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 a type I hypersensitivity reaction? What is atopic?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
IL 15; IL 12 - interferon Beta and interferon alpha
Fab portion

2. What is muromonab - CD3 (OKT3)
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

3. Type Iv hypersensitivity is...
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
delayed!
IgG
A j chain

4. What is the presentation of scid? treatment?
IgM
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
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
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

5. What is immune complex disease? give an example.
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
The igA found in breast milk
No because no peptide fragment!
IL 5

6. What links the adaptive and innate immunity?
Complement activation (active in both)
Barrel hoop basement membrane fenestrations
IL 3; supports growth and differentiation of bone marrow stem cells
IgE

7. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Anti viral and anti tumor
Axillary
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Wiskott Aldrich syndrome

8. which antibodies prevent antigens from binding mucosal surfaces?
Axillary
Th cells fail to produce interferon gamma; a lot of IgE
IgA
Cells that stil have weird parts of their membrane that macrophages usually bite off

9. What are the autoantibodies for drug induced lupus?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
...
Antihistone
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

10. What is the late phase reaction of anaphylaxis allergy? what mediates it?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
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)
Superior mesenteric
Chronic granulomatous disease

11. What are target cells?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Cells that stil have weird parts of their membrane that macrophages usually bite off

12. How fast does it occur?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
The patient could become cyanotic in the OR!
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

13. What cytokines are released by Th1 cells?
False! B cell class switching requires a second signal
Edema and necrosis in that region
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
Interferon gamma and IL 2

14. What is the white pulp of the spleen?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
MS
Anti alpha subunit 3 of collagen on type IV bm
T cell activation; no with CD 4 or CD 8

15. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
MHC I - CD16 - CD56
IgE
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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

16. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
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
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Basophils! THey want IG E class switch!
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

17. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Its main effect is a defect in Ab opsonization for killing
Macrophages - Dendritic cells - B cells
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

18. What is the pathogenesis of a hypersensitivity reaction?
Humoral
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
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

19. Which MHC presents intracellular peptides? how so?
Bind FcG for antibody dependent cellular cytotoxicity
MHC I; from RER with help of the B2 microglobulin
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
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

20. 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).
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!
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
By transcytosis
Activate macrophages

21. Give an example of someone who could get hyperacute transplant rejection.
IL 3; supports growth and differentiation of bone marrow stem cells
Anti mitochondrial
Previous transfusion; pregnant woman whose fetus had paternal antigens
Fc

22. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
By transcytosis
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
Acts as second signal on B cells to induce class switching to IgE and IgG
Cross link

23. What is the main function of interferons?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Receiving preformed Antibodies
Negative!

24. What is the main cytokine that activates eosinophils?
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
IL 5
Delayed type hypersensitivity
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

25. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
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
Alternative splicing of mRNA
Cells that stil have weird parts of their membrane that macrophages usually bite off

26. What is the toxicity of muromonab?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
delayed!
Superior mesenteric
encapsulated

27. which antibodies can bind complement?
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
A - B - C; all the D's
Superficial inguinal
IgM and IgG

28. which cytokine inhibits TH2 cells? secreted by who?
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!
Edema and necrosis in that region
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Interferon gamma; Th1

29. The idiotype; the Fc portion determines the...
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
isotype
Anti TSh receptor
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

30. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
SP infections
False! B cell class switching requires a second signal
The patient could become cyanotic in the OR!

31. What are howell jolly bodies?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Bind FcG for antibody dependent cellular cytotoxicity
Activate macrophages
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

32. What is oprelevkin? and What is it used for?
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!
Recom IL 11; thrombocytopenia
Antimicrosomal and antithyroglobulin
lowest concentration

33. What is the treatment of acute transplant rejection?
Cyclosporine - OKT3
...
type four
DM type I and RA

34. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
All MHC 1/CD8
Paracortex; viral infection
Th2; Th1
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

35. Which diseases are associated with DR5?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Pernicious Anemia and Hashimotos
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Type IV

36. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
active complement pathway
NK cells
MHC I - CD16 - CD56

37. What are the PALS?
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
Inferior mesenteric
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
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

38. What are the three types of lymphocytes?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Axillary
B - T - and NK cells
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

39. 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?
Anti smooth muscle
Antidesmoglein
TNF alpha and IL1
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

40. Which antibodies can be multimeric?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Th cells fail to produce interferon gamma; a lot of IgE
IgM and IgA
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

41. 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
CRP - C3b - IgM
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Anti topoisomerase

42. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
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
Alternative splicing of mRNA
In the germinal center of secondary follicles (In the paler center)
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

43. Which type of selection of thymic development provides central tolerance?
Daclizumab; prevent ACUTE rejection of renal transplant
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Negative selection
When you select for which MHC it will have; take out the lymphs that self react

44. What is the autoantibody for SLE that is nonspecific? Specific?
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
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

45. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
NK cells

46. What lymph node drains the thigh?
Superficial inguinal
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
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
encapsulated

47. Monomer in circulation - ___ when secreted
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
dimer
T cell dysfunction
Superficial inguinal

48. What are C1 - C2 - C3 - C4 important for?
IL 1 and IL 6
Severe pyogenic infections early in life
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
Viral neutralization of igM and IgG!

49. IgM can fix complement but...
Immunosuppression after kidney transplantation
cannot cross placenta
Not thymus - BM
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

50. What are the autoantibodies for type I diabetes mellitus?
Anti glutamate carboxylase and anti insulin
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
not Ab mediated