Immunity Regulation Flashcards
How does the immune system deal with invaders?
- Ab response to prevent attachment and entry of microbes (extracellular organisms)
- T cell-mediated response that mediate the activation of APCs and killing infected cells with intracellular microbes
What does the helper T cell do after activation?
- Secrete cytokines (IL-4) that help B cells produce Abs (TH2)
- Secrete IFN that stimulates complement (TH1)
T helper (TH) cells
CD4+ and bind to MHC class 2
TH3: TGF-beta
TH17: IL-17A
T Cytotoxic cells (CTL)
CD8+ and binds to MHC class 1
TC1: IFN
TC2: IL-4 and IL-5
Cytotoxic T lymphocytes kills target cell by the release of what?
Perforin
Granzymes
Perforin
A pier forming protein that causes cell to burst
Granzymes
Proteases that induce apoptosis (programmed cell death)
Cell death
Normal process involving old, surplus or abnormal cells that can interfere with normal tissue function or induced by infection, toxicity and trauma
Apoptosis (PCD)
Programmed cell death
Activated only when cell must die
Ex: old, surplus, abnormal cell
Why are the 2 pathways for apoptosis cell death
Intrinsic: mitochondrion (oxidants, radiants)
Extrinsic: death receptor - CD95 (TNF, CD95L)
Necrosis
Cells severely damaged by trauma, toxicity or microbial invasion
Largely unregulated, nflammatory process
What can trigger necrosis or apoptosis?
Microbial agents
How does CTL kill infected target which ways?
Directly and indirectly
Direct CTL apoptosis
Interaction of ligand (CD95L) on T cells and receptor (CD95) on infected target
Leads to apoptotic signal
Indirect CTL apoptosis
Release of proteilytic enzymes such as granzymes and perforins
Outcomes of apoptosis (PCD)
Clumping of chromatin
Apoptotic bodies
Cell bedding
Nuclear fragmentation
Loss of organelles
How are T cells classified?
- Type of secretion
- Expression of surface molecules (CD4 and CD8)
Which cytokines activate macrophages?
IL-2, IFN-Y, IFN-a/b, TNF-a, TNF-b, GM-CSF
Which cytokines suppress macrophages?
IL-10, IL-4, IL-13, TGF-b
Tolerance
The state of unresponsiveness that involves T and B cells
1. Central (self, clonal deletion)
2. Peripheral (in response to Ags, clonal anergy)
Central/ self tolerance
Develops early in life to preserve our body from attack by our own immune system
T cells responsive to own cells are deleted I’m thymus
Example of self tolerance
Bovine dizygotic (non identical twins)
Blood mixed between 2 calves because reactive T cells in twins were deleted in the thymus early in life
How are self Ags recognized in the thymus?
Ags are expressed on surface of thymic epithelium by promiscuous gene expression
Ags transported from outside thymus by DCs/MACs
Negative selection of T cell tolerance
Elimination of T cells that don’t recognize MHC and are reactive to self Ags
Positive selection of T cell tolerance
Selection of T cells that react moderately with MHC and aren’t reactive to self Ags
What mechanisms affect immune response?
- Inadequate immune response
- Excessive immune response leading to autoimmunity/ hypersensitivity
- Slowly metabolized Ags
- Form of Ag (polymeric or momomeric)
- Type of APC
- Abs or Ag-Ab immune complexes
Ag-Ab immune complexes
Excessive production of Abs trigger an inhibitory feedback mechanism
In some diseases excess Ags in blood form complexes
Consequences if Ag-Ab immune complexes
Deposition of organs, increased infection due to inhibition of Ab synthesis
Maternal Abs interfere with vaccination of newborn through neg feedback process
