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. Which cytokines do Th2 release and For what?
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
pathogenesis
pale central germinal centers
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

2. What is the toxicity of muromonab?
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
T cell and antibody mediated vascular damage due to MHC non self being recognized as self by self lymphocytes and resulting in attack of the foreign antigens it presents (all of them); months to years after; no :(
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

3. What are the function of B cells?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Paracortex; viral infection

4. what secretes IL 4?
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
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Basophils! THey want IG E class switch!

5. What lymph node drains the duodenum - jejunum?
Barrel hoop basement membrane fenestrations
Antihistone
Celiac
Superior mesenteric

6. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
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
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)
Previous transfusion; pregnant woman whose fetus had paternal antigens
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

7. Other than stimulating fever - what else does IL 6 do?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Stimulate the liver to release acute phase reactants
Antimicrosomal and antithyroglobulin
heavy chains

8. Which disease is associated with B8?
Graves
When you select for which MHC it will have; take out the lymphs that self react
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
Anti Jo -1

9. what ensure that a memory response is generated?
Sinusitis - otitis media - pneumonia
If there is class switching and plasma cell production (that is when memory cells are produced)
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Severe pyogenic infections early in life

10. What are the autoantibodies for goodpastures syndrome?
IgM and IgG
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
IgG
Anti alpha subunit 3 of collagen on type IV bm

11. 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).
Anemias (esp due to renal failure)
carboxy terminal
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!
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

12. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Th cells fail to produce interferon gamma; a lot of IgE
T cell activation; no with CD 4 or CD 8
Delayed type hypersensitivity
Cells that stil have weird parts of their membrane that macrophages usually bite off

13. which cytokine inhibits TH2 cells? secreted by who?
Interferon gamma; Th1
Hemochromatosis
Anti Jo -1
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

14. What is the main cytokine that activates eosinophils?
IL 5
secondary
Fc
Basophils! THey want IG E class switch!

15. __________ are a part of the innate system.
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Local infection/inflammation; infection of the ln itself; metastasis
NK cells
Bind FcG for antibody dependent cellular cytotoxicity

16. The ______ in the BM are DN - the DP are in the cortex of thymus
T cell precursor
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
CRP - C3b - IgM
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

17. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
pentamer
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
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

18. What are the autoantibodies for myasthenia gravis?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Anti Ach receptor
By transcytosis
Macrophages - Dendritic cells - B cells

19. Describe the complement independent Type II hypersenstivity reaction. Give an example.
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
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

20. What are the major functions of Antibodies?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

21. What is three common causes of severe combined immunodef? What is the result of all three?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
In the germinal center of secondary follicles (In the paler center)

22. describe the classic complement pathway.
IgAs in mothers breast milk!
Anti TSh receptor
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
The igA found in breast milk

23. What are the three types of APCs?
Cyclosporine - OKT3
Macrophages - Dendritic cells - B cells
Severe pyogenic infections early in life
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

24. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
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
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

25. 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
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Fab portion
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

26. which type of immunity is slow but long lasting? as opposed to...
Rheumatic arthritis
Active; passive - fast but short half life (3 weeks!)
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

27. What is the clinical use for azathioprine?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
...

28. What does Interferon alpha and beta do? how?
Increases expression of MHC I and MHC II and also activates NK cells
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

29. A lymph node is a ________ lymphoid organ.
IgA
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
secondary
Superficial inguinal

30. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
IgA
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Daclizumab; prevent ACUTE rejection of renal transplant

31. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Activate macrophages
Basophils! THey want IG E class switch!
TLR ad nuclear receptors
Axillary

32. What are the symptoms of serum sickness?
IgM and IgG
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
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

33. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Hereditary angioedema; PNH
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Its main effect is a defect in Ab opsonization for killing

34. What is the defect in hyper IgM syndrome? What are the lab results?
dimer
Activates Th1 helper cells; Macrophages
Antibody mediated cytotoxicity; either complement dependent or complement independent
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

35. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Thrombocytopenia
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Chronic granulomatous disease

36. Give three examples of bacteria that use antigenic variation and how.
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Viral neutralization of igM and IgG!
In the germinal center of secondary follicles (In the paler center)

37. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

38. The pathogenesis of contact dermatitis is ________ hypersensitivity
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
A - B - C; all the D's
type four

39. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Alternative splicing of mRNA
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Superficial inguinal

40. What is recomb gamma interferon used for?
Activate macrophages
opsonizes
Chronic granulomatous disease
RNA segment reassortment

41. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
In any situation where immunologically competent cells are transplanted into immunologically crippled recipient; graft rejects all the cells due to foreign proteins resulting in severe organ dysfunction
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
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
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

42. What is chronic mucocutaneous candidiasis d/t?
Antibody mediated cytotoxicity; either complement dependent or complement independent
T cell dysfunction
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

43. What does IgA pick up from epithelial cells before being secreted?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Receiving preformed Antibodies
Secretory component
Alternative splicing of mRNA

44. What is the pathology of acute transplant rejection? is it reversible?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Humoral
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Anti TSh receptor

45. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Rheumatic arthritis
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

46. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
Anti Ach receptor
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
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
isotype

47. Which antibodies can be multimeric?
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
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
IgM and IgA
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

48. What is muromonab - CD3 (OKT3)
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
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

49. What are some catalase positive organisms?
S. aureus - E. Coli - aspergillus
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Not thymus - BM
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

50. What are the autoantibodies for wegeners granulomatosis?
DM type I and RA
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Secretory component
Local infection/inflammation; infection of the ln itself; metastasis