*NIH takes action to bolster research on Myalgic Encephalomyelitis/Chronic Fatigue Syndrome
October 29, 2015 (For Immediate Release: Thursday)
many of the published studies are based on small study
populations and have not been replicated."
"An an effort to remedy this situation, NIH will design a clinical study in the NIH Clinical Center with plans to enrol individuals who developed fatigue following a rapid onset of symptoms suggestive of an acute infection. The study will involve researchers from NINDS, the National Institute of Allergy and Infectious Diseases, National Institute of Nursing Research and National Heart, Lung, and Blood Institute."
----qute from National Institutes of Health (NIH) at the US Department of Health & Human Services;
*Temple University Health System. "Bacterial biofilms may play a role in lupus, research finds."
ScienceDaily. ScienceDaily, 6 July 2015.
"Lupus, multiple sclerosis, and type-1 diabetes are among more than a score of diseases in which the immune system attacks the body. But why the immune system begins its misdirected assault has remained a mystery. Now, researchers have shown that bacterial communities known as biofilm play a role in the development of the autoimmune disease systemic lupus erythematosus -- a discovery that may provide important clues about several autoimmune ailments."
length analysis in Chronic Fatigue Syndrome
ER Unger, J Murray, LP Oakley, JM Lin, MS Rajeevan
- Centers for Disease Control and Prevention, Atlanta, GA
Date: April 2016 (Vol. 30, #1 Supplement, lb459)
Our results indicate that CFS should be included in the list of conditions associated with telomere shortening. Further work is needed to evaluate if the shortening has functional significance in CFS.
Nevada Center for Biomedical Research (NVCBR)
Date: May 28, 2016
Rem: This is the new WPI site
NVCBR researchers seek to discover the underlying causes of a spectrum of acquired diseases with the greatest impact on the immune system and the brain. Our key studies surround aberrant immunity, the gut/brain axis, inflammation, chronic infection, genetic susceptibility, and autoantibodies.
Journal of Immunology (Vol 196, #1 Supplement, 137.4)
Date: May 1, 2016
of gut-associated pDCs to express membrane bound
APRIL and BAFF prevents their ability to promote low-affinity
IgA expression in ME/CFS
Vincent C Lombardi(1), Svetlana F Khaiboullina(1), Kenny L De
Meirleir(1), Tanja Mijatovic(2), Jan Hulstaert(3)
1 Nevada Ctr. for Biomed. Res.
2 R.E.D Lab., Belgium
3 General Hosp. Jan Portaels, Belgium
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a heterogeneous illness characterized by a number of comorbid conditions; gastrointestinal (GI) dysregulation make up one subgroup of this disease. IgA is the most abundant antibody isotype found in mucosal secretions including the gut. In a process of class switch recombination (CSR), that relies on the interaction of plasmacytoid dendritic cells (pDCs) with B cells, in a T cell independent (TI) manner, low-affinity IgA are produced that limit the adhesion of commensal bacteria to intestinal epithelia without neutralizing them. These low-affinity antibodies also limit bacterial overgrowth and potential bacterial translocation thus maintaining gut homeostasis. This process is known as 'immune exclusion'. Two ligands on the surface of pDCs that are obligatory for the process; the membrane bound form of APRIL and BAFF. The upregulation of APRIL and BAFF on the surface of pDCs is dependent on low-level expression of type I interferon (IFN) which is produced by intestinal stromal cells in response to Toll-like receptor (TLR) engagement. Previous studies suggest that peripheral pDCs are significantly lower in subjects with ME/CFS when compared to controls and studies conducted by us further suggest these cells likely redistribute from the periphery to the gut. We have observed that, in contrast to controls, gut-associated pDCs in subjects with ME/CFS lack APRIL and BAFF expression. These data support a model of gut pathology in ME/CFS whereby dysregulated pDCs fail to promote the production of low-affinity IgA through the process of TI activation of B cells, thereby leading to bacterial overgrowth, dysbiosis, bacterial translocation and systemic immune activation.
(c) 2016 American Association of Immunologists, Inc.
