New Stanford University data clarifies immune dysfunction/infection in cancer, ME/CFS, MS

September 15th, 2017 by Amy Proal

Mark Davis and his lab at Stanford University are on fire! They recently released fascinating data (some unpublished) on patients with cancer, Lyme disease, MS and ME/CFS. Davis discussed this data at a recent Open Medicine Foundation meeting. The talk was recorded and I HIGHLY encourage you to watch it!

New Davis Lab Findings:

Davis starts by confirming that ME/CFS is characterized by high levels of systemic inflammation. In fact, in concert with Dr. Jose Montoya at Stanford, Davis detected elevated cytokines (inflammatory molecules) in the blood of patients with ME/CFS. First, this cytokine activation distinguished the ME/CFS patients from healthy controls: does anyone still want to argue that the ME/CFS is psychosomatic!? (please tell me no). Second, patients with more severe cases of ME/CFS demonstrated greater cytokine activation; indicating that ME/CFS disease progression is characterized by increased immune dysfunction over time. 

In another series of experiments, Davis looked at T cells responses in ME/CFS and related inflammatory conditions. T cells are part of the adaptive immune response: the branch of the immune system that creates antibodies in response to specific microbes or pathogens. Davis used a novel assay developed at Stanford to obtain T cell sequences from the tissues/blood of patients with colon cancer, MS, Lyme disease, and ME/CFS.

In all four diseases, T cells were activated in a manner not observed in healthy control subjects. To be specific, the team observed massive clonal expansion of the T cells – both in tumor tissue and in the blood of patients with MS, ME/CFS, and Lyme disease.

T cell expansion in healthy subjects as compared to patients with Lyme disease, MS, and ME/CFS

T cell expansion in healthy subjects as compared to patients with Lyme disease, ME/CFS and MS. Unpublished data by Mark Davis Lab, Stanford University.

What does this mean? In simple terms, T cell clonal expansion indicates that the T cells became increasingly activated against a “target.” This activation caused the cells to divide and proliferate. As Davis explains, this “target” could be a pathogen or dysregulated human tissue.

Davis leans towards the “target” being a pathogen, stating that antibodies driving T cell proliferation are likely formed “originally against some pathogen peptide.” In some cases, these “pathogen peptides” may cross react with similarly structured human peptides – causing the immune system to accidentally target human tissue. This is exactly in line with the new model of autoimmune/inflammatory disease I’ve described on this site.

Indeed, Davis’ next goal is to further study the activated T cells in his samples. He hopes to correlate the T cell activity with the presence of specific pathogens (and the antibodies created in response to their presence). This could lead to a better understanding of exact microbes involved in driving cancer, MS, ME/CFS etc.

CONSIDERATIONS: Davis’ data strongly suggests that in cancer, MS, Lyme disease, and ME/CFS the immune system is activated against an infectious threat. This threat could be one pathogen, or it could be many pathogens acting together (in a community).

I support the latter possibility: I suspect that T cells are activated in these conditions as part of a generalized response to microbiome dysbiosis or imbalance. However it is very possible that certain microbes in these communities play a larger role than others in driving disease processes (these microbes are often referred to as “keystone” pathogens.”)

Also, the same general pattern of T cell clonal expansion was observed in cancer, autoimmune disease, and infectious disease. This strongly supports what I have long advocated: different inflammatory conditions, commonly studied in isolation, may actually result from the same root causes. This overlap certainly explains the high levels of co-morbidity observed between patients with different diagnoses! If this is true we should be studying these illnesses TOGETHER, with an increased focus on multidisciplinary research.

Finally, the T cell activation Davis observed in patients with ME/CFS could serve as an excellent biomarker for the disease. In my opinion, we do not need to know the exact microbial species involved for the data to be useful. Nor does it matter that other related diseases demonstrate a similar pattern. For the sake of treatment, all we need to know is that patients with ME/CFS show different T cell activity than that of healthy subjects.

T cell expansion in colon carcinomas (tumors)

T cell expansion in colon carcinomas (tumors). Figure: Mark Davis Lab, Stanford University.


2 thoughts on “New Stanford University data clarifies immune dysfunction/infection in cancer, ME/CFS, MS


    Hi Amy, I have just found your website.
    I´m a medical oncologist from Brazil and also a ME/CFS patient.
    Regarding the Tcell clonal expansion in colon tumors, could it be that they are just reacting agaainst a specific tumoral antigen and not against a pathogen?

    1. Amy Proal Post author

      Oi Paulo,

      Glad to hear from someone in Brazil! Part of my family lives in Sao Paulo. Sorry you’re also suffering from ME/CFS.

      Regarding tumoral antigens – yes they could/do cause T cells to activate. However there are an increasing number of reported oncogenic viral antigens. And an increasing number of cancers being tied to infectious processes. For example, dramatic, continual alterations in the microbiome were reported during the development of tumors in a murine model of inflammation-driven colon cancer. These changes were directly responsible for tumor development:

      I’m interested by the fact that patients with Lyme disease and ME/CFS showed T cells patterns similar to the cancer subjects. Especially Lyme – a known infectious condition.

      Also I think we must better consider why specific tumoral antigens are generated in the first place. Intracellular pathogens often dysregulate human gene expression, which could drive at least part of the mutations associated with tumoral antigens.

      I really look forward to when the Davis Lab formally publishes their data, so that we can get much more context on these preliminary results:)



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