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 is the end result of complement activation? what bugs are this important for? through what pathway and why?
Complement activation (active in both)
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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
Anti Ach receptor

2. What is the main cytokine released by T cells? What does it do
IL 3; supports growth and differentiation of bone marrow stem cells
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
B - T - and NK cells
IL 4

3. What are the autoantibodies for graves?
Anti TSh receptor
Basophils! THey want IG E class switch!
Anti smooth muscle
Daclizumab; prevent ACUTE rejection of renal transplant

4. Which is the main antibody that provides passive immunity to infants?
IgE
By transcytosis
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
IgG

5. Type IV hypersensitivity is i...
Anti Jo -1
not Ab mediated
In the germinal center of secondary follicles (In the paler center)
Activate macrophages

6. What lymph node drains the stomach?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Anti glutamate carboxylase and anti insulin
Celiac
False! B cell class switching requires a second signal

7. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
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
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Influenza; antigenic shift; antigenic drift
Superior mesenteric

8. What are MHC's necessary for? By themselves?
secondary
IgA
Daclizumab; prevent ACUTE rejection of renal transplant
T cell activation; no with CD 4 or CD 8

9. What is chronic mucocutaneous candidiasis d/t?
T cell dysfunction
Negative!
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
CD56

10. In thymic development - What is the positive selection? negative selections?
Fab portion
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
When you select for which MHC it will have; take out the lymphs that self react
Its main effect is a defect in Ab opsonization for killing

11. What are the two signals required for Th1 cells? what happens after then activated?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Fc
MHC class molecules bind to KIRS or CD94 to prevent killing
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

12. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
lowest concentration
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

13. What are the autoantibodies for pernicious anemia?
When you select for which MHC it will have; take out the lymphs that self react
Anti IF
Negative nitroblue tetrazolium reduction test
IgM and IgG

14. where do somatic hypermutation and class switching occur?
Liver! (they are proteins circulating in the blood)
Hereditary angioedema; PNH
In the germinal center of secondary follicles (In the paler center)
Anti U1 RNP (ribonucleoprotein)

15. What are the autoantibodies for polymyositis and dermatomyositis?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Inferior mesenteric
Anti Jo -1

16. What is the common variable immunodeficiency ? How is it different from Brutons?
cannot cross placenta
MHC II - B7
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
Paracortex

17. What are the two signals to kill for NK cells?
Negative nitroblue tetrazolium reduction test
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

18. What is the pathogenesis of a hypersensitivity reaction?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Interferon gamma and IL 2
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
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

19. 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?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
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
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Anti topoisomerase

20. What does granzyme do? who secretes it?
Barrel hoop basement membrane fenestrations
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Its a serine protease that activates apoptosis; NK and CD8
pathogenesis

21. What does interferon gamma do? What two type of cells does it attack mostly?
Anti topoisomerase
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
IgAs in mothers breast milk!
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

22. What is the autoantibody for SLE that is nonspecific? Specific?
Humoral
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
IgE
MS - hay fever - SLE - goodpastures

23. Describe the Mannose Lectin pathway
IgAs in mothers breast milk!
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
IL 1 and IL 6
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

24. What bugs can actually infect the lymph node itself?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
A j chain
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

25. 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?
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
Paracortex
Yes
C5a

26. What is the late phase reaction of anaphylaxis allergy? what mediates it?
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
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)
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

27. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
IgM and IgD
Cells that stil have weird parts of their membrane that macrophages usually bite off

28. What are superantigens? give two examples.
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
T
...
heavy chains

29. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
MHC II - B7
Cross link
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
not Ab mediated

30. what secretes IL 4?
Basophils! THey want IG E class switch!
Glycoproteins; HLA
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

31. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
A recomb cytokine of IL 2; RCC and metastatic melanoma
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
Local infection/inflammation; infection of the ln itself; metastasis

32. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
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
DM type I
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
IgG

33. What is the main function of IL 8?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Active; passive - fast but short half life (3 weeks!)
A chemotactic factor for neutrophils
Its main effect is a defect in Ab opsonization for killing

34. The Fc region is found on the...
secondary
Lymphocytes
False! B cell class switching requires a second signal
carboxy terminal

35. what mediates the type II hypersensitivity? What are the two different methods?
isotype
Antibody mediated cytotoxicity; either complement dependent or complement independent
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
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!

36. What are the autoantibodies for autoimmune hepatitis?
Immunoflourescent staining of tissue biopsies
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Anti smooth muscle

37. Which antibodies can be multimeric?
IgM and IgA
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Increases expression of MHC I and MHC II and also activates NK cells
SP infections

38. What are the main cell surface proteins on B cells?
No because no peptide fragment!
Superficial inguinal
acute phase reactants
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

39. in which immunodef order do you see a lot of pus? no pus?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
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
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

40. What is the most common selective Ig deficiency? What is the presentation?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Antibody mediated cytotoxicity; either complement dependent or complement independent
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
...

41. What are C1 - C2 - C3 - C4 important for?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Viral neutralization of igM and IgG!

42. What is a type I hypersensitivity reaction? What is atopic?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
In the germinal center of secondary follicles (In the paler center)
Anti topoisomerase
opsonizes

43. How does igA cross the epithelium?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
In the germinal center of secondary follicles (In the paler center)
By transcytosis
MHC I; from RER with help of the B2 microglobulin

44. In general What are T cells good for?
Negative selection
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Anti viral and anti tumor

45. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Celiac
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
IgA
Activates Th1 helper cells; Macrophages

46. How do you test for type III hypersensitivity?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Immunoflourescent staining of tissue biopsies
T cell activation; no with CD 4 or CD 8
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

47. What is colostrum?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
T cell activation; no with CD 4 or CD 8
The igA found in breast milk

48. What are the autoantibodies for systemic sclerosis?
IgG
Anti topoisomerase
...
neutrophilia!

49. Name 5 ways Antibody diversity is generated?
Superior mesenteric
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
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Glycoproteins; HLA

50. What is the presentation of Brutons agammaglobulinemia?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
TNF alpha and IL1
Hereditary angioedema; PNH
Anti alpha subunit 3 of collagen on type IV bm