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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. What are the mediators that mast cells release?
Receiving preformed Antibodies
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

2. What are the main symptoms of T cell immunodeficiencies?
DM type I
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

3. What are the function of B cells?
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
Digeorge syndrome - 22q11 deletion resulting in failure to develop 3rd and 4th pharyngeal pouches; cardiac and great vessel congenital defects - tetany from hypocalcemia - recurrent viral/fungal infections from T cell deficiency; hypoPTH - hypoCa - a
Interferon gamma and IL 2
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

4. The idiotype; the Fc portion determines the...
isotype
Graves
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
IgM and IgA

5. How fast does it occur?
Axillary
Celiac
T cell precursor
The patient could become cyanotic in the OR!

6. What are the three types of APCs?
IgM and IgG
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Macrophages - Dendritic cells - B cells

7. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
MS
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Recom IL 11; thrombocytopenia
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

8. From where do cytokines come from?
Its a serine protease that activates apoptosis; NK and CD8
Lymphocytes
cannot cross placenta
Negative nitroblue tetrazolium reduction test

9. What are the labs in brutons agammaglobulinemia?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Th cells fail to produce interferon gamma; a lot of IgE
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Severe pyogenic infections early in life

10. other than eat and bite RBCs what else do Macrophages of spleen do>
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
Anti mitochondrial
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
Remove encapsulated bacateria

11. What are some sinopulmonary infections?
Sinusitis - otitis media - pneumonia
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Activates cytotoxic CD 8 T cells as second signal
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

12. The two heavy chains of an antibody contribute to the...
Fab portion
heavy chains
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
IL 4 - 5 - 10 - 6

13. Which are the only two antiinflammatory cytokines?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
pathogenesis
TGF beta and IL 10
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

14. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Superior mesenteric
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Influenza; antigenic shift; antigenic drift

15. What lymph node drains the sigmoid colon?
Inferior mesenteric
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
IgM and IgA
MS - hay fever - SLE - goodpastures

16. is IgM an opsonizer?
opsonizes
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Negative!
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

17. What are the autoantibodies for Celiac disease?
Superficial inguinal
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

18. What is the defect in hyper IgM syndrome? What are the lab results?
Pernicious Anemia and Hashimotos
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
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

19. Which antibody mediates immunity to worms? how?
Superior mesenteric
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
TLR ad nuclear receptors
IgE; by activating eosinophils

20. What does interferon gamma do? What two type of cells does it attack mostly?
Glycoproteins; HLA
Sinusitis - otitis media - pneumonia
...
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

21. Only the _______ contribute to the Fc region
heavy chains
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
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!
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

22. The MALT/GALT are not...
encapsulated
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
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
RNA segment reassortment

23. __________ are a part of the innate system.
NK cells
type four
Superficial inguinal
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

24. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
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!
Bind FcG for antibody dependent cellular cytotoxicity
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

25. What lymph node drains the upper limb?
Steroid responsive nephrotic syndrome
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Rheumatic arthritis
Axillary

26. What are the autoantibodies for primary biliary cirrhosis?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Anti alpha subunit 3 of collagen on type IV bm
Anti mitochondrial
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

27. What are the autoantibodies for goodpastures syndrome?
Immunoflourescent staining of tissue biopsies
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Anti alpha subunit 3 of collagen on type IV bm
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

28. describe the pathogenesis of delayed type IV hypersensitivity
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Alternative splicing of mRNA
Recom IL 11; thrombocytopenia

29. what characterizes an arthus reaction?
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
A chemotactic factor for neutrophils
Edema and necrosis in that region
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

30. can igG cross the placenta?
Influenza; antigenic shift; antigenic drift
Yes
Anti U1 RNP (ribonucleoprotein)
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

31. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Alternative splicing of mRNA
IL 1 and IL 6
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
carboxy terminal

32. What do mature naive B lymphocytes express?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
IgM and IgD
mesenchymal
Receiving preformed Antibodies

33. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
Acts as second signal on B cells to induce class switching to IgE and IgG
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Hereditary angioedema; PNH

34. What is the pathogenesis of acute transplant rejection? When does it occur?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
A recomb cytokine of IL 2; RCC and metastatic melanoma
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

35. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
carboxy terminal

36. which B and T cell disorder presents with specifically low IgM?
Cross link
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
Wiskott Aldrich syndrome
Secretory component

37. What is a type I hypersensitivity reaction? What is atopic?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Activates cytotoxic CD 8 T cells as second signal
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
TNF alpha and IL1

38. What kinds of receptors activate innate immunity?
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
IL 4 - 5 - 10 - 6
Antihistone
TLR ad nuclear receptors

39. What is filgrastim and sargramostim? and What is it used for?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

40. What is the presentation of scid? treatment?
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
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

41. What are the autoantibodies for myasthenia gravis?
IgG
Negative nitroblue tetrazolium reduction test
Anti Ach receptor
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

42. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
Hemochromatosis
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
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
encapsulated

43. where are complements produced?
Paracortex; viral infection
IgM and IgD
In the germinal center of secondary follicles (In the paler center)
Liver! (they are proteins circulating in the blood)

44. What are the autoantibodies for Mixed connective tissue disease?
Anti Ach receptor
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Anti U1 RNP (ribonucleoprotein)
Thrombocytopenia

45. How does the alternative pathway lead to MAC activation?
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
A - B - C; all the D's
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
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

46. What is muromonab - CD3 (OKT3)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Th2; Th1
CD21 on B cells (although there is T cell lymphocytosis in EBV)
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

47. How is the thymus organized? what happens in each section?
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
Axillary
type four
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

48. What is the white pulp of the spleen?
A chemotactic factor for neutrophils
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Interferon gamma; Th1
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

49. other than C3a - what other complement acts as an anaphyloxin?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
A chemotactic factor for neutrophils
C5a
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

50. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Interferon gamma; Th1
T
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)