Test your basic knowledge |

USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

Instructions:

Answer 50 questions in 15 minutes.
If you are not ready to take this test, you can study here.
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. What are the cell surface proteins for Macrophages? which two are for opsonins?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Alternative splicing of mRNA
IL 3; supports growth and differentiation of bone marrow stem cells
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

2. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
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
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
...
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

3. A lymph node is a ________ lymphoid organ.
Previous transfusion; pregnant woman whose fetus had paternal antigens
Hemochromatosis
Fab portion
secondary

4. Which disease is associated with HLA A3?
Hemochromatosis
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
IL 15; IL 12 - interferon Beta and interferon alpha
dimer

5. 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
IgM
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
A chemotactic factor for neutrophils

6. How does complement link innate and adaptive?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
delayed!
type four
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

7. What is digoxin immune Fab used for?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
B - T - and NK cells
Antidote for digoxin intoxication
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

8. What does IL 2 do?
NK cells
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Activates cytotoxic CD 8 T cells as second signal

9. what happens in a deficiency of C1 esterase inhibitor? DAF?
NK cells
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Hereditary angioedema; PNH

10. What are the autoantibodies for polymyositis and dermatomyositis?
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
CD21 on B cells (although there is T cell lymphocytosis in EBV)
If there is class switching and plasma cell production (that is when memory cells are produced)
Anti Jo -1

11. 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?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
except hyperacute
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

12. Which diseases are associated with DR4?
Th2; Th1
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
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
DM type I and RA

13. What bugs can actually infect the lymph node itself?
CD56
All MHC 1/CD8
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

14. What are the autoantibodies for drug induced lupus?
Carbohydrate
Pernicious Anemia and Hashimotos
Antihistone
except hyperacute

15. Give three examples of bacteria that use antigenic variation and how.
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
IgM
T cell activation; no with CD 4 or CD 8
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

16. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
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
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!

17. what results in symptoms of shock in an acute hemolytic transfusion reaction?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Superior mesenteric

18. What type of side chains are found on Fc region of an antibody?
Carbohydrate
Humoral
Hereditary angioedema; PNH
T

19. What are superantigens? give two examples.
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Not thymus - BM
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
Superficial inguinal

20. 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
C5a
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

21. How is sirolimus different from tacrolimus?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Previous transfusion; pregnant woman whose fetus had paternal antigens
heavy chains
Immunosuppression after kidney transplantation

22. What is serum sickness? give an example.
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
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
MHC II - B7
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

23. Name two endogenous pyrogens
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
IL 1 and IL 6
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
2 heavy chains and two light chains

24. What is the treatment of acute transplant rejection?
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
IgE; by activating eosinophils
Activates Th1 helper cells; Macrophages
Cyclosporine - OKT3

25. IgM can fix complement but...
Liver! (they are proteins circulating in the blood)
cannot cross placenta
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
TGF beta and IL 10

26. What is the pathogenesis of a hypersensitivity reaction?
Superficial inguinal
Superficial inguinal
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

27. What are the autoantibodies for Mixed connective tissue disease?
MS - hay fever - SLE - goodpastures
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Anti U1 RNP (ribonucleoprotein)
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

28. What are the main symptoms of B cell immunodeficiencies?
IL 4
MHC I; from RER with help of the B2 microglobulin
mesenchymal
SP infections

29. What is the presentation of common variable immunodef? and What are the labs?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Superior mesenteric
T cell dysfunction
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

30. What is the main function of interferons?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Cells that stil have weird parts of their membrane that macrophages usually bite off
Sinusitis - otitis media - pneumonia

31. What are the autoantibodies for hashimotos?
Th2; Th1
Antimicrosomal and antithyroglobulin
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
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

32. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Complement activation (active in both)
Its main effect is a defect in Ab opsonization for killing
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

33. Which type of selection of thymic development provides central tolerance?
If there is class switching and plasma cell production (that is when memory cells are produced)
Negative selection
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Chronic granulomatous disease

34. The alternative pathway is the only constutively...
active complement pathway
Stimulate the liver to release acute phase reactants
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
CD56

35. What cytokines are released by Th1 cells?
Interferon gamma and IL 2
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
heavy chains
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

36. 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?
Para aortic
pentamer
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
Fc

37. IgE has the ___________ in the serum
T cell activation; no with CD 4 or CD 8
cannot cross placenta
lowest concentration
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

38. What are the labs in brutons agammaglobulinemia?
Its main effect is a defect in Ab opsonization for killing
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
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
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

39. What is recomb alpha interferon used for?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Cyclosporine - OKT3
Axillary
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

40. Which diseases are associated with DR5?
Activates cytotoxic CD 8 T cells as second signal
Anemias (esp due to renal failure)
Pernicious Anemia and Hashimotos
Immunosuppression after kidney transplantation

41. Which HLA's are included in MHC I? MHC II?

Warning: Invalid argument supplied for foreach() in /var/www/html/basicversity.com/show_quiz.php on line 183

42. What is the white pulp of the spleen?
Anti viral and anti tumor
Wiskott Aldrich syndrome
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
T cell activation; no with CD 4 or CD 8

43. The idiotype; the Fc portion determines the...
pentamer
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
isotype
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

44. What is recomb gamma interferon used for?
Anti topoisomerase
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Histamine; post capillary venules - vasodilation
Chronic granulomatous disease

45. What is the common variable immunodeficiency ? How is it different from Brutons?
cannot cross placenta
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
...
CD21 on B cells (although there is T cell lymphocytosis in EBV)

46. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Its a serine protease that activates apoptosis; NK and CD8
pathogenesis
...

47. what characterizes an arthus reaction?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Edema and necrosis in that region
Immunoflourescent staining of tissue biopsies
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

48. other than eat and bite RBCs what else do Macrophages of spleen do>
Thrombocytopenia
pathogenesis
Paracortex; viral infection
Remove encapsulated bacateria

49. What are the two signals to kill for NK cells?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Alternative splicing of mRNA
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
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

50. What is the pathogenesis of a candida skin test?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Delayed type hypersensitivity
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
MHC class molecules bind to KIRS or CD94 to prevent killing