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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

Instructions:

Answer 50 questions in 15 minutes.
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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 howell jolly bodies?
pathogenesis
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Viral neutralization of igM and IgG!
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

2. which cytokine inhibits TH2 cells? secreted by who?
Interferon gamma; Th1
Activates cytotoxic CD 8 T cells as second signal
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
Rheumatic arthritis

3. What are the autoantibodies for myasthenia gravis?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Basophils! THey want IG E class switch!
Anti Ach receptor
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

4. What are the autoantibodies for pemphigus bulgaris?
Its a serine protease that activates apoptosis; NK and CD8
CRP - C3b - IgM
Activate macrophages
Antidesmoglein

5. What is the main function of IL 12? other than macrophages who else can release IL 12?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Antibody mediated cytotoxicity; either complement dependent or complement independent

6. what will NK cells do to cells covered in IgG Ab? why?
Antihistone
TLR ad nuclear receptors
Cyclosporine - OKT3
Kill them because they have CD16 on them that recognize the FcG portion

7. What is the presentation of Brutons agammaglobulinemia?
IgM and IgA
Hemochromatosis
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Cytokine IL 10 secreted by Th2

8. What is thrombopoietin used for?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Thrombocytopenia
Lymphocytes

9. Which cytokines do Th2 release and For what?
IgAs in mothers breast milk!
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Steroid responsive nephrotic syndrome
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

10. What happens when a T helper cell in the paracortical section encounters an antigen? a cytotoxic t cell? a B cell in the cortical section?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
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
cannot cross placenta
Humoral

11. T/F B cells do not require a second signal
Anti glutamate carboxylase and anti insulin
Fab portion
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
False! B cell class switching requires a second signal

12. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Para aortic
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

13. 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?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
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
Antibody mediated cytotoxicity; either complement dependent or complement independent
Complement activation (active in both)

14. What is the toxicity of azathioprine?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Inferior mesenteric
...
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

15. What does it mean if there are igM in the serum at birth?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
IgE; by activating eosinophils
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

16. Which disease is associated with B8?
Interferon gamma; Th1
Graves
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
Barrel hoop basement membrane fenestrations

17. What is three common causes of severe combined immunodef? What is the result of all three?
IgA
Superficial inguinal
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Secretory component

18. which type of immunity is slow but long lasting? as opposed to...
Active; passive - fast but short half life (3 weeks!)
IL 4
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

19. In general What are T cells good for?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Type IV
Anti viral and anti tumor
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

20. What are the major functions of Antibodies?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Inferior mesenteric
A chemotactic factor for neutrophils
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

21. what mediates the type II hypersensitivity? What are the two different methods?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Antibody mediated cytotoxicity; either complement dependent or complement independent
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
Influenza; antigenic shift; antigenic drift

22. What is filgrastim and sargramostim? and What is it used for?
Anti IF
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
RNA segment reassortment
By transcytosis

23. where do somatic hypermutation and class switching occur?
acute phase reactants
secondary
In the germinal center of secondary follicles (In the paler center)
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

24. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Cyclosporine - OKT3
The igA found in breast milk

25. What are MHC's necessary for? By themselves?
T cell activation; no with CD 4 or CD 8
Steroid responsive nephrotic syndrome
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

26. What are the autoantibodies for hashimotos?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
TGF beta and IL 10
Antimicrosomal and antithyroglobulin
MHC I; from RER with help of the B2 microglobulin

27. 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?
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
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
In the germinal center of secondary follicles (In the paler center)

28. What are the autoantibodies for other vasculitides?
TGF beta and IL 10
No because no peptide fragment!
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

29. What does CD16 on NK cells do?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Barrel hoop basement membrane fenestrations
Celiac
Bind FcG for antibody dependent cellular cytotoxicity

30. IgE has the ___________ in the serum
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
lowest concentration
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Negative selection

31. What can cause a lymph node enlargement?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
IgM and IgA
If there is class switching and plasma cell production (that is when memory cells are produced)
Local infection/inflammation; infection of the ln itself; metastasis

32. give an example of how influenza does a major antigenic shift.
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
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
IL 3; supports growth and differentiation of bone marrow stem cells
RNA segment reassortment

33. What are the T cell functions?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Pernicious Anemia and Hashimotos
Cytokine IL 10 secreted by Th2
active complement pathway

34. What is anergy? why does this occur?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
IgM and IgA
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

35. what bacteria are a splenectomy patient most susceptible to? why?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Axillary
TLR ad nuclear receptors
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

36. what results in symptoms of shock in an acute hemolytic transfusion reaction?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
TGF beta and IL 10
type four
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

37. What are C1 - C2 - C3 - C4 important for?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Wiskott Aldrich syndrome
Viral neutralization of igM and IgG!
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

38. What type of side chains are found on Fc region of an antibody?
Fc
Carbohydrate
...
opsonizes

39. IgM can exist as a _______ also
IL 4
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
pentamer
If there is class switching and plasma cell production (that is when memory cells are produced)

40. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
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
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
Type IV
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

41. What is the general structure of an Ab?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
2 heavy chains and two light chains
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Its a serine protease that activates apoptosis; NK and CD8

42. What links the adaptive and innate immunity?
IgE
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
S. aureus - E. Coli - aspergillus
Complement activation (active in both)

43. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Sinusitis - otitis media - pneumonia
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

44. Which helper T cells' development is induced by IL 4? IL 12?
Th2; Th1
Superior mesenteric
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
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

45. Which is the most abundant antibody in blood?
IgG
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
acute phase reactants
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

46. What is the autoantibody for SLE that is nonspecific? Specific?
The patient could become cyanotic in the OR!
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
IL 3; supports growth and differentiation of bone marrow stem cells

47. To what portion of the Antibody do the complements bind?
Fc
Hereditary angioedema; PNH
Its main effect is a defect in Ab opsonization for killing
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

48. Describe the Mannose Lectin pathway
TGF beta and IL 10
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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
TNF alpha and IL1

49. What is the pathogenesis of a candida skin test?
Delayed type hypersensitivity
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
type four
MS - hay fever - SLE - goodpastures

50. Monomer in circulation - ___ when secreted
Antibody mediated cytotoxicity; either complement dependent or complement independent
dimer
IL 15; IL 12 - interferon Beta and interferon alpha
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.