Investigation of mast cell toll-like receptor 3 in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis and Systemic Mastocytosis participants using the novel application of autoMACS magnetic separation and flow cytometry
2017
Background: Viral infections and hypersensitivities are commonly reported by Chronic Fatigue Syndrome/Myalgic
Encephalomyelitis (CFS/ME) patients. Mast Cells (MC) uniquely mediate type 1 hypersensitivities and resolve viral
infections via toll-like receptor 3 (TLR3).
Objective: To characterise and compare mast cell progenitors (MCPs) in CFS/ME participants with a known MC
disorder, Systemic mastocytosis (SM), and secondly, to investigate the role of MC TLR3 in CFS/ME participants
following Polyinosinic:polycytidylic acid (Poly I:C) stimulation.
Methods: A total of 11 International Consensus Criteria defined CFS/ME participants (40.42 ± 10.31), 9 World Health
Organisation defined systemic mastocytosis (SM) participants (47.00 ± 10.37) and 12 healthy controls (HC) (36.36 ± 9.88)
were included. Following autoMACS magnetic separation, CD117+/LinMCPs
were stimulated with Poly I:C for 24hr.
MCP purity (CD117 and Lin2), maturity (CD34 and FceRI), interaction receptors and ligands (CD154 and HLA-DR),
and SM-specific (CD2 and CD25) markers were measured using flow cytometry.
Results: There was a significant decrease in HLA-DR+/CD154-
expression between CFS/ME and SM groups pre and post
Poly I:C stimulation. There were no significant differences in maturity MCPs, CD154, and CD2/CD25 expression between
groups pre and post Poly I:C stimulation.
Conclusion: This pilot investigation provides a novel methodology to characterise MCPs in a rapid, inexpensive and
less invasive fashion. We report a significant decrease in HLA-DR+/CD154-
expression between CFS/ME and SM
participants, and an observed increase in HLA-DR/CD154+
expression post Poly I:C stimulation in CFS/ME
participants. Peripheral MCPs may be present in CFS/ME pathophysiology, however further investigation is required to
determine their immunological role.
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