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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. So antibodies are the effectors for the humoral response. List some of their functions.
TNF alpha and IL1
pathogenesis
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

2. what secretes IL 4?
Fc
Paracortex; viral infection
Cross link
Basophils! THey want IG E class switch!

3. How is i Th1 helper cell inhibited?
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
Cytokine IL 10 secreted by Th2
Anti TSh receptor
carboxy terminal

4. What are the labs in brutons agammaglobulinemia?
Anti topoisomerase
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Immunosuppression after kidney transplantation
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

5. The alternative pathway is the only constutively...
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
active complement pathway
opsonizes
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

6. IgM can exist as a _______ also
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
pentamer
Superficial inguinal

7. How is the antigen loaded onto a MHC II?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Anti glutamate carboxylase and anti insulin
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
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

8. What is the main function of TNF alpha? How does it do this?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
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!
IgM and IgD
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

9. What are the cell surface proteins for Macrophages? which two are for opsonins?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Hereditary angioedema; PNH

10. What is an example of a parasite showing antigenic variation?
MS
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Anti SS- A (anti RO) and Anti SS- B
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

11. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Cells that stil have weird parts of their membrane that macrophages usually bite off
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

12. How do you test for type III hypersensitivity?
Immunoflourescent staining of tissue biopsies
Anti glutamate carboxylase and anti insulin
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
dimer

13. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Alternative splicing of mRNA
Receiving preformed Antibodies
Humoral

14. Which is the most abundant antibody in blood?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Activates cytotoxic CD 8 T cells as second signal
No because no peptide fragment!
IgG

15. What happens when a T helper cell in the paracortical section encounters an antigen? a cytotoxic t cell? a B cell in the cortical section?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
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
cannot cross placenta
When you select for which MHC it will have; take out the lymphs that self react

16. What are the autoantibodies for wegeners granulomatosis?
Axillary
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

17. What are the autoantibodies for drug induced lupus?
Anti glutamate carboxylase and anti insulin
Kill them because they have CD16 on them that recognize the FcG portion
Influenza; antigenic shift; antigenic drift
Antihistone

18. What are the autoantibodies for hashimotos?
MHC II - B7
IgG
Antibody mediated cytotoxicity; either complement dependent or complement independent
Antimicrosomal and antithyroglobulin

19. What is three common causes of severe combined immunodef? What is the result of all three?
Remove encapsulated bacateria
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
If there is class switching and plasma cell production (that is when memory cells are produced)
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

20. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
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
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

21. What is hereditary angioedema? What are the C3 levels?
Superficial inguinal
Axillary
SP infections
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

22. which cytokine inhibits TH2 cells? secreted by who?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
secondary
Interferon gamma; Th1
IgG

23. What are the main symptoms of T cell immunodeficiencies?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Anti U1 RNP (ribonucleoprotein)
not Ab mediated

24. what characterizes an arthus reaction?
Edema and necrosis in that region
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
MS - hay fever - SLE - goodpastures
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

25. What does interferon gamma do to be antiviral?
pale central germinal centers
Increases expression of MHC I and MHC II and also activates NK cells
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Bind FcG for antibody dependent cellular cytotoxicity

26. What is anergy? why does this occur?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Wiskott Aldrich syndrome
Superficial inguinal
IL 1 and IL 6

27. How does complement link innate and adaptive?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
MHC class molecules bind to KIRS or CD94 to prevent killing
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

28. What is the late phase reaction of anaphylaxis allergy? what mediates it?
S. aureus - E. Coli - aspergillus
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)
Glycoproteins; HLA
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

29. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
Barrel hoop basement membrane fenestrations
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
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
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

30. 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
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
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Anemias (esp due to renal failure)

31. What is the presentation of scid? treatment?
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
Anti alpha subunit 3 of collagen on type IV bm
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

32. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
IgE; by activating eosinophils
Anti smooth muscle
Anti SS- A (anti RO) and Anti SS- B
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

33. __________ are a part of the innate system.
pentamer
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
NK cells
A chemotactic factor for neutrophils

34. Which antibodies can be multimeric?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Anti SS- A (anti RO) and Anti SS- B
Basophils! THey want IG E class switch!
IgM and IgA

35. In thymic development - What is the positive selection? negative selections?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
When you select for which MHC it will have; take out the lymphs that self react
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

36. The Fc region is found on the...
carboxy terminal
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
Fab portion
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)

37. What lymph node drains the stomach?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Its a serine protease that activates apoptosis; NK and CD8
Celiac
Negative nitroblue tetrazolium reduction test

38. What are the autoantibodies for autoimmune hepatitis?
Anti topoisomerase
T
Anti smooth muscle
IgAs in mothers breast milk!

39. What lymph node drains the breast?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Axillary
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

40. which antibody activate mast cells - basophils - and eosinophils?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Thrombocytopenia
IgE
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

41. which cells have more complete tolerance - B or T cells?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
IL 4 - 5 - 10 - 6
IgM and IgD
T

42. What are some sinopulmonary infections?
Rheumatic arthritis
Anti TSh receptor
Sinusitis - otitis media - pneumonia
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

43. Only the _______ contribute to the Fc region
Barrel hoop basement membrane fenestrations
heavy chains
lowest concentration
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

44. What is digoxin immune Fab used for?
T cell precursor
Negative!
Antidote for digoxin intoxication
Macrophages - Dendritic cells - B cells

45. What is the pathology in hyperacute transplant rejection?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
If there is class switching and plasma cell production (that is when memory cells are produced)
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Fab portion

46. What is the pathology seen in chronic transplant rejection?
DM type I
Fc
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
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

47. Which is the main antibody in the delayed or secondary response to an antigen?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
IgG
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

48. What is the main function of interferons?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Stimulate the liver to release acute phase reactants
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Anti viral and anti tumor

49. What is the mode of inheritance of Chediak Higashi syndrome? What is the disease d/t? What does it result in? What is the presentation?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Para aortic
When you select for which MHC it will have; take out the lymphs that self react

50. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
carboxy terminal
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1