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15 Cards in this Set

  • Front
  • Back

most bacteria and parasites replicate in:
- endosomes and lysosomes that form the vesiclular system

antigens that bind to MHC I:
- viruses in the cytosal
- cytosolic pathogens are degraded in cytosal, bind to MHC I, presented to CD8T ->, killed

antigens that bind to MHC II
- intravesicular pathogens
- degraded in endocytic vesicles, low pH
- MHC II/peptide complex -> CD4T (helper)
- APC activated -> kill intravesicular bacteria or parasite

facultative antigen presenting cells:
- cells that can be induced to present antigens
- low levels of pagocytosis
- astrocytes (Macrophages of the brain) -> MHC II

MHC I (endodenous) pathway of antigen presentation
- leads to presentation of MHCI bound peptides to CD8+ T cells
- antigen is processed within cytosol (by proteasomes)
- processed peptides are transported across the ER membrane
- MHCI peptide complexes are formed in the ER and are transported through the conventional secretory pathway to the cell surface

MHCI presentation pathway:
- partly folded MHC I alpha chains bind to calnexin until beta2- microglobulin binds
- alpha:beta2m complex released from calnexin, binds a complex of chaperone proteins (calreticulin, Erp57) and binds to TAP via tapasin
- proteosome: cytosolic protein -> peptide fragment
- TAP delivers a peptide -> MHC I, complete folding, released from TAP, exported

MHC II processing (endocytic/exogenous) pathway of antigen presention
- leads to presentation of MHC II bound peptides to CD4+ T cells
- antigen is processed within endocytic vesicles
- upon its synthesis MHC II moves through endocytic pathway and binds antigenic peptides en route to the cell surface of an APC.

MHC II presentation pathway
- invariant chain (Ii) forms a complex with MHC II molecules, blocking the binding of peptides
- Ii is cleaved in an acidified endosome, leaving a short peptide fragment, CLIP, still bound to the MHC II
- CHP block the binding of antigen peptides to MHC II
- HLA DM bind to MHC II -> releasing CLIP, peptides bind
- MHC II travels to the surface

supramolecular adhesion complex (SMAC)
clustering of T and B receptors leads to the formation of an organized structure

immunological synapse
- formation of SMAC in T cells leads to formation of SMAC in APC.
- contact between T cell and APC is highly organized interface call immunological synpase

LFA-1, ICAM-1:
- T cell initially binds APC through low-affinity LFA-1, ICAM-1 interactions
- adhesion molecules
- if T is specific for the antigen presented by the APC -> conformational change in LFA -> increase affinity and prolong cell-cell contact

activation of naive T cells requires 2 independent signals delivered by the same APC
1st: recognition of MHC I or II
2nd: co-stimulatory molecule

the principal co-stimulatory molecules expressed on APCs are B7:
molecules which bind T cell protein CD28

T cell activation through the TCR and CD28 leads to the:
increased expression of CTLA4, an inhibitory receptor for B7 molecules

At a minimum, activation of T cells requires:
a specific signal via the TcR-MHC/peptide complex and a non-specific signal via CD28-B7 molecules