(MS), lacking a fully elucidated mode of action. We assessed the
immunomodulatory effects of laquinimod in vitro on human B cells from
healthy or MS patients, cultured alone or with CD4(+) T cells.
Laquinimod modulated B cell markers, mainly by increasing the regulatory
ones CD25, IL10 and CD86, and decreased IL4, while increasing IL10 and
TGFβ in both B and T cells, in a B cell-mediated manner. These findings
shed additional light on the mechanisms underlying the effects of
laquinimod in MS and potentially other immune-mediated diseases.
This is all well and dandy and reports that laquinimod can have an inhibitory effect on B cell markers and increasing the regulatory ones such as increasing IL-10 and TGFbeta. However as laquinimod is a rather useless drug at slowing relapses what does this really mean? Does it mean that these immune responses are irrelevant to the mechanisms of relapse? There was however some evidence that whilst it was not good at slowing relapse rates it may have been better at affecting the accumulation of disability. Is this due to B cell activity? Unless the pharma company do more studies.that I doubt will happen..we will never know.