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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. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Receiving preformed Antibodies
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Cells that stil have weird parts of their membrane that macrophages usually bite off
RNA segment reassortment

2. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
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
IgG
Antibody mediated cytotoxicity; either complement dependent or complement independent
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

3. Which disease is associated with DR3?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Hereditary angioedema; PNH
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
DM type I

4. What is the marginal zone of the spleen? what happens there?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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
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

5. What links the adaptive and innate immunity?
Complement activation (active in both)
Not thymus - BM
T
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

6. Which diseases are associated with DR5?
Pernicious Anemia and Hashimotos
IL 4
Th2; Th1
RNA segment reassortment

7. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Chronic granulomatous disease
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Not thymus - BM
MHC II - B7

8. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
Superficial inguinal
except hyperacute
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
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

9. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
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
Recom IL 11; thrombocytopenia
Celiac

10. which antibody is involved in the primary response or immediate response to an antigen?
Superficial inguinal
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
A - B - C; all the D's
IgM

11. which cytokine inhibits TH2 cells? secreted by who?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Interferon gamma; Th1
T cell precursor
When you select for which MHC it will have; take out the lymphs that self react

12. What is thrombopoietin used for?
Antidote for digoxin intoxication
C5a
Macrophages - Dendritic cells - B cells
Thrombocytopenia

13. What is Aldesleukin? What is it used for
A recomb cytokine of IL 2; RCC and metastatic melanoma
Inferior mesenteric
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
RNA segment reassortment

14. What is three common causes of severe combined immunodef? What is the result of all three?
T cell precursor
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
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

15. What lymph node drains the breast?
Axillary
Macrophages - Dendritic cells - B cells
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
Histamine; post capillary venules - vasodilation

16. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Severe pyogenic infections early in life
Local infection/inflammation; infection of the ln itself; metastasis
TNF alpha and IL1
Activates Th1 helper cells; Macrophages

17. What is the clinical use for azathioprine?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Lymphocytes
...

18. which of the hypersensitivity reactions is not Ab mediated?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
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
Bind FcG for antibody dependent cellular cytotoxicity
Type IV

19. What are the major functions of Antibodies?
IgM
opsonizes
Cytokine IL 10 secreted by Th2
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

20. What is the presentation of Brutons agammaglobulinemia?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
IL 15; IL 12 - interferon Beta and interferon alpha
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

21. What is the pathogenesis of a hypersensitivity reaction?
B - T - and NK cells
Barrel hoop basement membrane fenestrations
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
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

22. 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?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
MHC I - CD16 - CD56
IgM and IgA

23. What are the autoantibodies for pemphigus bulgaris?
Influenza; antigenic shift; antigenic drift
Antidesmoglein
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
isotype

24. So antibodies are the effectors for the humoral response. List some of their functions.
Superficial inguinal
IgAs in mothers breast milk!
MHC class molecules bind to KIRS or CD94 to prevent killing
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

25. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Graves
TGF beta and IL 10
...

26. What are the function of B cells?
Activates cytotoxic CD 8 T cells as second signal
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

27. Describe the complement independent Type II hypersenstivity reaction. Give an example.
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
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
Kill them because they have CD16 on them that recognize the FcG portion

28. What lymph node drains the duodenum - jejunum?
...
Superior mesenteric
Kill them because they have CD16 on them that recognize the FcG portion
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

29. which cells have more complete tolerance - B or T cells?
T
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
DM type I
Anti viral and anti tumor

30. What is the presentation of scid? treatment?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Fab portion
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
pale central germinal centers

31. What is the pathogenesis of a candida skin test?
Yes
Delayed type hypersensitivity
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
IgG

32. Describe the capsular structure of a lymph node; What are the functions of the LN?
Macrophages - Dendritic cells - B cells
neutrophilia!
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
Acts as second signal on B cells to induce class switching to IgE and IgG

33. what cytokine does basophils secrete?
IL 4
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
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

34. What lymph node drains the thigh?
Activates Th1 helper cells; Macrophages
MS - hay fever - SLE - goodpastures
Superficial inguinal
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

35. In general What are T cells good for?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Anti viral and anti tumor
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
Remove encapsulated bacateria

36. How fast does it occur?
The patient could become cyanotic in the OR!
Steroid responsive nephrotic syndrome
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Anti alpha subunit 3 of collagen on type IV bm

37. What is recomb alpha interferon used for?
Cyclosporine - OKT3
Basophils! THey want IG E class switch!
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
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

38. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T 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
IgE; by activating eosinophils
Popliteal

39. Which is the main antibody that provides passive immunity to infants?
IgG
Increases expression of MHC I and MHC II and also activates NK cells
TLR ad nuclear receptors
Carbohydrate

40. What are the labs in brutons agammaglobulinemia?
IL 15; IL 12 - interferon Beta and interferon alpha
Antibody mediated cytotoxicity; either complement dependent or complement independent
Histamine; post capillary venules - vasodilation
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

41. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Anti smooth muscle
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Anti topoisomerase

42. What are the autoantibodies for pernicious anemia?
Negative!
Anti IF
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
TLR ad nuclear receptors

43. describe the pathogenesis of delayed type IV hypersensitivity
Cells that stil have weird parts of their membrane that macrophages usually bite off
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Severe pyogenic infections early in life
Secretory component

44. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Axillary
TNF alpha and IL1
Severe pyogenic infections early in life
Th cells fail to produce interferon gamma; a lot of IgE

45. What is the clinical use for sirolimus? what should you combine it with?
IL 5
TLR ad nuclear receptors
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)
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

46. 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?
Celiac
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
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Anti glutamate carboxylase and anti insulin

47. What is hereditary angioedema? What are the C3 levels?
Th cells fail to produce interferon gamma; a lot of IgE
MS - hay fever - SLE - goodpastures
Chronic granulomatous disease
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

48. What is the pathogenesis of acute transplant rejection? When does it occur?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Activates cytotoxic CD 8 T cells as second signal
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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

49. What do multimeric antibodies require for assembly?
acute phase reactants
IgE; by activating eosinophils
Immunoflourescent staining of tissue biopsies
A j chain

50. What are the two signals required for Th1 cells? what happens after then activated?
dimer
No because no peptide fragment!
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Anti mitochondrial