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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.
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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. which of the hypersensitivity reactions is not Ab mediated?
Lymphocytes
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
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Type IV

2. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
pentamer
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
IgM and IgA

3. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
It is a localized type III hypersensitivity reaction to an external antigen; localized instead of systemic; ?; intradermal injection of the antigen results in antibody production and antigen antibody complexes deposit in the skin
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
Negative nitroblue tetrazolium reduction test
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!

4. What is epo used for?
Anti viral and anti tumor
cannot cross placenta
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 :(
Anemias (esp due to renal failure)

5. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
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
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Bind FcG for antibody dependent cellular cytotoxicity
Macrophages - Dendritic cells - B cells

6. How does complement link innate and adaptive?
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
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
S. aureus - E. Coli - aspergillus
Anti SS- A (anti RO) and Anti SS- B

7. How does the alternative pathway lead to MAC activation?
Activates Th1 helper cells; Macrophages
IL 1 and IL 6
Interferon gamma; Th1
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

8. Name the three opsonins
Superior mesenteric
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
CRP - C3b - IgM
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

9. What is the marginal zone of the spleen? what happens there?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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
Interferon gamma and IL 2
Anti smooth muscle

10. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
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
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
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
Viral neutralization of igM and IgG!

11. 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?
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
not Ab mediated
Carbohydrate
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

12. can igG cross the placenta?
lowest concentration
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Yes
Glycoproteins; HLA

13. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
Steroid responsive nephrotic syndrome
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 :(
delayed!
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

14. 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)?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Graves
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
acute phase reactants

15. What are superantigens? give two examples.
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
No because no peptide fragment!
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
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

16. How fast does it occur?
Cyclosporine - OKT3
The patient could become cyanotic in the OR!
T cell precursor
An acidified endosome with the antigen fuses with the MHC which causes the release of the invariant chain Which is sitting in spot of antigen and stabilizing the MHC II

17. What are C1 - C2 - C3 - C4 important for?
A recomb cytokine of IL 2; RCC and metastatic melanoma
Kill them because they have CD16 on them that recognize the FcG portion
Viral neutralization of igM and IgG!
If there is class switching and plasma cell production (that is when memory cells are produced)

18. describe the pathogenesis of delayed type IV hypersensitivity
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
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
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Antimicrosomal and antithyroglobulin

19. What are the two signals required for T cells? what happens after?
active complement pathway
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Kill them because they have CD16 on them that recognize the FcG portion
Paracortex; viral infection

20. What is Aldesleukin? What is it used for
A recomb cytokine of IL 2; RCC and metastatic melanoma
Lymphocytes
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
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

21. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
All MHC 1/CD8
Negative!
MHC class molecules bind to KIRS or CD94 to prevent killing

22. How is the antigen loaded onto a MHC II?
The patient could become cyanotic in the OR!
An acidified endosome with the antigen fuses with the MHC which causes the release of the invariant chain Which is sitting in spot of antigen and stabilizing the MHC II
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Anemias (esp due to renal failure)

23. What is the most common selective Ig deficiency? What is the presentation?
Stimulate the liver to release acute phase reactants
Lymphocytes
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
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

24. What is serum sickness? give an example.
Recom IL 11; thrombocytopenia
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
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
Carbohydrate

25. give an example of how influenza does a major antigenic shift.
RNA segment reassortment
Active; passive - fast but short half life (3 weeks!)
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
Anti IF

26. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
carboxy terminal
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
IgM and IgA
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

27. Which cytokines do Th2 release and For what?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
IL 5
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

28. How do you test for type III hypersensitivity?
Immunoflourescent staining of tissue biopsies
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
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

29. is IgM an opsonizer?
not Ab mediated
For some reason a mature naive B lymphocyte got away from tolerance and the result was a production an Ab on its surface with an Fab region that recognized the alpha 3 collagen subunit on the BM as non self. It then gets activated by a Th2 cell (enti
IgE
Negative!

30. what ensure that a memory response is generated?
IL 3; supports growth and differentiation of bone marrow stem cells
CRP - C3b - IgM
DM type I and RA
If there is class switching and plasma cell production (that is when memory cells are produced)

31. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
secondary
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Superficial inguinal

32. Describe the complement independent Type II hypersenstivity reaction. Give an example.
Macrophages - Dendritic cells - B cells
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
In the germinal center of secondary follicles (In the paler center)

33. What does granulysin do?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

34. what prevents NK cells from killing normal cells if their default is to kill?
Anti mitochondrial
DM type I
Basophils! THey want IG E class switch!
MHC class molecules bind to KIRS or CD94 to prevent killing

35. Which diseases are associated with DR5?
Pernicious Anemia and Hashimotos
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
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
Alternative splicing of mRNA

36. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Superior mesenteric
Superficial inguinal

37. What lymph node drains the thigh?
CRP - C3b - IgM
Its main effect is a defect in Ab opsonization for killing
Viral neutralization of igM and IgG!
Superficial inguinal

38. What is the main function of IL 8?
A chemotactic factor for neutrophils
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Cytokine IL 10 secreted by Th2
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

39. What is the most common example of passive immunity?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
IgAs in mothers breast milk!

40. What does IgA pick up from epithelial cells before being secreted?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Secretory component
Cytokine IL 10 secreted by Th2
active complement pathway

41. What lymph node drains the lateral side of the dorsum of the foot?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Popliteal
Pernicious Anemia and Hashimotos

42. What is the receptor for EBV? On what cells is that located?
Negative nitroblue tetrazolium reduction test
Aut. Dominant; C1 esterase inhibitor deficiency resulting in continued C1 which results in increased C2 and C4 cleavage products which have anaphyltoxic activity and result in swelling of face and oropharynx
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

43. where are complements produced?
Liver! (they are proteins circulating in the blood)
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
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
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

44. 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
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Increases expression of MHC I and MHC II and also activates NK cells
Glycoproteins; HLA

45. What happens in a secondary follicle?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
It is a localized type III hypersensitivity reaction to an external antigen; localized instead of systemic; ?; intradermal injection of the antigen results in antibody production and antigen antibody complexes deposit in the skin
MHC II - B7

46. what characterizes an arthus reaction?
Edema and necrosis in that region
IL 5
heavy chains
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

47. What does interferon gamma do? What two type of cells does it attack mostly?
Immunosuppression after kidney transplantation
IgG
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Activates Th1 helper cells; Macrophages

48. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Anti glutamate carboxylase and anti insulin
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
IgM and IgD

49. in which immunodef order do you see a lot of pus? no pus?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
active complement pathway
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Interferon gamma and IL 2

50. which interleukin receptor is required for NK development? activation?
IL 15; IL 12 - interferon Beta and interferon alpha
IL 1 and IL 6
Paracortex; viral infection
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening