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27 Cards in this Set

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T lymphocyte (T cell)
T cell
HLA (Human histocompatability Antigen)
HLA
MHC (Major Histocompatability Complex)
MHC
Hypersensitivity reactions
1) Type 1- mast cell/ basophil mediated

2) Type 2- direct attack on cells/ tissues by antibodies

3) Type 3- damage secondary to deposition of immune complexes (IgG- Ag)

4) Type 4- T cell / macrophage mediated (delayed type hypersensitivity)
Eicosanoids


1) Prostaglandins

2) Leukotrines
A)

1)


2)
CYTOKINES:
CYTOKINES
IL1
CELL SOURCE: macrophages, B cells, NK cells

TARGET CELLS: endothelium, fibroblasts, astrocytes

EFFECTS: Lymph activation, mac stimulation, increase leukocytes, endothelium adhesion, acute phase proteins, fevers
IL2
CELL SOURCE: T cells

TARGET CELLS: T cells, NK cells

EFFECTS: T cell and NK cell activation and proliferation
IL4
CELL SOURCE: T cells, TH2 cells, mast cells

TARGET CELLS: B cells, T cells

EFFECTS: B cell GF, isotype switching to IgE, TH2 differentiation, suppress TH1 cells
IL10
CELL SOURCE: T cells, TH2 cells

TARGET CELLS: TH1 cells

EFFECTS: B cell gf, isotype switching to IgA, wosinophil growth
IL12
CELL SOURCE: monocytes, APC

TARGET CELLS: TH1 cells

EFFECTS: inhibition of cytokine synthesis and macrophage function
TNF alpha
CELL SOURCE: lymphocytes, macs, mast cells

TARGET CELLS: many cells

EFFECTS: proinflammatory, endothelial activation, shock, acute phase proteins, PMN activation
IFN gamma
CELL SOURCE: NK cells, T cells

TARGET CELLS: macs, B cells, endothelium, DCs

EFFECTS: increased MHC class II expression, mac activation, IgG class switching, suppress TH2 cells
TGF beta
CELL SOURCE: most cells

TARGET CELLS: most cells

EFFECTS: antiviral, increased MHC I expression
CHEMOKINES
CHEMOKINES
MAST CELLS
*
EOSINOPHILS
*
MACROPHAGES/ MONOCYTES
*
VASCULITIS
*
ANAPHYLAXIS
*
OPSONIZATION
*
Describe TYPE 1 HS.

1) What is anayphylaxis?

2) What happens with the induction of IgE response?

3) What's the difference between primary and secondary mediators?
* It is mast cell, basophil mediated

1) Can have anyphylaxis: systemic and localized. Examples are asthma, allergic rhinitis

2) Get induction of IgE response after antigen exposure- - TH2 cells as well

3) Primary: preformed mediators
Secondary: synthesized mediators
Describe Type 2 HS.

1) What diseases are associated with this? (6)

2) What is the mechanism of Type 2 HS?
* Direct attack on cells. tissues by antibodies

1) Hemolytic anemia, erythroblastosis fatalis, Goodpasture syndrome, Myesthenia gravis, Rheumatic fever, Graves' disease

2)
- So get induction of anti- self antibodies, and antibodies bind to self- constituents
- Complement fixation/ activation
- Tissue lysis/ opsonization/ phagocytosis/ cell- mediated cytotoxicity
Describe Type 3 HS.
1) What diseases are associated with this? (5)
* damage secondary to deposition of immune complexes (IgG- Ag)

1) Glomerulonephritis, serum sickness, polyarteritis nodosa, arthus reaction

- Get induction of antibodies and form Ab- Ag complexes
- Deposition of copmlexes in tissues or on cells
- Complement activation and prod of comp factos
- Neutrophil attraction and degranulation and tissue destruction
Describe Type 4 HS.

1) What diseases/ reactions are associated with this? (3)

2) What are major characteristics
* T-cell/ macrophage mediated/ DTH

1) Tuberculin reaction, granuloma formation, contact dermatitis

2)
- Must first get sensitization of T cells
- Ag processing and presentation
- Rechallenge or chronic Ag challenge
- Production of cytokines and chemokines
- Attract other cells and actication of macs
- Form giant cells
- Activate CD8 cytotoxic T cells
- Form granulomas
Describe the significance of Graft/ Tranplant rejection.
* Combination of HS reaction types 2- 4, but not type 1
What are the 4 types of transplant rejection?
1) Ab mediated: hyperacute rejection, thrombosis vessel attack

2) Acute rejection: host becomes sensitized to donor tissue
- Cellular and Ab mediated
- Get attack on vessels (vasculitis), parenchymal attack and damage

3) Chronic rejection: mixed mechanism, but many macs and T cells and plasma
- Extensive and longstanding damage and fibrosis to graft

4) Graft vs. Host disease
- Can have acute and chronic
- Tranplanted tissue attack the host
- See in skin, liver, GI tracts are most affected