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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. Give an example of someone who could get hyperacute transplant rejection.
Previous transfusion; pregnant woman whose fetus had paternal antigens
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Barrel hoop basement membrane fenestrations
Antihistone

2. What kinds of receptors activate innate immunity?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
TLR ad nuclear receptors
Superficial inguinal
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

3. What are howell jolly bodies?
Superior mesenteric
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
IgG

4. What is the white pulp of the spleen?
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
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Severe pyogenic infections early in life
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

5. when can graft versus host disease? What is the result?
Previous transfusion; pregnant woman whose fetus had paternal antigens
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
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
Anti viral and anti tumor

6. What is Aldesleukin? What is it used for
Histamine; post capillary venules - vasodilation
opsonizes
Glycoproteins; HLA
A recomb cytokine of IL 2; RCC and metastatic melanoma

7. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
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 4
MHC I - CD16 - CD56

8. What is an example of a parasite showing antigenic variation?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Bind FcG for antibody dependent cellular cytotoxicity
Daclizumab; prevent ACUTE rejection of renal transplant
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

9. What is the mechanism for sirolimus? what else it known as?
Binds to Mtor which (like tacrolimus and cyclosporine just in a different pathway) inhibits IL 2 production and thus t cell proliferation in response to IL 2 producton
Macrophages - Dendritic cells - B cells
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Influenza; antigenic shift; antigenic drift

10. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Antidesmoglein
Kill them because they have CD16 on them that recognize the FcG portion
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
Alternative splicing of mRNA

11. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
2 heavy chains and two light chains
All MHC 1/CD8
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

12. What does IL 2 do?
Anti SS- A (anti RO) and Anti SS- B
Activates cytotoxic CD 8 T cells as second signal
Steroid responsive nephrotic syndrome
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

13. Give three examples of bacteria that use antigenic variation and how.
lowest concentration
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

14. What is chronic mucocutaneous candidiasis d/t?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
NK cells
not Ab mediated
T cell dysfunction

15. Name 5 ways Antibody diversity is generated?
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
delayed!
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Interferon gamma and IL 2

16. What are some catalase positive organisms?
Its a serine protease that activates apoptosis; NK and CD8
S. aureus - E. Coli - aspergillus
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Carbohydrate

17. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
except hyperacute
Rheumatic arthritis
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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

18. What is the toxicity of azathioprine?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
...
carboxy terminal

19. The secondary follicles have __________; primary follicles are dense
Para aortic
Hereditary angioedema; PNH
pale central germinal centers
Negative!

20. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
Axillary
Influenza; antigenic shift; antigenic drift
CD21 on B cells (although there is T cell lymphocytosis in EBV)
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

21. How fast does it occur?
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!
Anti alpha subunit 3 of collagen on type IV bm
The patient could become cyanotic in the OR!
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

22. What are superantigens? give two examples.
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
Superior mesenteric
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
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

23. What is recomb gamma interferon used for?
Its main effect is a defect in Ab opsonization for killing
Chronic granulomatous disease
...
Antidote for digoxin intoxication

24. The MALT/GALT are not...
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
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
encapsulated

25. What does granzyme do? who secretes it?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Chronic granulomatous disease
Its a serine protease that activates apoptosis; NK and CD8
Superficial inguinal

26. What does IgA pick up from epithelial cells before being secreted?
Not thymus - BM
When you select for which MHC it will have; take out the lymphs that self react
Secretory component
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

27. What are the autoantibodies for goodpastures syndrome?
Anti alpha subunit 3 of collagen on type IV bm
Fab portion
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
IgG

28. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Anti mitochondrial
Glycoproteins; HLA
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
The igA found in breast milk

29. From where do cytokines come from?
dimer
Lymphocytes
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Type IV

30. where are complements produced?
Interferon gamma; Th1
The igA found in breast milk
DM type I
Liver! (they are proteins circulating in the blood)

31. What does CD16 on NK cells do?
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
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Antidote for digoxin intoxication
Bind FcG for antibody dependent cellular cytotoxicity

32. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
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
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
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Type IV

33. So antibodies are the effectors for the humoral response. List some of their functions.
SP infections
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Antihistone

34. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
A chemotactic factor for neutrophils
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Daclizumab; prevent ACUTE rejection of renal transplant
T cell dysfunction

35. What is the main cytokine that activates eosinophils?
IL 5
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
neutrophilia!

36. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Immunoflourescent staining of tissue biopsies
Negative nitroblue tetrazolium reduction test
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

37. where do NK cells develop?
Pernicious Anemia and Hashimotos
heavy chains
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Not thymus - BM

38. What cytokines are released by Th1 cells?
Secretory component
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
pale central germinal centers
Interferon gamma and IL 2

39. What is the main function of TNF alpha? How does it do this?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Remove encapsulated bacateria

40. What is the clinical use for sirolimus? what should you combine it with?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Interferon gamma; Th1
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

41. what prevents NK cells from killing normal cells if their default is to kill?
MHC class molecules bind to KIRS or CD94 to prevent killing
Fab portion
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Graves

42. What cytokines to Th2 secrete?
IL 4 - 5 - 10 - 6
Anti Jo -1
lowest concentration
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

43. What are the symptoms of serum sickness?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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
NK cells
Activates cytotoxic CD 8 T cells as second signal

44. What does IL 4 do?
B - T - and NK cells
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
S. aureus - E. Coli - aspergillus
Acts as second signal on B cells to induce class switching to IgE and IgG

45. In general What are T cells good for?
Anti viral and anti tumor
carboxy terminal
IL 1 and IL 6
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

46. Which disease is associated withB B27?
Axillary
Viral neutralization of igM and IgG!
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Axillary

47. What is the presentation of scid? treatment?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
pale central germinal centers
IgM and IgG
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

48. What type of side chains are found on Fc region of an antibody?
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
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Superior mesenteric
Carbohydrate

49. What is a factor that is a predictor for a bad transplantation?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
...
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
active complement pathway

50. 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?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Its a serine protease that activates apoptosis; NK and CD8
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
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