NorthWest Biotherapeutics Inc (NWBO)

[sentiment_stocks]

One thing that stood out to me about T Cell Receptors in that link you provided was this…

Cytotoxic T lymphocyte TCRs recognise epitopes displayed by MHC class I molecules on the surface of almost every cell in the body, so it can distinguish between ‘self’-antigens and foreign antigens (viral-infected cells), as well as being sensitive to the amount of self-antigen presented (increased number of self-antigens in malignant cells).
https://www.ebi.ac.uk/interpro/potm/2005_3/Page1.htm

So it sounds as if that is due to the epitopes displayed by the “major histocompatibility complex” (MHC) present on the antigen. So when TCRs are able to differentiate between self and non-self antigens, then the T-cells can go to work.

The definition of MHC indicates this…

Major histocompatibility complex (MHC), group of genes that code for proteins found on the surfaces of cells that help the immune system recognize foreign substances. MHC proteins are found in all higher vertebrates. In human beings the complex is also called the human leukocyte antigen (HLA) system.

But it seems that this isn’t always the case. If MHC molecules aren’t present on the antigen, then the TCR’s can’t tell the difference… I think anyway. And so when MHC is lost or down regulated, are the TCRs rendered incapacitated?

In their MAGE trials, KITE is engineering T cells with TCRs to treat solid tumors. But If they engineer a T cell with a TCR designed to recognize the MHC protein on the cancer gene, if there is no MHC present on the cancer cell itself… how will that improve the T cells’ odds of identifying that particular cancer cell and eliminating it?

Anyway, it’s been very interesting to read about this subject thus far. Anyone feel free to correct my understanding of the science here. Thanks for the links.