Immune surveillance by T cells is essential for the control of spontaneous B cell lymphomas

[Christopher]

02 February 2014

The concept of immune surveillance was proposed long ago36, but few studies have examined the cellular and molecular requirements for this process directly21, 37. A recent report showed that the Epstein-Barr virus–derived antigen LMP1 expressed under the control of B cell–specific regulatory elements can directly activate T cell–mediated immune surveillance, leading to efficient deletion of LMP1-transgenic B cells, thereby preventing development of B lymphoma38. Although that study demonstrated the critical role of T cells in the control of lymphomas driven by a viral antigen, it did not clarify the role of immune surveillance in the pathogenesis of spontaneous B cell lymphomas that do not express foreign or pathogen-associated antigens. Our study demonstrates for the first time, to our knowledge, the ability of T cells to prevent spontaneous lymphoma development triggered

http://www.nature.com/nm/journal/vaop/ncurrent/full/nm.3442.html

 

[anciendaze]

I've asked oncologists how often cells with neoplastic potential arise and are eliminated by active immune response in healthy people. The answers I get basically indicate that they don't know because it isn't cancer until it proliferates. Some have added that immune function is not compromised until late in the disease.

This is true for general immune function, but understanding of specific immune compromise, as in the case of those subsets of T-cells which perform this function against a particular pathogen, is still very poor. We saw evidence that highly specific immune dysfunction is possible in ME/CFS patients in recent research by Carmen Scheibenbogen's group in Berlin. The most striking aspect had to do with a missing response to EBNA-1, a protein produced at the very beginning of the replication cycle.

As I understand things, (and this is a limited understanding,) LMP1 is formed fairly late in the sequence of events leading to EBV replication. Expression of this, and especially some mutant forms of the gene, seems to be connected with metastasis. It appears to perform dual, opposing roles: first, it signals on cell membranes that a cell is actively infected, enabling immune response to eliminate those cells; second, it interferes with the ability of the cell to adhere to membranes. Once cells with oncogenic properties cease to be confined to membranes they are much more likely to become metastatic. This is the point at which it becomes much, much harder to control or eliminate a neoplasm.