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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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1. 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?
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
When you select for which MHC it will have; take out the lymphs that self react
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
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

2. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Fab portion
Severe pyogenic infections early in life
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

3. What is the main function of interferons?
MS - hay fever - SLE - goodpastures
Inferior mesenteric
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
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

4. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Activate macrophages
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
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

5. 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?
acute phase reactants
Fc
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
Interferon gamma; Th1

6. What are the autoantibodies for autoimmune hepatitis?
Paracortex
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Anti smooth muscle
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

7. What is the most common selective Ig deficiency? What is the presentation?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
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
RNA segment reassortment
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

8. which of the transplant rejections is antibody mediated? why does it occur?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
active complement pathway
T
Macrophages - Dendritic cells - B cells

9. To what disease do the autoantibodies to IgG (rheumatoid factor)?
acute phase reactants
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Rheumatic arthritis
Superficial inguinal

10. What is Aldesleukin? What is it used for
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
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
A recomb cytokine of IL 2; RCC and metastatic melanoma
T cell precursor

11. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
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
Popliteal
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

12. which cytokine inhibits TH2 cells? secreted by who?
Superior mesenteric
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Interferon gamma; Th1
type four

13. which antibodies prevent antigens from binding mucosal surfaces?
Para aortic
Type IV
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
IgA

14. What are the symptoms of serum sickness?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Anemias (esp due to renal failure)
A chemotactic factor for neutrophils

15. Which MHC presents intracellular peptides? how so?
Celiac
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
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
MHC I; from RER with help of the B2 microglobulin

16. What does granzyme do? who secretes it?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Its a serine protease that activates apoptosis; NK and CD8
Pernicious Anemia and Hashimotos

17. What is the mechanism for sirolimus? what else it known as?
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
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Receiving preformed Antibodies
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

18. What are the two signals to kill for NK cells?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
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
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Axillary

19. What does it mean if there are igM in the serum at birth?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
IgM
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Negative!

20. What are the two signals required for T cells? what happens after?
Th cells fail to produce interferon gamma; a lot of IgE
MHC II - B7
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

21. What is the pathogenesis of a candida skin test?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Delayed type hypersensitivity
Cyclosporine - OKT3

22. What is the pathogenesis of a hypersensitivity reaction?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
CD56
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

23. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
2 heavy chains and two light chains
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
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
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

24. What happens in a secondary follicle?
Antidote for digoxin intoxication
Bind FcG for antibody dependent cellular cytotoxicity
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
IgM and IgA

25. The Fc region is found on the...
Hemochromatosis
Complement activation (active in both)
delayed!
carboxy terminal

26. How is the thymus organized? what happens in each section?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Anemias (esp due to renal failure)
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
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

27. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
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
Th2; Th1
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
carboxy terminal

28. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
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
MS - hay fever - SLE - goodpastures
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

29. __________ are a part of the innate system.
Its a serine protease that activates apoptosis; NK and CD8
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
NK cells
Carbohydrate

30. What is the pathology in hyperacute transplant rejection?
2 heavy chains and two light chains
IgE
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
dimer

31. What does granulysin do?
IgA
Negative nitroblue tetrazolium reduction test
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

32. Which diseases are associated with DR2?
acute phase reactants
secondary
MS - hay fever - SLE - goodpastures
No because no peptide fragment!

33. What are the three types of lymphocytes?
Antidote for digoxin intoxication
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
B - T - and NK cells
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

34. What is serum sickness? give an example.
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
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
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
A recomb cytokine of IL 2; RCC and metastatic melanoma

35. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
Anti alpha subunit 3 of collagen on type IV bm
In the germinal center of secondary follicles (In the paler center)
Cyclosporine - OKT3
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

36. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
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
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
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

37. ________ regulate the cell mediated response.
Thrombocytopenia
Humoral
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

38. Which disease is associated with HLA A3?
Macrophages - Dendritic cells - B cells
Anti alpha subunit 3 of collagen on type IV bm
isotype
Hemochromatosis

39. what ensure that a memory response is generated?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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
If there is class switching and plasma cell production (that is when memory cells are produced)
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

40. What lymph node drains the scrotum?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
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
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Superficial inguinal

41. What are the autoantibodies for polymyositis and dermatomyositis?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
IgM or IgG antibodies coat the antigen and result in activation of MAC complex via the classical pathway OR fixed macrophages in the spleen phagoctyose the opsonized (C3b or igG) antigens - ex penicillin reaction; IgM AIHA - anti B IgMs in a group A
Anti Jo -1
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

42. What are the autoantibodies for hashimotos?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Antimicrosomal and antithyroglobulin
IL 5
Influenza; antigenic shift; antigenic drift

43. What is epo used for?
Anemias (esp due to renal failure)
pale central germinal centers
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
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

44. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Th2; Th1
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
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
B - T - and NK cells

45. The secondary follicles have __________; primary follicles are dense
CD21 on B cells (although there is T cell lymphocytosis in EBV)
pale central germinal centers
MS - hay fever - SLE - goodpastures
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

46. What does IgA pick up from epithelial cells before being secreted?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Cytokine IL 10 secreted by Th2
Secretory component
Antimicrosomal and antithyroglobulin

47. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
IgM and IgG
IL 4
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

48. Give an example of someone who could get hyperacute transplant rejection.
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
opsonizes
Previous transfusion; pregnant woman whose fetus had paternal antigens
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

49. What are the autoantibodies for type I diabetes mellitus?
Anti glutamate carboxylase and anti insulin
Paracortex
When you select for which MHC it will have; take out the lymphs that self react
MHC II - B7

50. Leukocyte adhesion defect presents with...
neutrophilia!
TGF beta and IL 10
Histamine; post capillary venules - vasodilation
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

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USMLE Step 1 Immunology

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