Journal of IiME Volume 6 Issue 1 (June 2012) Professor Klimas said the most important thing that has come out of her group recently is the discovery of very low perforin (which she described as “the killing stuff of the cell”). She said that very low perforin levels in the cytotoxic T cell matters, because the anti-viral defence is impaired. In ME/CFS the perforin is half what it should be. She emphasised that in addition to poor cell function, the cells are very activated and very stimulated, and there are consequences of an activated cell – what is seen is not only “this big immune activation, but apoptosis – a lot of cell death”, resulting in a constant drive to make more cells, especially neutrophils and lymphocytes. Thus there is “a constant drive to keep the system in overdrive in trying to keep up with cell loss”. Her group has also seen a CD26 cell receptor in ME/CFS – this is seen in an activated cell, and the number of cells expressing this receptor is elevated, even though there are fewer molecules per cell. This matters, because the number of these activated receptors on the cell determines the function of that cell (which cannot “activate up” the function). Professor Klimas summarised all this as (i) an over-activated system; (ii) a system that is not functional and (iii) what she described as “the stuff of the cell – the thing you need to make the cell function well – being under-produced”. She then spoke about neuropeptide Y, which is a very important neuropeptide of interest to the vascular biologists’ findings in ME/CFS. It has a large number of regulatory functions, including the immune system and the autonomic system. It is a biomarker. They looked at more than 100 patients and found a significant difference between ME/CFS patients and controls. Professor Klimas said this is important. She went on to speak about clinical correlates: they had found that people who had low cognitive difficulties had good T cell function but Invest in ME (Charity Nr. 1114035) people who had very high cognitive difficulties had the poorest T cell function, so there is a definite clinical correlate. This correlate has also been shown with NK cells, and once again she emphasised that this immune connection matters. She discussed the fact that genomics have put some focus on the HPA axis dysregulation and said that IL-6 is associated with the intensity of that dysregulation. She mentioned the role of infection, saying she herself had needed to be convinced about the role of viruses and it was the work of Dr Peterson that had convinced her. Peterson had shown transmissible living virus in spinal fluid cultures of ME/CFS patients (which definitely should not be there): “You should not be able to culture anything out of anybody’s spinal fluid in the way of a virus or bacteria or anything – it’s not OK. That was impressive”. Professor Klimas went on to talk about enteroviruses in ME/CFS: “Enteroviruses keep reappearing – they keep coming back (into the picture). Most recently at our conference in January (the IACFS/ME conference in Florida), Dr Chia from Los Angeles had looked at more than 100 intestinal biopsies (and showed) slide and slide after slide with enteroviruses – it was phenomenal”. She said that people had previously looked at enteroviruses in muscle, but “looking at the intestine was a place no-one had ever looked before, and yet the intestine is, beyond the skin, the second biggest immune system component you have, and a tremendous place to have a lot of antigen exposure and a good reason to have chronic immune activation”. She then pointed out that the genomics work is very exciting as applied to immunology and virology, as it replicates the immune data by a completely different method. Professor Klimas began her lecture by saying: “People are finding things that fit. This all makes sense. It’s a very exciting time because the puzzle www.investinme.org Page 78 of 108
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