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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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1. What is the pathology of acute transplant rejection? is it reversible?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
neutrophilia!
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

2. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
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
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Recom IL 11; thrombocytopenia

3. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
Immunoflourescent staining of tissue biopsies
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Paracortex

4. Which diseases are associated with DR5?
Pernicious Anemia and Hashimotos
Antidote for digoxin intoxication
IL 1 and IL 6
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

5. What is oprelevkin? and What is it used for?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Th cells fail to produce interferon gamma; a lot of IgE
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
Recom IL 11; thrombocytopenia

6. describe the classic complement pathway.
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Paracortex; viral infection
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

7. What are the autoantibodies for wegeners granulomatosis?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Activates cytotoxic CD 8 T cells as second signal
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
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

8. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Cells that stil have weird parts of their membrane that macrophages usually bite off
Th cells fail to produce interferon gamma; a lot of IgE
Antihistone

9. How is i Th1 helper cell inhibited?
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
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Cytokine IL 10 secreted by Th2

10. Other than stimulating fever - what else does IL 6 do?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
isotype
Stimulate the liver to release acute phase reactants
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

11. Describe the Mannose Lectin pathway
A - B - C; all the D's
Internal iliac
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
Interferon gamma and IL 2

12. other than eat and bite RBCs what else do Macrophages of spleen do>
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Remove encapsulated bacateria
MS - hay fever - SLE - goodpastures
MHC II - B7

13. 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?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
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
except hyperacute
Macrophages - Dendritic cells - B cells

14. In thymic development - What is the positive selection? negative selections?
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
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
When you select for which MHC it will have; take out the lymphs that self react
Remove encapsulated bacateria

15. What are howell jolly bodies?
MHC class molecules bind to KIRS or CD94 to prevent killing
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
T
Anti topoisomerase

16. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
If there is class switching and plasma cell production (that is when memory cells are produced)
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
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
Sinusitis - otitis media - pneumonia

17. other than C3a - what other complement acts as an anaphyloxin?
C5a
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Cross link
delayed!

18. Describe complement dependent Type II hypersensitivity. Give an example.
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
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)
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

19. What cytokines to Th2 secrete?
Thrombocytopenia
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
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
IL 4 - 5 - 10 - 6

20. A lymph node is a ________ lymphoid organ.
Carbohydrate
Th2; Th1
MHC II - B7
secondary

21. which antibodies prevent antigens from binding mucosal surfaces?
Anti viral and anti tumor
IgA
Wiskott Aldrich syndrome
2 heavy chains and two light chains

22. What are the main Cell surface proteins on T cells?
RNA segment reassortment
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
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

23. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
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
Inferior mesenteric
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

24. What happens in a deficiency of C3?
Anemias (esp due to renal failure)
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Cytokine IL 10 secreted by Th2

25. What is the common variable immunodeficiency ? How is it different from Brutons?
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
Sinusitis - otitis media - pneumonia
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
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

26. What is the toxicity of azathioprine?
opsonizes
Antimicrosomal and antithyroglobulin
neutrophilia!
...

27. What does Interferon alpha and beta do? how?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
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
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

28. 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?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
IL 4 - 5 - 10 - 6
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Antidesmoglein

29. What are the mediators that mast cells release?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
isotype
CRP - C3b - IgM
Stimulate the liver to release acute phase reactants

30. What are the autoantibodies for primary biliary cirrhosis?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
A recomb cytokine of IL 2; RCC and metastatic melanoma
Anti mitochondrial
Viral neutralization of igM and IgG!

31. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
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
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
type four
dimer

32. What does IgA pick up from epithelial cells before being secreted?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Secretory component
Basophils! THey want IG E class switch!
CD56

33. To what disease do the autoantibodies to IgG (rheumatoid factor)?
T
Remove encapsulated bacateria
Rheumatic arthritis
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

34. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Superficial inguinal
A j chain
Daclizumab; prevent ACUTE rejection of renal transplant

35. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Cross link
pathogenesis
heavy chains
except hyperacute

36. ________ regulate the cell mediated response.
Humoral
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
Thrombocytopenia
Barrel hoop basement membrane fenestrations

37. How fast does it occur?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
The patient could become cyanotic in the OR!
...
In the germinal center of secondary follicles (In the paler center)

38. describe the pathogenesis of delayed type IV hypersensitivity
MS - hay fever - SLE - goodpastures
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Antidesmoglein
A - B - C; all the D's

39. What is serum sickness? give an example.
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
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
The igA found in breast milk

40. What are the autoantibodies for Mixed connective tissue disease?
acute phase reactants
Anti U1 RNP (ribonucleoprotein)
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Activate macrophages

41. What is the most common selective Ig deficiency? What is the presentation?
Inferior mesenteric
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
NK cells
RNA segment reassortment

42. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
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
Antidesmoglein
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

43. What is the clinical use of Muromonab?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Immunosuppression after kidney transplantation
IgG
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

44. What are superantigens? give two examples.
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
All MHC 1/CD8
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
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

45. Type IV hypersensitivity is i...
Yes
Immunosuppression after kidney transplantation
Active; passive - fast but short half life (3 weeks!)
not Ab mediated

46. What is the pathology in hyperacute transplant rejection?
Activates cytotoxic CD 8 T cells as second signal
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Antidote for digoxin intoxication
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

47. Describe the capsular structure of a lymph node; What are the functions of the LN?
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
Macrophages - Dendritic cells - B cells
SP infections
opsonizes

48. What is the pathogenesis of a hypersensitivity reaction?
Alternative splicing of mRNA
Paracortex; viral infection
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
Activate macrophages

49. What are the autoantibodies for autoimmune hepatitis?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Anti smooth muscle
Its main effect is a defect in Ab opsonization for killing
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

50. which cytokine inhibits TH2 cells? secreted by who?
Antidote for digoxin intoxication
Anti Ach receptor
Interferon gamma; Th1
Antimicrosomal and antithyroglobulin

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USMLE Step 1 Immunology

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