SEATTLE, May 15 (Reuters Health) - When stimulated with a myelin protein, T cells from women with multiple sclerosis (MS) produce high levels of a "damaging" inflammatory cytokine but do not produce a regulatory cytokine.
"At the moment there is no difference in the way we treat males and females [with MS]. Very possibly there should be a difference," Dr. Clara M. Pelfrey of the Cleveland Clinic Foundation in Ohio told Reuters Health.
Noting that women develop MS three times more often than men, but current treatments focus only on suppressing the inflammatory response, she said that "maybe [treatment] should be promoting the opposite response, the regulatory response."
In a talk here today at the annual meeting of the American Association of Immunologists, Dr. Pelfrey described her team's studies of 22 patients with various stages of multiple sclerosis and 22 healthy controls. In both cases, the patients were evenly split between men and women.
The researchers used a sensitive assay to measure the levels of interferon-gamma, an inflammatory cytokine, and interleukin-5, a regulatory cytokine, after stimulating peripheral blood cells with a series of peptides from proteolipid protein. Proteolipid protein makes up 50% of myelin, Dr. Pelfrey noted.
T cells from all women, regardless of whether they had the disease, produced significantly higher levels of interferon-gamma than T cells from men. Although women with MS produced the highest levels of the cytokine, the difference did not reach statistical significance, Dr. Pelfrey said.
In the case of interleukin-5, she and her group tested 17 MS patients and 11 healthy controls and found that women with MS produced absolutely none of the cytokine. Since healthy males also produced no interleukin-5, Dr. Pelfrey noted that both disease and gender were "truly linked" statistically in this case.
"That really was very striking, and suggested a skewing towards the inflammatory response," she said. "That's encouraging in a sense, that we have something we can point a finger at now and say, 'Well, that's very likely one of the mediators or a major mediator in the disease process'," referring to interleukin-5.
This skewing towards the inflammatory response in women has support from studies in mice, Dr. Pelfry said. She noted that the inflammatory response in women tends to switch to the regulatory response during pregnancy so that their bodies do not reject the fetus. "It's thought that maybe females in general have a stronger inflammatory response to counteract that--in other words, so we don't die of infection when we're pregnant."
She said she would like to recruit more patients to make sure that the
observed cytokine responses are specific for different stages of the disease.