Maybe? But as TCR activated in the Tc the pd-1 expressed less so the activation increases?
Note that some tumors with could be started by viruses express b7-h1 and MHC1 like pd.
https://link.springer.com/chapter/10.1007/978-1-4615-1971-3_67
It appears that cells that interact with the follicular dendritic cells FDC have B7-2. What is the receptor on FDC for B7-2?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193370/
B7-H1 induces il-10 (mitochondria/ nuclear antigens p. dendritic )
https://www.ncbi.nlm.nih.gov/pubmed/21830424
B7-1 and B7-2 both induce il-4 (outside antigens: langerhans)
https://www.ncbi.nlm.nih.gov/pubmed/7577797
when antigens are in the mitochondria/nuclear area
PD-1 on CD8
https://www.ncbi.nlm.nih.gov/pubmed/29654146
PDL-1 (B7-H1) binding PD1 converts TH1 into T regulatory
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3235958/
B7-H1 and antigen responses not cytotoxic responses
http://www.bloodjournal.org/content/97/6/1809?sso-checked=true
Which brings the possibility:
B7-1 costimulates cd8 cells but not B7-2
https://www.ncbi.nlm.nih.gov/pubmed/8543795
B7-1 as a ligand for pd-1
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2707944/
B7-2 appears on Langerhans and marginal zone B cells that bring antigens to the follicular dendritic cell.
The langerhans use the conduit. Reticular cells produce CXCL13 which attracts B and T cells. These cells may also become FDC which holds the antigen for the B cells.
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