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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 MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Glycoproteins; HLA
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Edema and necrosis in that region

2. How does complement link innate and adaptive?
Chronic granulomatous disease
Fab portion
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
IgG

3. What are howell jolly bodies?
RNA segment reassortment
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
encapsulated
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

4. What is the cause of thymic aplasia? What is its presentation? What are the labs?
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
Complement activation (active in both)
All MHC 1/CD8
Activates Th1 helper cells; Macrophages

5. What is recomb beta interferon used for?
Anti TSh receptor
MS
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Activates cytotoxic CD 8 T cells as second signal

6. The ______ in the BM are DN - the DP are in the cortex of thymus
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
T cell precursor
Barrel hoop basement membrane fenestrations
Cytokine IL 10 secreted by Th2

7. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
type four
A recomb cytokine of IL 2; RCC and metastatic melanoma
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

8. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Graves
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
except hyperacute
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

9. what ensure that a memory response is generated?
T cell precursor
If there is class switching and plasma cell production (that is when memory cells are produced)
T
IL 15; IL 12 - interferon Beta and interferon alpha

10. What are the cell surface proteins on NK cells?
Tetanus - Botulinum - HBV - Rabies
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
secondary
MHC I - CD16 - CD56

11. what cell surface proteins are on all APCs?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Antibody mediated cytotoxicity; either complement dependent or complement independent
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
MHC II - B7

12. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Superficial inguinal
Its main effect is a defect in Ab opsonization for killing
...
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)

13. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
A recomb cytokine of IL 2; RCC and metastatic melanoma
Fc
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

14. What bugs can actually infect the lymph node itself?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
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
Th2; Th1

15. What lymph node drains the anal canal (below the pectinate line)?
Immunosuppression after kidney transplantation
Sinusitis - otitis media - pneumonia
TLR ad nuclear receptors
Superficial inguinal

16. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
DM type I and RA
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
Anti SS- A (anti RO) and Anti SS- B
MHC class molecules bind to KIRS or CD94 to prevent killing

17. What does CD16 on NK cells do?
A j chain
IL 3; supports growth and differentiation of bone marrow stem cells
Immunoflourescent staining of tissue biopsies
Bind FcG for antibody dependent cellular cytotoxicity

18. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Interferon gamma and IL 2
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Activates Th1 helper cells; Macrophages
IL 5

19. What is the most common example of passive immunity?
IgM and IgA
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
IgAs in mothers breast milk!
CD56

20. What lymph node drains the testes?
Para aortic
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Carbohydrate

21. A lymph node is a ________ lymphoid organ.
secondary
Acts as second signal on B cells to induce class switching to IgE and IgG
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

22. hat is the presentation of Jobs syndrome or Hyper IgE?
The igA found in breast milk
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
MHC I - CD16 - CD56
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

23. The Fc region is found on the...
carboxy terminal
The patient could become cyanotic in the OR!
A chemotactic factor for neutrophils
No because no peptide fragment!

24. What is the main function of IL 8?
A chemotactic factor for neutrophils
isotype
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

25. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
Local infection/inflammation; infection of the ln itself; metastasis
Hereditary angioedema; PNH
IgE; by activating eosinophils
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

26. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
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
Influenza; antigenic shift; antigenic drift
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

27. Complements are...
acute phase reactants
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
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

28. Which helper T cells' development is induced by IL 4? IL 12?
Th2; Th1
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Negative!

29. What are the autoantibodies for other vasculitides?
Interferon gamma and IL 2
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
T cell dysfunction

30. Give an example of someone who could get hyperacute transplant rejection.
delayed!
Previous transfusion; pregnant woman whose fetus had paternal antigens
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

31. The alternative pathway is the only constutively...
C5a
active complement pathway
TLR ad nuclear receptors
Anti TSh receptor

32. What is the presentation of Brutons agammaglobulinemia?
If there is class switching and plasma cell production (that is when memory cells are produced)
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
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
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

33. What do multimeric antibodies require for assembly?
A j chain
When you select for which MHC it will have; take out the lymphs that self react
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!
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

34. What are the autoantibodies for Celiac disease?
MS - hay fever - SLE - goodpastures
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

35. What is the autoantibody for SLE that is nonspecific? Specific?
MHC class molecules bind to KIRS or CD94 to prevent killing
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
Its a serine protease that activates apoptosis; NK and CD8
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

36. what mediates the type II hypersensitivity? What are the two different methods?
Kill them because they have CD16 on them that recognize the FcG portion
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
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)
Antibody mediated cytotoxicity; either complement dependent or complement independent

37. Which is the main antibody in the delayed or secondary response to an antigen?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Previous transfusion; pregnant woman whose fetus had paternal antigens
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
IgG

38. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Rheumatic arthritis
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
Fab portion
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

39. What is the presentation of scid? treatment?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Anti SS- A (anti RO) and Anti SS- B
All MHC 1/CD8
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

40. What are the function of B cells?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Active; passive - fast but short half life (3 weeks!)
B - T - and NK cells

41. What is the toxicity of azathioprine?
Basophils! THey want IG E class switch!
...
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
pentamer

42. Which type of selection of thymic development provides central tolerance?
acute phase reactants
Local infection/inflammation; infection of the ln itself; metastasis
Negative selection
opsonizes

43. IgG...
Pernicious Anemia and Hashimotos
Carbohydrate
opsonizes
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

44. 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?
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
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
opsonizes
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

45. Name 5 ways Antibody diversity is generated?
IgG
Immunoflourescent staining of tissue biopsies
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
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

46. What lymph node drains the stomach?
MHC I - CD16 - CD56
Celiac
Complement activation (active in both)
Its main effect is a defect in Ab opsonization for killing

47. give an example of how influenza does a major antigenic shift.
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Immunosuppression after kidney transplantation
RNA segment reassortment

48. what cytokine does basophils secrete?
opsonizes
IL 4
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
type four

49. What are the major functions of Antibodies?
Histamine; post capillary venules - vasodilation
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Chronic granulomatous disease
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

50. What are the labs in brutons agammaglobulinemia?
Antimicrosomal and antithyroglobulin
Antidesmoglein
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class