※ "BAFF and APRIL" とは
"Nurselike cells express BAFF and APRIL, which can promote survival of chronic lymphocytic leukemia cells via a paracrine pathway distinct from that of SDF-1α"
Mitsufumi Nishio,Tomoyuki Endo,Nobuhiro Tsukada,Junko Ohata,Shinichi Kitada,John C. Reed,Nathan J. Zvaifler, and Thomas J. Kipps
Author Affiliations From the
Department of Medicine, University of California, San Diego, La Jolla; and The
Burnham Institute, La Jolla, CA.
Accepted March 28, 2005.
Copyright © 2005 by The American Society of Hematology
Expression Of BAFF In T Cells In Active Systemic Lupus Erythematosus: The Role Of BAFF In T cell-dependent B Cell Pathogenic Autoantibody Production
S. Morimoto; S. Nakano; T. Watanabe; Y. Tamayama; A. Mitsuo; Y. Nakiri; J. Suzuki; K. Nozawa; H. Amano; Y. Tokano; T. Kobata; Y. Takasaki
Prominent role for plasmacytoid dendritic cells in mucosal T cell-independent IgA induction.
Immunity. 2011; 34(2):247-57 (ISSN: 1097-4180)
Abe Y; Asano J; Sato T; Liu J; Iwata M; Ohteki T
Department of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.
Although both conventional dendritic cells (cDCs) and plasmacytoid dendritic cells (pDCs) are present in the gut-associated lymphoid tissues (GALT), the roles of pDCs in the gut remain largely unknown. Here we show a critical role for pDCs in T cell-independent (TI) IgA production by B cells in the GALT. When pDCs of the mesenteric lymph nodes (MLNs) and Peyer's patches (PPs) (which are representative GALT) were cultured with naive B cells to induce TI IgA class switch recombination (CSR), IgA production was substantially higher than in cocultures of these cells with cDCs. IgA production was dependent on APRIL and BAFF production by pDCs. Importantly, pDC expression of APRIL and BAFF was dependent on stromal cell-derived type I IFN signaling under steady-state conditions. Our findings provide insight into the molecular basis of pDC conditioning to induce mucosal TI IgA production, which may lead to improvements in vaccination strategies and treatment for mucosal-related disorders.
Biological Research, Vol. 49, #1, p 27
Date: May 31, 2016
Novel identification and characterisation of Transient receptor potential melastatin 3 ion channels on Natural Killer cells and
B lymphocytes: effects on cell signalling in Chronic fatigue syndrome/Myalgic encephalomyelitis patients
T. Nguyen(1,2,*), D. Staines(3,4), B. Nilius(5), P. Smith(3), S. Marshall-Gradisnik(3,4)
1 The National Centre for Neuroimmunology and Emerging Diseases, Menzies Health Institute, Griffith University, Parklands Drive, Southport,
Mailbox 68, Gold Coast, 4222, Australia.
2 School of
Medical Science, Griffith University, Gold Coast, Australia
3 The National Centre for Neuroimmunology and Emerging Diseases, Menzies Health Institute, Griffith University, Parklands Drive, Southport,
Mailbox 68, Gold Coast, 4222, Australia.
4 School of Medical Science, Griffith University, Gold Coast, Australia.
5 Department of Molecular Cell Biology, Laboratory of Ion Channel Research, KU Leuven University, 49 Herestraat, Leuven, B-3000, Belgium.
author. Email: email@example.com
Received: 26 January 2016
Accepted: 9 May 2016
Published: 31 May 2016
The results from this preliminary investigation identify, for the first time, TRPM3 surface expression on both NK and B lymphocytes in healthy controls. We also report for the first time, significant reduction in TRPM3 cell surface expression in NK and B lymphocytes, as well as decreased intracellular calcium within specific conditions in CFS/ME patients. This warrants further examination of these pathways to elucidate whether TRPM3 and impaired calcium mobilisation has a role in CFS/ME.
Keywords: Chronic fatigue syndrome - Transient receptor potential - Calcium signalling - Myalgic encephalomyelitis
* "TRPM3" とは
（TRP channel は"一過性受容器電位チャネル", Transient receptor potential ion channel, TRPM の”M"は”Melastatin"=メラスタチン）
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