Interleukin-2 therapy does not exacerbate multiple sclerosis

Multiple sclerosis (MS) is an inflammatory and demyelinating disease of the CNS in which cytokines play a crucial role. Pro-inflammatory cytokines interleukin (IL)-1β, IL-2, interferon (IFN)-gamma, and tumor necrosis factor (TNF) (T helper [Th] 1-type cytokines) increase before and during relapses. There also is an increased production of anti-inflammatory cytokines such as IL-4 and IL-10 (Th2-type cytokines) after relapse. Administration of IFN-gamma has been shown to induce exacerbations of the disease.¹ Based on the concept that an imbalance between Th1 and Th2 cytokines is critical to disease activity, various approaches for achieving an immune deviation from a Th1 to a Th2 phenotype are currently under investigation as potential treatments for MS. IL-2, a Th1-type cytokine and proliferation signal for T lymphocytes, is effective against some metastatic malignancies. It, however, also induces neurologic side effects in these patients, most commonly a reversible encephalopathy. Recently eight patients were described who developed neurologic deficits and multiple white and gray matter lesions on MRI during IL-2 treatment.² It was hypothesized that this syndrome might represent immunologically mediated damage.

Here we describe our findings in a patient with secondary progressive MS who was treated with recombinant human IL-2 for metastatic renal cell carcinoma.

Case report. A diagnosis …