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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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Answer 50 questions in 15 minutes.
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1. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Its main effect is a defect in Ab opsonization for killing
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Anti alpha subunit 3 of collagen on type IV bm
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

2. describe the classic complement pathway.
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Negative nitroblue tetrazolium reduction test
Alternative splicing of mRNA
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

3. What is the main cytokine released by T cells? What does it do
Anti Jo -1
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
Basophils! THey want IG E class switch!
IL 3; supports growth and differentiation of bone marrow stem cells

4. To what portion of the Antibody do the complements bind?
Fc
Sinusitis - otitis media - pneumonia
MS - hay fever - SLE - goodpastures
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 is the most common selective Ig deficiency? What is the presentation?
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
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
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
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

6. What type of side chains are found on Fc region of an antibody?
Receiving preformed Antibodies
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
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
Carbohydrate

7. which of the hypersensitivity reactions is not Ab mediated?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Type IV
Lymphocytes
Local infection/inflammation; infection of the ln itself; metastasis

8. What are the autoantibodies for graves?
Anti TSh receptor
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
The igA found in breast milk
A j chain

9. what happens in a deficiency of C1 esterase inhibitor? DAF?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Anemias (esp due to renal failure)
TLR ad nuclear receptors
Hereditary angioedema; PNH

10. What are target cells?
Immunosuppression after kidney transplantation
Histamine; post capillary venules - vasodilation
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Cells that stil have weird parts of their membrane that macrophages usually bite off

11. Which disease is associated with DR7?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Steroid responsive nephrotic syndrome
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
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

12. What are the main Cell surface proteins on T cells?
MHC I - CD16 - CD56
Brain - eyes - placenta/fetus - testicles; because they can have an antigen in there and not get attacked by immune system because dont have contact with immune system via blood and lymph; if an infection occurs such that trauma results in exposure t
isotype
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

13. What are the function of B cells?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
pentamer
If there is class switching and plasma cell production (that is when memory cells are produced)

14. IgG...
A recomb cytokine of IL 2; RCC and metastatic melanoma
A chemotactic factor for neutrophils
opsonizes
Superior mesenteric

15. Leukocyte adhesion defect presents with...
By transcytosis
All MHC 1/CD8
neutrophilia!
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

16. What are the symptoms of serum sickness?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Hereditary angioedema; PNH
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

17. Name two endogenous pyrogens
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
IL 1 and IL 6
Pernicious Anemia and Hashimotos
In the germinal center of secondary follicles (In the paler center)

18. What is epo used for?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
delayed!
Anemias (esp due to renal failure)
Viral neutralization of igM and IgG!

19. What are the autoantibodies for myasthenia gravis?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
B - T - and NK cells
Anti Ach receptor
In the germinal center of secondary follicles (In the paler center)

20. What is the clinical use of Muromonab?
active complement pathway
Immunosuppression after kidney transplantation
IgM and IgA
mesenchymal

21. What are the labs in brutons agammaglobulinemia?
Para aortic
IL 4 - 5 - 10 - 6
Lymphocytes
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

22. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Viral neutralization of igM and IgG!
pathogenesis
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

23. How do you test for chronic granulomatous disease?
...
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Negative nitroblue tetrazolium reduction test
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

24. What are the autoantibodies for drug induced lupus?
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
Th2; Th1
Antihistone
Recom IL 11; thrombocytopenia

25. What is the white pulp of the spleen?
Fab portion
acute phase reactants
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

26. what ensure that a memory response is generated?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
IgM and IgA
If there is class switching and plasma cell production (that is when memory cells are produced)
active complement pathway

27. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
lowest concentration
Active; passive - fast but short half life (3 weeks!)
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

28. other than eat and bite RBCs what else do Macrophages of spleen do>
Delayed type hypersensitivity
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Remove encapsulated bacateria
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

29. What is anergy? why does this occur?
Active; passive - fast but short half life (3 weeks!)
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

30. What does IL 10 do? who is secreted by?
IL 4 - 5 - 10 - 6
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory 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
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

31. What are the PALS?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Celiac
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
IgM

32. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
MHC I - CD16 - CD56
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

33. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
Interferon gamma and IL 2
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
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
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

34. is IgM an opsonizer?
Negative!
Recom IL 11; thrombocytopenia
Daclizumab; prevent ACUTE rejection of renal transplant
TGF beta and IL 10

35. Name 5 ways Antibody diversity is generated?
cannot cross placenta
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
MS
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

36. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
IgG
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

37. Type IV hypersensitivity is i...
Hereditary angioedema; PNH
IgA
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 :(
not Ab mediated

38. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
DM type I
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Anti viral and anti tumor
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

39. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
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
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
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

40. What is the main function of interferons?
Active; passive - fast but short half life (3 weeks!)
Rheumatic arthritis
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
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!

41. what characterizes an arthus reaction?
IgE; by activating eosinophils
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Edema and necrosis in that region
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

42. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
IgM and IgD
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
A recomb cytokine of IL 2; RCC and metastatic melanoma

43. what prevents NK cells from killing normal cells if their default is to kill?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
All MHC 1/CD8
MHC class molecules bind to KIRS or CD94 to prevent killing

44. Only the _______ contribute to the Fc region
IgG
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
heavy chains
Steroid responsive nephrotic syndrome

45. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
MS
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 :(
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

46. What are the main cell surface proteins on B cells?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
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
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Its main effect is a defect in Ab opsonization for killing

47. What is the defect in hyper IgM syndrome? What are the lab results?
If there is class switching and plasma cell production (that is when memory cells are produced)
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
A j chain

48. How fast does it occur?
The patient could become cyanotic in the OR!
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Anemias (esp due to renal failure)
IgAs in mothers breast milk!

49. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Paracortex; viral infection
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
Para aortic
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

50. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Sinusitis - otitis media - pneumonia
Histamine; post capillary venules - vasodilation
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
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

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USMLE Step 1 Immunology

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