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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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1. 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
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

2. What are the major functions of Antibodies?
IgG
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
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
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

3. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

4. How does the alternative pathway lead to MAC activation?
IL 5
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
Alternative splicing of mRNA
carboxy terminal

5. The pathogenesis of contact dermatitis is ________ hypersensitivity
All MHC 1/CD8
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
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
type four

6. How is sirolimus different from tacrolimus?
mesenchymal
Delayed type hypersensitivity
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Macrophages - Dendritic cells - B cells

7. IgE has the ___________ in the serum
IgE
lowest concentration
IL 3; supports growth and differentiation of bone marrow stem cells
Anti TSh receptor

8. ________ regulate the cell mediated response.
Humoral
T cell dysfunction
TNF alpha and IL1
Cyclosporine - OKT3

9. For which toxins are preformed antibodies (passive) given?
Tetanus - Botulinum - HBV - Rabies
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
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
dimer

10. What does CD16 on NK cells do?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Bind FcG for antibody dependent cellular cytotoxicity
Superficial inguinal
S. aureus - E. Coli - aspergillus

11. Describe complement dependent Type II hypersensitivity. Give an example.
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Remove encapsulated bacateria
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
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

12. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Glycoproteins; HLA
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

13. What are the three types of lymphocytes?
By transcytosis
B - T - and NK cells
MHC I - CD16 - CD56
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

14. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
Thrombocytopenia
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Cyclosporine - OKT3
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

15. What is the general structure of an Ab?
2 heavy chains and two light chains
Not thymus - BM
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Hereditary angioedema; PNH

16. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
IgG
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Severe pyogenic infections early in life

17. What is Aldesleukin? What is it used for
Rheumatic arthritis
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
Receiving preformed Antibodies
A recomb cytokine of IL 2; RCC and metastatic melanoma

18. 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
Hereditary angioedema; PNH
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

19. What is the marginal zone of the spleen? what happens there?
CRP - C3b - IgM
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
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Anti smooth muscle

20. What are the autoantibodies for graves?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
...
Anti TSh receptor
If there is class switching and plasma cell production (that is when memory cells are produced)

21. What type of fenestrations are found in the red pulp of the spleen?
Carbohydrate
Barrel hoop basement membrane fenestrations
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
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

22. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
CD56
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
TNF alpha and IL1
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

23. What are the autoantibodies for other vasculitides?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
IgM and IgG
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
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

24. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
encapsulated
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
The patient could become cyanotic in the OR!
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 :(

25. What are the T cell functions?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
S. aureus - E. Coli - aspergillus
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Celiac

26. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
MHC II - B7
Paracortex; viral infection
Steroid responsive nephrotic syndrome
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

27. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
A B and T cell disorder; X linked recessive; progressive deletion of B and T cells; thrombocytopenic purpura - infections - eczema; high IgE and IgA but low IgM
Macrophages - Dendritic cells - B cells

28. hat is the presentation of Jobs syndrome or Hyper IgE?
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
Sinusitis - otitis media - pneumonia
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Type IV

29. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
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
RNA segment reassortment

30. where do somatic hypermutation and class switching occur?
In the germinal center of secondary follicles (In the paler center)
Carbohydrate
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Histamine; post capillary venules - vasodilation

31. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
The interstitial tissue of a lymph node is structured into the cortex on the outside Which is densely cellular which transitions into the paracortex Which is less dense and then the medulla Which is least dense. The cells that inhabit these tissues a
Interferon gamma; Th1
B - T - and NK cells
Th cells fail to produce interferon gamma; a lot of IgE

32. What lymph node drains the upper limb?
Axillary
Negative selection
DM type I
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

33. To what portion of the Antibody do the complements bind?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Fc
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

34. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
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
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Pernicious Anemia and Hashimotos
The igA found in breast milk

35. Which are the only two antiinflammatory cytokines?
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
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
TGF beta and IL 10
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

36. Describe the Mannose Lectin pathway
By transcytosis
Immunoflourescent staining of tissue biopsies
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
Viral neutralization of igM and IgG!

37. What is the presentation of hyperIgM syndrome?
Severe pyogenic infections early in life
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
IgE; by activating eosinophils
RNA segment reassortment

38. What lymph node drains the duodenum - jejunum?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Superior mesenteric
Pernicious Anemia and Hashimotos
NK cells

39. What is the presentation of common variable immunodef? and What are the labs?
The interstitial tissue of a lymph node is structured into the cortex on the outside Which is densely cellular which transitions into the paracortex Which is less dense and then the medulla Which is least dense. The cells that inhabit these tissues a
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
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
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

40. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Secretory component
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Receiving preformed Antibodies

41. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
IgM and IgA
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

42. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
Increases expression of MHC I and MHC II and also activates NK cells
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Negative nitroblue tetrazolium reduction test
Daclizumab; prevent ACUTE rejection of renal transplant

43. What are the PALS?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Th2; Th1
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
IL 5

44. What are four results of a splenectomy?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
opsonizes

45. Monomer in circulation - ___ when secreted
pale central germinal centers
dimer
Activates Th1 helper cells; Macrophages
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

46. In general What are T cells good for?
IgG
Anti viral and anti tumor
acute phase reactants
Cells that stil have weird parts of their membrane that macrophages usually bite off

47. Give an example of someone who could get hyperacute transplant rejection.
Previous transfusion; pregnant woman whose fetus had paternal antigens
No because no peptide fragment!
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
cannot cross placenta

48. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Cells that stil have weird parts of their membrane that macrophages usually bite off
heavy chains
IL 3; supports growth and differentiation of bone marrow stem cells
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

49. What are the autoantibodies for sjorgens syndrome?
MHC class molecules bind to KIRS or CD94 to prevent killing
Anti SS- A (anti RO) and Anti SS- B
Receiving preformed Antibodies
Anti alpha subunit 3 of collagen on type IV bm

50. where are complements produced?
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
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
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
Liver! (they are proteins circulating in the blood)

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USMLE Step 1 Immunology

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