Until now, researchers thought that immune cells could suppress inflammatory reactions.

Instead, they found that more immune cells increase inflammatory response and reduce inflammation – a finding that could offer a clue for future treatments of inflammatory diseases such as rheumatoid arthritis, inflammatory bowel disease and psoriasis.

Scientists are using a mouse model of pain-induced depression to understand how the immune system works, and whether this process contributes to certain clinical syndromes, epidemics and behaviors such as opioid use disorder.

The mice exhibited a dramatic decrease in meaningful pain symptoms, as well as an absolutely freezing of the ability to perform complex thinking tasks.

They also displayed a remarkable inflammatory reaction, which heightened pain sensitivity and increased inflammation.

IF the immune cells’ effects are replicated with humans, it has the potential to influence treatments for severe pain that have little hope of long-term efficacy due to the unreliability of the pain symptoms; immune dysfunction oftentimes immunosuppressed.

Titled “Effects of multiple functional checkpoint blockade, ” by Dennis Waldor, Ph.D., which was published in Nature Immunology, this work draws on the understanding of laboratory models of non-inflammatory developmental states, with an emphasis on defensive immune response.

“Unintended side effects of pain-induced depression frequently appear in animal models where pain is not taken very seriously, which means that pain-transmitting cells have adapted to ‘no pain, no equal’ and indeed the optimal pain coping mechanism is not thought to exist,” says Waldor, who holds the Everest Chair and directs the Division of Pain Medicine at Boston Medical Center (BMC).

Targeting receptors that act directly on a subset of immune cells is currently being explored as a promising way to treat chronic pain, which still remains a major challenge.

McCrieg Bundy, Ph.D., who co-authored the research, and other authors believe that the modulation of immune cells should serve as a starting point to treat inflammatory pain, which affects nearly 2 of every 3 women in the United States over the age of 20.

“We think there is an important way of modeling pain that will not have an obvious effect on the treatment of chronic pain,” says Bundy, who also is a professor of neurology and formal neurobiology in the UCSF College of Medicine.

“We have been trying to extend our model to humans, and found that that our model has the potential to be applied to the clinical management of chronic pain, which is what we want to do in the context of our lab and exploring pain in mice.”