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SMCI RAMSAY 2018: “Characterization of Janus kinase (JAK) activation profiles in ME/CFS subgroups”, Lombardi

Discussion in 'BioMedical ME/CFS Research' started by Andy, Oct 10, 2018 at 9:52 AM.

  1. Andy

    Andy Committee Member

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    Ramsay 2018 award recipient
    https://solvecfs.org/ramsay-2018-meet-prof-vincent-lombardi-phd/
     
    MEMarge, Indigophoton, Rosie and 10 others like this.
  2. Helen

    Helen Senior Member (Voting Rights)

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    Congratulations Prof. Lombardi and your team!

    It looks like we are getting closer to a treatment if the study will show positive results.
     
    MEMarge, Rosie, Indigophoton and 4 others like this.
  3. jaded

    jaded Established Member (Voting Rights)

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    This research follows on from Prof Lombardi’s and Prof Kenny De Meirleir’s (KDM) prior collaborative work on the appearance of pDCs in gut biopsies of ME patients and potential resulting inflammation.

    https://www.ncbi.nlm.nih.gov/m/pubmed/23422476/?i=7&from=De Meirleir, Kenny

    And their humoral immunity profiling work:

    https://www.ncbi.nlm.nih.gov/m/pubmed/27981498/?i=3&from=De Meirleir, Kenny

    Given that KDM is medical director of the WPI (about to be renamed from Nevada Center for Biomedical Reserch - NVCBR) this work has the potential to translate into clinical trials with JAK/STAT inhibitors. Very exciting.
     
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  4. Dolphin

    Dolphin Senior Member (Voting Rights)

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  5. Sasha

    Sasha Senior Member (Voting Rights)

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    RAMSAY 2018: MEET PROF. VINCENT LOMBARDI, PHDOCTOBER 9, 2018
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    “Characterization of Janus kinase (JAK) activation profiles in ME/CFS subgroups”

    A project summary as written by Prof. Vincent Lombardi, PhD:

    Several investigators have reported that ME/CFS is characterized by a dysregulation of inflammatory cytokines; small peptides that are critical for cell-to-cell communication.

    When inflammatory cytokines bind to their cognate cellular receptor, a signaling cascade is triggered that ultimately result in the activation of inflammatory response genes. It is likely that this process plays a significant role in the pathophysiology of ME/CFS, as it does with several other inflammatory disease.

    Most hematopoietic cytokine receptor signaling is mediated by a family of tyrosine kinases referred to as Janus kinases (JAKs) and their downstream transcription factors, referred to as STATs (signal transducers and activators of transcription).

    Several diseases that are characterized by chronic cytokine-associated inflammation such as rheumatoid arthritis, multiple sclerosis and systemic lupus erythematosus are being successfully treated or the subject of clinical trials with drugs that inhibit the activation of JAKs.

    In that ME/CFS is also characterized by systemic inflammatory cytokine production, it is reasonable to propose that some of the same drugs that are being used or developed to treat the aforementioned inflammatory diseases, may also be efficacious in treating ME/CFS.

    Therefore, the overarching goal of our study is to identify specific JAK activation profiles of distinct ME/CFS subgroups, thereby addressing the feasibility of using JAK inhibitors to treat ME/CFS.

    Our study may additionally provide compelling evidence to justify conducting clinical trials to evaluate the efficacy of JAK inhibitors for the treatment of ME/CFS.​


    I've broken the text up for ease of reading. The original is here:

    https://solvecfs.org/ramsay-2018-meet-prof-vincent-lombardi-phd/

    @Emily Taylor - Congratulations to Solve on having funded such interesting projects! :) Can I put a plea in for Solve to break up mega-paragraphs on your site where you describe the research? Many PWME have difficulty reading such large blocks of text.
     
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