“Characterization of Janus kinase (JAK) activation profiles in ME/CFS subgroups”
PI: Vincent Lombardi, PhD
University of Nevada, Reno
Vincent Lombardi (PhD), an established ME/CFS researcher, is studying activation of janus kinase (JAK), a signaling pathway involved in cytokine activity, in individuals with ME/CFS. Working with expert clinician Kenny De Meirleir (MD), JAK activation profiles of a large well-defined cohort of patients and control subjects will be assessed. Previous research has shown that inhibition of JAKs is an effective strategy for treating immune-mediated diseases that are characterized by elevated inflammatory cytokines. In fact, JAK inhibitors are being used or trialed in indications characterized by chronic cytokine-associated inflammation such as multiple sclerosis and rheumatoid arthritis. Therefore, this investigation could lead directly to treatments that are already FDA-approved for other conditions, increasing the potential for translational benefit to patients.
“We are honored and grateful to have received the SMCI Ramsay award to understand the Janus kinase activation profile of ME/ CFS. We would also like to express our unwavering commitment to helping those who suffer with this devastating disease.” -Prof. Lombardi
Read coverage of Dr. Lombardi and Dr. De Meirleir’s immunosignature research here
Read the research team’s study abstract below:
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.