure to blood products with IgA? tetany?retained primary teeth? peripheral neuropathy?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

22. 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
secondary
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
lowest concentration

23. What does IL 2 do?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Activates cytotoxic CD 8 T cells as second signal
Kill them because they have CD16 on them that recognize the FcG portion
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

24. What are the symptoms of serum sickness?
Negative!
Celiac
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
By transcytosis

25. How is the thymus organized? what happens in each section?
Superior mesenteric
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
opsonizes
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

26. What are the two signals required for Th1 cells? what happens after then activated?
Carbohydrate
Antidote for digoxin intoxication
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
The igA found in breast milk

27. What does granzyme do? who secretes it?
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
Lymphocytes
Its a serine protease that activates apoptosis; NK and CD8
IgE; by activating eosinophils

28. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
...
Activate macrophages
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

29. which of the transplant rejections is antibody mediated? why does it occur?
IL 15; IL 12 - interferon Beta and interferon alpha
Internal iliac
Daclizumab; prevent ACUTE rejection of renal transplant
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

30. What lymph node drains the thigh?
Its a serine protease that activates apoptosis; NK and CD8
Superficial inguinal
IgM and IgA
Negative selection

31. What is the white pulp of the spleen?
Edema and necrosis in that region
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Interferon gamma; Th1
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

32. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
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
Thrombocytopenia
MS

33. How is i Th1 helper cell inhibited?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Cytokine IL 10 secreted by Th2
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Sinusitis - otitis media - pneumonia

34. __________ are a part of the innate system.
NK cells
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Basophils! THey want IG E class switch!

35. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
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
Anti alpha subunit 3 of collagen on type IV bm
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

36. which antibody activate mast cells - basophils - and eosinophils?
B - T - and NK cells
Steroid responsive nephrotic syndrome
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
IgE

37. Which disease is associated with HLA A3?
Hemochromatosis
IgM
Viral neutralization of igM and IgG!
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

38. What type of side chains are found on Fc region of an antibody?
Carbohydrate
Activates cytotoxic CD 8 T cells as second signal
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
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

39. What is the autoantibody for SLE that is nonspecific? Specific?
Paracortex; viral infection
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

40. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Daclizumab; prevent ACUTE rejection of renal transplant
Delayed type hypersensitivity
Negative selection
T cell dysfunction

41. Leukocyte adhesion defect presents with...
neutrophilia!
IgG
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Remove encapsulated bacateria

42. What are the two signals required for B cell class switching? Which is the second signal?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Its main effect is a defect in Ab opsonization for killing
Celiac

43. IgE has the ___________ in the serum
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
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
lowest concentration
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

44. What is serum sickness? give an example.
Cyclosporine - OKT3
Acts as second signal on B cells to induce class switching to IgE and IgG
cannot cross placenta
Type III hypersensitivity where an exogenous antigen results in a systemic antigen antibody complex disease (takes around 5 days after exposure for the Abs to develop); immune complexes then fix in tissue and activate complement resulting in tissue d

45. What is passive immunity?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Receiving preformed Antibodies
A j chain
All MHC 1/CD8

46. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
delayed!
Glycoproteins; HLA
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
Daclizumab; prevent ACUTE rejection of renal transplant

47. How does complement link innate and adaptive?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
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
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

48. what secretes IL 4?
Increases expression of MHC I and MHC II and also activates NK cells
Axillary
Anti TSh receptor
Basophils! THey want IG E class switch!

49. What is the common variable immunodeficiency ? How is it different from Brutons?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
TLR ad nuclear receptors

50. Which type of selection of thymic development provides central tolerance?
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
heavy chains
Steroid responsive nephrotic syndrome
Negative selection