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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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Answer 50 questions in 15 minutes.
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1. What are superantigens? give two examples.
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
If there is class switching and plasma cell production (that is when memory cells are produced)
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
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

2. 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?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
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
No because no peptide fragment!
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

3. What is Aldesleukin? What is it used for
A recomb cytokine of IL 2; RCC and metastatic melanoma
Severe pyogenic infections early in life
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
MHC class molecules bind to KIRS or CD94 to prevent killing

4. Which diseases are associated with DR4?
DM type I and RA
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Stimulate the liver to release acute phase reactants

5. 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?
If there is class switching and plasma cell production (that is when memory cells are produced)
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
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

6. What does CD16 on NK cells do?
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
Kill them because they have CD16 on them that recognize the FcG portion
Bind FcG for antibody dependent cellular cytotoxicity
Active; passive - fast but short half life (3 weeks!)

7. What are MHC's necessary for? By themselves?
Anemias (esp due to renal failure)
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
T cell activation; no with CD 4 or CD 8

8. Leukocyte adhesion defect presents with...
encapsulated
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
neutrophilia!
False! B cell class switching requires a second signal

9. What is recomb alpha interferon used for?
Interferon gamma; Th1
Paracortex
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Alternative splicing of mRNA

10. How is sirolimus different from tacrolimus?
C5a
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
MHC II - B7
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

11. What happens in a deficiency of C3?
Th cells fail to produce interferon gamma; a lot of IgE
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Anti mitochondrial
Its a serine protease that activates apoptosis; NK and CD8

12. describe the classic complement pathway.
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
neutrophilia!
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Thrombocytopenia

13. What is thrombopoietin used for?
Immunosuppression after kidney transplantation
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Thrombocytopenia
Anti topoisomerase

14. Which is the main antibody that provides passive immunity to infants?
SP infections
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
T
IgG

15. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
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
Hemochromatosis
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
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 :(

16. How does the alternative pathway lead to MAC activation?
lowest concentration
MS
MS - hay fever - SLE - goodpastures
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

17. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Alternative splicing of mRNA
mesenchymal
Antibody mediated cytotoxicity; either complement dependent or complement independent
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

18. How does igA cross the epithelium?
Secretory component
Anti alpha subunit 3 of collagen on type IV bm
Superficial inguinal
By transcytosis

19. What is the most common selective Ig deficiency? What is the presentation?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
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
T cell dysfunction
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

20. What is the cause of thymic aplasia? What is its presentation? What are the labs?
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
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

21. How is the antigen loaded onto a MHC II?
Its main effect is a defect in Ab opsonization for killing
Delayed type hypersensitivity
Interferon gamma and IL 2
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

22. What is the main function of IL 12? other than macrophages who else can release IL 12?
NK cells
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Celiac

23. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
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
isotype
Carbohydrate

24. What are four results of a splenectomy?
In the germinal center of secondary follicles (In the paler center)
lowest concentration
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
A chemotactic factor for neutrophils

25. What are target cells?
Cells that stil have weird parts of their membrane that macrophages usually bite off
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
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
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

26. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
Graves
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
Cross link
All MHC 1/CD8

27. Which is the most abundant antibody in blood?
IgG
Superficial inguinal
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
Fab portion

28. which antibody is involved in the primary response or immediate response to an antigen?
IgM
TGF beta and IL 10
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

29. give an example of how influenza does a major antigenic shift.
RNA segment reassortment
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
C5a

30. What is the receptor for EBV? On what cells is that located?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Receiving preformed Antibodies
CD21 on B cells (although there is T cell lymphocytosis in EBV)
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

31. What is the marginal zone of the spleen? what happens there?
Fc
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Found in the red pulp; contains the cords of billroth or the splenic parenchyma that have APCs/Macrophages that closely interact with the basement membrane of the vasculature and where RBCs squeeze through into the parenchyma and interact with Macrop
Remove encapsulated bacateria

32. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Its main effect is a defect in Ab opsonization for killing
isotype
A j chain

33. What are the three types of APCs?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Paracortex
Negative selection
Macrophages - Dendritic cells - B cells

34. What are the main Cell surface proteins on T cells?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
carboxy terminal

35. What is the pathogenesis of a hypersensitivity reaction?
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
IgG
A j chain
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

36. IgM can exist as a _______ also
Celiac
Anti IF
pentamer
Negative nitroblue tetrazolium reduction test

37. Which diseases are associated with DR5?
Paracortex; viral infection
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Pernicious Anemia and Hashimotos
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

38. What are the autoantibodies for autoimmune hepatitis?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Its main effect is a defect in Ab opsonization for killing
Anti smooth muscle
Paracortex; viral infection

39. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
type four
except hyperacute
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

40. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
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
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

41. Describe complement dependent Type II hypersensitivity. Give an example.
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
secondary
SP infections

42. What lymph node drains the upper limb?
mesenchymal
IgM and IgD
Axillary
Activate macrophages

43. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
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
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
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

44. What is the toxicity of azathioprine?
not Ab mediated
IL 15; IL 12 - interferon Beta and interferon alpha
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
...

45. How fast does it occur?
Remove encapsulated bacateria
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Humoral
The patient could become cyanotic in the OR!

46. What is the presentation of common variable immunodef? and What are the labs?
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
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
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

47. which cells have more complete tolerance - B or T cells?
T
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
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

48. What is the pathology seen in chronic transplant rejection?
Antidesmoglein
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Liver! (they are proteins circulating in the blood)
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

49. What does IgA pick up from epithelial cells before being secreted?
Secretory component
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
CRP - C3b - IgM
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

50. What links the adaptive and innate immunity?
Daclizumab; prevent ACUTE rejection of renal transplant
Superior mesenteric
Complement activation (active in both)
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

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USMLE Step 1 Immunology

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