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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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1. What are the autoantibodies for systemic sclerosis?
MHC I - CD16 - CD56
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
Barrel hoop basement membrane fenestrations
Anti topoisomerase

2. What do mature naive B lymphocytes express?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Inferior mesenteric
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
IgM and IgD

3. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
IgG
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

4. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
DM type I
Macrophages - Dendritic cells - B cells
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Anti Ach receptor

5. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Complement activation (active in both)
B - T - and NK cells
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

6. what will NK cells do to cells covered in IgG Ab? why?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Kill them because they have CD16 on them that recognize the FcG portion
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Negative nitroblue tetrazolium reduction test

7. What is the pathogenesis of a hypersensitivity reaction?
not Ab mediated
pathogenesis
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
Hereditary angioedema; PNH

8. What are the autoantibodies for Mixed connective tissue disease?
Anti U1 RNP (ribonucleoprotein)
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

9. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
A recomb cytokine of IL 2; RCC and metastatic melanoma
Histamine; post capillary venules - vasodilation
Popliteal

10. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Previous transfusion; pregnant woman whose fetus had paternal antigens
Antidesmoglein
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
Chronic granulomatous disease

11. What cytokines to Th2 secrete?
IL 4 - 5 - 10 - 6
False! B cell class switching requires a second signal
Kill them because they have CD16 on them that recognize the FcG portion
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

12. Which are the only two antiinflammatory cytokines?
TGF beta and IL 10
Pernicious Anemia and Hashimotos
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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

13. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Basophils! THey want IG E class switch!
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
pentamer
MHC class molecules bind to KIRS or CD94 to prevent killing

14. Which diseases are associated with DR5?
Celiac
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
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Pernicious Anemia and Hashimotos

15. What is a type I hypersensitivity reaction? What is atopic?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
When you select for which MHC it will have; take out the lymphs that self react
Graves
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

16. How is the thymus organized? what happens in each section?
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
SP infections
IgE; by activating eosinophils
T

17. What lymph node drains the testes?
not Ab mediated
Anti TSh receptor
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Para aortic

18. What is passive immunity?
Its main effect is a defect in Ab opsonization for killing
Hemochromatosis
except hyperacute
Receiving preformed Antibodies

19. To what portion of the Antibody do the complements bind?
lowest concentration
Anti alpha subunit 3 of collagen on type IV bm
Fc
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

20. What type of side chains are found on Fc region of an antibody?
Graves
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Carbohydrate
pathogenesis

21. 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).
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
IgG
Cyclosporine - OKT3
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!

22. What is the cause of thymic aplasia? What is its presentation? What are the labs?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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
Type IV

23. What is the mechanism for sirolimus? what else it known as?
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
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
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

24. What is the toxicity of azathioprine?
Cells that stil have weird parts of their membrane that macrophages usually bite off
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
...

25. What is filgrastim and sargramostim? and What is it used for?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Delayed type hypersensitivity
Secretory component
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

26. What is the pathology of acute transplant rejection? is it reversible?
Remove encapsulated bacateria
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
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Superficial inguinal

27. What is the presentation of hyperIgM syndrome?
Severe pyogenic infections early in life
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
Anti smooth muscle
opsonizes

28. 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)
TLR ad nuclear receptors
CRP - C3b - IgM
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

29. What lymph node drains the upper limb?
Steroid responsive nephrotic syndrome
Axillary
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

30. For which toxins are preformed antibodies (passive) given?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Tetanus - Botulinum - HBV - Rabies
Anti viral and anti tumor

31. where do somatic hypermutation and class switching occur?
Delayed type hypersensitivity
In the germinal center of secondary follicles (In the paler center)
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
Not thymus - BM

32. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
neutrophilia!
Paracortex; viral infection
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

33. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Daclizumab; prevent ACUTE rejection of renal transplant
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
not Ab mediated
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

34. 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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
IL 1 and IL 6

35. What are the autoantibodies for type I diabetes mellitus?
Anti glutamate carboxylase and anti insulin
Anti IF
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 :(
isotype

36. describe the pathogenesis of delayed type IV hypersensitivity
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Yes
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

37. Which is the main antibody in the delayed or secondary response to an antigen?
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
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
IgG
Receiving preformed Antibodies

38. What are some catalase positive organisms?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
CD21 on B cells (although there is T cell lymphocytosis in EBV)
S. aureus - E. Coli - aspergillus

39. What is the main cytokine released by T cells? What does it do
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
IL 3; supports growth and differentiation of bone marrow stem cells
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
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

40. What lymph node drains the anal canal (below the pectinate line)?
Superficial inguinal
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
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

41. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
SP infections
Antidesmoglein
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 :(
Histamine; post capillary venules - vasodilation

42. What are the main symptoms of T cell immunodeficiencies?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Tetanus - Botulinum - HBV - Rabies
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

43. What are C1 - C2 - C3 - C4 important for?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Viral neutralization of igM and IgG!

44. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
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
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
Daclizumab; prevent ACUTE rejection of renal transplant
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

45. In thymic development - What is the positive selection? negative selections?
lowest concentration
When you select for which MHC it will have; take out the lymphs that self react
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
Anti Ach receptor

46. What does IL 10 do? who is secreted by?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
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 the germinal center of secondary follicles (In the paler center)
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

47. Which disease is associated with B8?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Graves
DM type I and RA

48. IgG...
If there is class switching and plasma cell production (that is when memory cells are produced)
opsonizes
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
NK cells

49. other than C3a - what other complement acts as an anaphyloxin?
Internal iliac
Previous transfusion; pregnant woman whose fetus had paternal antigens
C5a
Hereditary angioedema; PNH

50. What is the most common example of passive immunity?
IgAs in mothers breast milk!
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

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USMLE Step 1 Immunology

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