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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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1. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
When you select for which MHC it will have; take out the lymphs that self react
Activate macrophages
Superior mesenteric
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

2. what mediates the type II hypersensitivity? What are the two different methods?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Antibody mediated cytotoxicity; either complement dependent or complement independent
Viral neutralization of igM and IgG!
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

3. What is the late phase reaction of anaphylaxis allergy? what mediates it?
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)
Tetanus - Botulinum - HBV - Rabies
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
Wiskott Aldrich syndrome

4. What cytokines to Th2 secrete?
Histamine; post capillary venules - vasodilation
IL 4 - 5 - 10 - 6
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Celiac

5. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

6. What is filgrastim and sargramostim? and What is it used for?
RNA segment reassortment
Defect in LFA 1 integrin (CD 18) protein on phagocytes (neutrophils!); recurrent bacterial infections - severe gingivitis - poor wound healing - absent pus formation - and delayed separation of the umbilicus; neutrophilia
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
In the germinal center of secondary follicles (In the paler center)

7. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
IL 5
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Cells that stil have weird parts of their membrane that macrophages usually bite off
TNF alpha and IL1

8. Monomer in circulation - ___ when secreted
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
dimer
Glycoproteins; HLA
C5a

9. What lymph node drains the duodenum - jejunum?
lowest concentration
IgM and IgD
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Superior mesenteric

10. What is recomb gamma interferon used for?
Th2; Th1
Chronic granulomatous disease
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Superficial inguinal

11. What are the autoantibodies for polymyositis and dermatomyositis?
Anti Jo -1
TGF beta and IL 10
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
For some reason a mature naive B lymphocyte got away from tolerance and the result was a production an Ab on its surface with an Fab region that recognized the alpha 3 collagen subunit on the BM as non self. It then gets activated by a Th2 cell (enti

12. What are the autoantibodies for type I diabetes mellitus?
Anti glutamate carboxylase and anti insulin
Influenza; antigenic shift; antigenic drift
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

13. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
except hyperacute
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
Anti IF

14. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Acts as second signal on B cells to induce class switching to IgE and IgG

15. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Local infection/inflammation; infection of the ln itself; metastasis
Yes
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

16. What lymph node drains the scrotum?
Histamine; post capillary venules - vasodilation
Superficial inguinal
delayed!
Anti U1 RNP (ribonucleoprotein)

17. What are the main Cell surface proteins on T cells?
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
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Thrombocytopenia

18. How do you test for type III hypersensitivity?
Alternative splicing of mRNA
MS - hay fever - SLE - goodpastures
Kill them because they have CD16 on them that recognize the FcG portion
Immunoflourescent staining of tissue biopsies

19. What is the presentation of hyperIgM syndrome?
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
IgM
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Severe pyogenic infections early in life

20. are Th cells involved in trapping of antigens of endotoxin/LPS?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Pernicious Anemia and Hashimotos
T cell precursor
No because no peptide fragment!

21. What are the autoantibodies for Celiac disease?
Wiskott Aldrich syndrome
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
IgG
A - B - C; all the D's

22. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Barrel hoop basement membrane fenestrations
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Axillary

23. What are the cell surface proteins on NK cells?
Antidote for digoxin intoxication
MHC I - CD16 - CD56
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
heavy chains

24. Complements are...
Axillary
acute phase reactants
mesenchymal
Stimulate the liver to release acute phase reactants

25. What is the clinical use for azathioprine?
Secretory component
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
...
Axillary

26. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Axillary
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

27. What is the pathology of acute transplant rejection? is it reversible?
Activates Th1 helper cells; Macrophages
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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

28. What is epo used for?
Th cells fail to produce interferon gamma; a lot of IgE
Anemias (esp due to renal failure)
Basophils! THey want IG E class switch!
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

29. What are the autoantibodies for graves?
Anti TSh receptor
Internal iliac
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
IgM

30. From where do cytokines come from?
Lymphocytes
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Influenza; antigenic shift; antigenic drift

31. What kinds of receptors activate innate immunity?
TLR ad nuclear receptors
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
IgM
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

32. 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
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Basophils! THey want IG E class switch!

33. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Antimicrosomal and antithyroglobulin
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
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
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

34. The lymphocytes are ________ origin
Anti SS- A (anti RO) and Anti SS- B
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
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
mesenchymal

35. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
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
...
Edema and necrosis in that region
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

36. What can cause a lymph node enlargement?
IL 3; supports growth and differentiation of bone marrow stem cells
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
Local infection/inflammation; infection of the ln itself; metastasis
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

37. In general What are T cells good for?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Kill them because they have CD16 on them that recognize the FcG portion
Alternative splicing of mRNA
Anti viral and anti tumor

38. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
A - B - C; all the D's
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

39. where are complements produced?
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
Liver! (they are proteins circulating in the blood)
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

40. What does IL 4 do?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Acts as second signal on B cells to induce class switching to IgE and IgG

41. The secondary follicles have __________; primary follicles are dense
pale central germinal centers
Viral neutralization of igM and IgG!
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

42. What does Interferon alpha and beta do? how?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Sinusitis - otitis media - pneumonia
C5a

43. A lymph node is a ________ lymphoid organ.
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
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
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
secondary

44. What lymph node drains the testes?
Recom IL 11; thrombocytopenia
Para aortic
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)
Type IV

45. The alternative pathway is the only constutively...
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
pathogenesis
Secretory component
active complement pathway

46. Give an example of someone who could get hyperacute transplant rejection.
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Previous transfusion; pregnant woman whose fetus had paternal antigens
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
opsonizes

47. What lymph node drains the lateral side of the dorsum of the foot?
IgG
Popliteal
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
...

48. where do somatic hypermutation and class switching occur?
In the germinal center of secondary follicles (In the paler center)
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
IL 4 - 5 - 10 - 6
Anti SS- A (anti RO) and Anti SS- B

49. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Alternative splicing of mRNA
isotype
Antidesmoglein
...

50. Name 5 ways Antibody diversity is generated?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
A recomb cytokine of IL 2; RCC and metastatic melanoma
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
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

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USMLE Step 1 Immunology

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