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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. Type Iv hypersensitivity is...
opsonizes
CRP - C3b - IgM
IL 5
delayed!

2. What is the defect in hyper IgM syndrome? What are the lab results?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
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
Axillary

3. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Interferon gamma and IL 2
Immunoflourescent staining of tissue biopsies
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

4. 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?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
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
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Cross link

5. What lymph node drains the scrotum?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Superficial inguinal
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
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

6. What are the labs in brutons agammaglobulinemia?
By transcytosis
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

7. What is the general structure of an Ab?
IgA
Rheumatic arthritis
...
2 heavy chains and two light chains

8. Which HLA's are included in MHC I? MHC II?

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9. To what disease do the autoantibodies to IgG (rheumatoid factor)?
...
Rheumatic arthritis
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

10. The Fc region is found on the...
carboxy terminal
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Macrophages - Dendritic cells - B cells
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

11. Type IV hypersensitivity is i...
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
not Ab mediated

12. what happens in a deficiency of C1 esterase inhibitor? DAF?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Chronic granulomatous disease
Hereditary angioedema; PNH
Its a serine protease that activates apoptosis; NK and CD8

13. What is an example of a parasite showing antigenic variation?
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
SP infections
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Delayed type hypersensitivity

14. can igG cross the placenta?
Yes
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
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
Barrel hoop basement membrane fenestrations

15. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
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
MHC class molecules bind to KIRS or CD94 to prevent killing
Cross link

16. 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
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Axillary

17. What are the autoantibodies for sjorgens syndrome?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Para aortic
In the germinal center of secondary follicles (In the paler center)
Anti SS- A (anti RO) and Anti SS- B

18. The idiotype; the Fc portion determines the...
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
isotype
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
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

19. What is recomb alpha interferon used for?
Antidesmoglein
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
dimer
Rheumatic arthritis

20. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
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
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

21. What is the white pulp of the spleen?
Steroid responsive nephrotic syndrome
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
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
...

22. Which disease is associated with HLA A3?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Superficial inguinal
Stimulate the liver to release acute phase reactants
Hemochromatosis

23. Give three examples of bacteria that use antigenic variation and how.
TNF alpha and IL1
RNA segment reassortment
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
The patient could become cyanotic in the OR!

24. What is the clinical use of Muromonab?
Antihistone
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Immunosuppression after kidney transplantation

25. Which disease is associated with DR3?
DM type I
Anti alpha subunit 3 of collagen on type IV bm
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

26. What is the main function of IL 12? other than macrophages who else can release IL 12?
Stimulate the liver to release acute phase reactants
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
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Steroid responsive nephrotic syndrome

27. What is the treatment of acute transplant rejection?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Cyclosporine - OKT3
DM type I and RA
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

28. which antibodies can bind complement?
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
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
IgM and IgG
Activates Th1 helper cells; Macrophages

29. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
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
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
TLR ad nuclear receptors
Cross link

30. which type of immunity is slow but long lasting? as opposed to...
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Recom IL 11; thrombocytopenia
Chronic granulomatous disease
Active; passive - fast but short half life (3 weeks!)

31. What does it mean if there are igM in the serum at birth?
Recom IL 11; thrombocytopenia
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
TNF alpha and IL1
lowest concentration

32. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
IL 1 and IL 6
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

33. describe the pathogenesis of delayed type IV hypersensitivity
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
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
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

34. which B and T cell disorder presents with specifically low IgM?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Wiskott Aldrich syndrome
T cell activation; no with CD 4 or CD 8
...

35. What are the autoantibodies for goodpastures syndrome?
Anti alpha subunit 3 of collagen on type IV bm
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Fc
A chemotactic factor for neutrophils

36. What cytokines are released by Th1 cells?
Basophils! THey want IG E class switch!
Inferior mesenteric
Interferon gamma and IL 2
Th2; Th1

37. What is the pathogenesis of acute transplant rejection? When does it occur?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Activate macrophages
Sinusitis - otitis media - pneumonia
TGF beta and IL 10

38. which cells have more complete tolerance - B or T cells?
T
Immunosuppression after kidney transplantation
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
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

39. In thymic development - What is the positive selection? negative selections?
A recomb cytokine of IL 2; RCC and metastatic melanoma
heavy chains
When you select for which MHC it will have; take out the lymphs that self react
Axillary

40. which antibody is involved in the primary response or immediate response to an antigen?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
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
IgM
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

41. What are the autoantibodies for type I diabetes mellitus?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Anti glutamate carboxylase and anti insulin
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Carbohydrate

42. What is the toxicity of muromonab?
Anti smooth muscle
Daclizumab; prevent ACUTE rejection of renal transplant
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

43. The ______ in the BM are DN - the DP are in the cortex of thymus
T cell precursor
Anti mitochondrial
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
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

44. What bugs can actually infect the lymph node itself?
Interferon gamma and IL 2
T cell activation; no with CD 4 or CD 8
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
IgM

45. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
Increases expression of MHC I and MHC II and also activates NK cells
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
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
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

46. 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?
Fab portion
IL 4 - 5 - 10 - 6
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
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

47. What type of side chains are found on Fc region of an antibody?
Carbohydrate
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

48. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Active; passive - fast but short half life (3 weeks!)
Paracortex
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Th cells fail to produce interferon gamma; a lot of IgE

49. what bacteria are a splenectomy patient most susceptible to? why?
lowest concentration
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
IgM and IgA
A - B - C; all the D's

50. What is a type I hypersensitivity reaction? What is atopic?
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
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Antidote for digoxin intoxication