Regulatory T-cells (Tregs) — immune cells that normally dampen immune and inflammatory responses by inhibiting the activity of pro-inflammatory immune cells — enabled mice in a model of multiple sclerosis to partly recover from limb and tail paralysis, scientists reported.
Tregs can do this by preventing a subtype of pro-inflammatory T-helper cells, called Th17, from interacting with another type of immune cell, called antigen-presenting cells (APCs), the team found. Tregs can also block calcium signaling in Th17 cells, further enhancing their ability to counteract Th17’s pro-inflammatory activity.
These findings help in understanding the molecular mechanisms at play in multiple sclerosis (MS), and may lead to new forms of treatment based on the use of T-cells.
The study, “Regulatory T cells suppress Th17 cell Ca2+ signaling in the spinal cord during murine autoimmune neuroinflammation,” was published in the journal PNAS.
“Building on our years of expertise in immunoimaging and calcium signaling, this study highlights Th17 and Treg cell interactions, their motility characteristics, and intracellular signaling, thus providing new insights into the pathophysiology [disease mechanisms] of MS,” Michael Cahalan, PhD, professor and chair of the department of Physiology and Biophysics at the University of California, Irvine (UCI) School of Medicine, and the study’s senior author, said in a press release.
“Our results illustrate how a regulatory T cell-based immunotherapy may be instrumental in limiting demyelination in MS,” Cahalan added.
The interaction between different types of immune cells is known to be vital for controlling the body’s immune and inflammatory responses, but it is still unclear how Tregs position themselves to counter the inflammatory activity of Th17 cells.
To address this and also investigate how Tregs interact with APCs and Th17 cells in the context of inflammation, the researchers used advanced high-resolution imaging to visualize portions of the spinal cord of mice with chronic experimental autoimmune encephalomyelitis (EAE), a disease that mimics MS in humans.
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