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What does innate immunity consist of?

Phagocytes - neutrophils and macrophages
NK cells
Plasma proteins - compliment, CRP, mannose-binding lectin


What is the job of NK cells, how are they regulated, and what do they secrete?

Killers of virus infected and tumor cells.
Activating receptors: activated by viral and stress-induced proteins
Inhibiting receptors: engaged by normal levels of MHC I
Secrete: IFN-y and TNF


What occurs with Tcell activation?

Release of cytokines, proliferation, differentiation into effector or memory cells.


What is the difference between TH1 and TH2 cells?

TH1: Release IL-2 and IFN-gamma. Tcell proliferation, macrophage activation, Ab production

TH2: Release IL-4, 5, 13. eosinophil activation and IgE synthesis


What are 2 subclasses of T regulatory cells?

Treg: Express CD4, CD25, and FoxP3. Suppress Tcell activity, APCs. Suppress autoreactive Tcells

adaptive regulatory Tcells: Express CD4 and upregulate CD25 in the periphery (MALT). induced by inflammation

Release IL-10 and TGF-B


CD8 cell function

Interact with MHC I (expressed on most cells). Activated by foreign peptide, self-restricted. Important in response to virus infection.


What effect does CD 21 have on Bcell activation?

amplifies. Binds complement component (Cdg) that is attached to pathogen surface. Amplifies BCR signal and Bcell response


What is the function of Dendritic cells? What is a follicular dendritic cell?

Dendritic cells: in epithelium and interstitium. major APC for CD4+ Tcells. Can migrate to lymph organs

Follicular dendritic cells: found in germinal centers of lymph follicles. Present to B cells -> activation


What chromosome houses MHC / HLA genes?

Chromosome 6


What genetec loci encode MHC I variable regions?



What genetic loci encode MHC II variable regions?

Subregions of HLA D:


What types of proteins are presented by MHC I and II?

MHC I: cytoplasmic antigens

MHC II: exogenous antigens


Type I hypersensitivity

Anaphylactic type
IgE mediated, TH2 dependent
Antigen -> dendritic cell -> presentation to Tcell -> TH2 activation, secretion of IL-4 -> Bcell activation -> IgE plasma cell -> IgE attaches to mast cells (first exposure)
Second exposure: allergen cross-links IgE on mast cell -> degranulation


What is released with degranulation of mast cells / basophils in the setting of allergic reaction?

1. Primary response - preformed mediators in granules: biogenic amines (histamine, adenosine), chemotactic factor (eosinophil), enzymes, proteoglycans

2. Secondary response - newly synthesized (later): PLP A2 activation -> leukotrienes (LTB4, C4, D4) and prostaglandins (PGD2), PAF
cytokine / chemokine secretion: Interleukins, TNFa, GM-CSF


What histopathologic findings are associated with Type I hypersensitivity?

Vascular: vasodilation, increased permeability, edema
-histamine, PAF, LTC4 and D4
Bronchial sm. muscle contractoin: biogenic amines, LTC4 and D4, PAF, PGD2
Increased secretion - mucinous metaplasia: histamine, PGD2
Infiltration - eosinophil, chron. inflamm. cels: eosinophil chemotactic factor, LTB4, PAF, TNFa


What is type II hypersensitivity?

Involves antibody binding to cell surfaces or tissue antigens.
May or may not involve complement
Results in cell destruction or cell/ tissue dysfunction


Examples of Type II hypersensitivity, w/ and w/o compliment.

Compliment dependent:
Autoimmune rxn to blood cells
Transfusion rxns, hemolytic disease of the newborn
Autoimmune skin-bistering (pemphigous vulgaris)
Goodpasture (Ab to glomerular and pulmonary basement membrane)

Antibody-dependent cell-mediated cytotoxicity (ADCC):
Response to parasite / malignant cells

Antibody mediated tissue dysfunction: no cell death
Myasthenia gravis, Graves


What are type III hypersensitivity reactions?

Immune complex mediated
Excess antigen -> immune complex formation and deposition in tissue -> complement activation -> acute inflammation / coagulation, tissue injury

Results in vasodilation, edema, necrosis


What is an Arthus Reaction?

Local immune complex disease
tissue necrosis resulting from acute immune complex vasculitis, usually elicited in the skin.

Immune complexes precipitate in vessel walls -> fibrinoid necrosis


What are 3 phases of Type III hypersensitivity?

1) immune complex formation (exogenous or endogenous antigen)
2) immune complex depisition (local or systemic)
3) tissue injury (complement activation (not at native site), acute inflammation, coagulation)


Examples of Type III hypersensitivity

Acute post-streptococcal glomerulonephritis
Polyarteritis Nodosa
Rheumatoid Arthritis


What type of necrosis is associated with Type III hypersensitivity?


Due to compliment activation and MAC -> coagulation -> fibrin deposition


What is the key pathologic finding in Type III hypersensitivity?

Acute necrotizing vasculitis of small to medium sized blood vessels


What is Type IV hypersensitivity?

Cell mediated: delayed or cytotoxic
Delayed: TH1 mediated
Cytotoxic: CD8 mediated


Examples of Type IV hypersensitivity

Delayed: TB and TB skin test, contact dermatitis (poison ivy), fungal infections

Cytotoxic: viral infection, tumor immunity, acute graft rejection



Produced by macrophages
Results in differentiation and activation of TH1 cells


Describe the Direct and Indirect pathways of transplant rejection

Direct: recipient Tcells recognize MHC on donor APCs. (Acute rejection)
--Paradoxical Mimicry
a) MHC-1 -> CD8+ Tcell proliferation and cytotoxic hypersensitivity. Results in apoptotic death of graft cells
b) MHC-II -> CD4+ Tcell proliferation (TH1) -> delayed type hypersensitivity. IL-2, TNF-a, and IFN-y ->Inflammatory response and tissue destruction by mobilized macrophages

Indirect: Usual mode of rejection (Chronic Rejection)
Host APCs present graft antigen on self-MHC II
CD4+ Tcell activation -> delayed type hypersensitivity and transplant rejection


What is rejection vasculitis?

Antibody mediated transplant rejection
a) hyperacute: preformed Ab
b) acute: induced Ab


What is hyperacute rejection?

Due to preformed antibody -> rejection vasculitis
w/in minutes - hours of transplant

immune complex formation and vascular deposition -> complement activation -> vasodilation, vascular permeability -> inflammatory infiltrate -> necrosis, hemorrhage, thrombosis -> infarction


How long after transplantation does acute rejection take place? What usually causes it?

days to weeks after transplant or later due to reduction in immunosuppression