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Patricia Inacio, PhD

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Patricia holds her PhD in cell biology from the University Nova de Lisboa, Portugal, and has served as an author on several research projects and fellowships, as well as major grant applications for European agencies. She also served as a PhD student research assistant in the Department of Microbiology & Immunology, Columbia University, New York, for which she was awarded a Luso-American Development Foundation (FLAD) fellowship.

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Articles by Patricia Inacio, PhD

May 1, 2018 News by Patricia Inacio, PhD

#AAN2018 — Ocrevus Lowers Immune Response to Vaccines in Relapsing MS, Phase 3 Trial Shows

Treatment with Ocrevus (ocrelizumab) is linked to a reduced immune response to vaccinations in patients with relapsing multiple sclerosis (MS), according to a Phase 3 trial. These results were recently presented at the 2018 American Academy of Neurology (AAN) Annual Meeting in Los Angeles in a presentation titled, “Effect of Ocrelizumab on Vaccine Responses in Patients With Multiple Sclerosis.” Genentech’s Ocrevus is an approved MS therapy that targets the CD20 protein located on the surface of B-cells, targeting the cells for destruction. B-cells are immune system cells involved, for example, in the production of antibodies necessary to fight off infection. At the AAN meeting, researchers reported that in MS patients, treatment with Ocrevus decreased the ability of B-cells to activate other immune cells, improving the rate of MS attacks. Penn Medicine neurologist Amit Bar-Or, MD, presented these findings, which showed that interactions between different classes of immune cells, such as B- and T-cells, promote MS attacks. Vaccination against infections is an important part of the management of patients with MS. So, in a second study (NCT02545868), researchers investigated the impact treatment with Ocrevus has on patient response to vaccines. They recruited 102 patients with relapsing MS and randomized them in two groups. In group A, 68 people received a single dose of 600 mg Ocrevus (administered into the blood); in group B, 34 patients received no disease-modifying therapy or interferon-beta. All patients were then administered vaccines for tetanus, seasonal flu, and pneumococcus. Patients in group A received the vaccines 12 weeks after they were treated with Ocrevus, while group B patients received the vaccines on day one. Researchers also tested patients’ response to a novel protein (an antigen) never "seen" by their immune system, called keyhole limpet hemocyanin (KLH) neoantigen. The vaccinations led to an immune system response in all patients, but the level of response in patients treated with Ocrevus was lower. A positive response to the tetanus vaccine at eight weeks after treatment was 23.9% in group A (Ocrevus) compared with 54.5% in group B (no treatment); the response to pneumococcus vaccination was 71.6% in group A and 100% in group B. After four weeks of treatment, the levels of antibodies against the different strains of the flu virus were lower in Ocrevus-treated patients than in the control group, ranging from 55.6% to 80.0% in the Ocrevus group compared with 75.0% to 97.0% in the controls. The immune response to the neoantigen KLH was also decreased in the Ocrevus group. "This study shows that while people with MS treated with ocrelizumab [Ocrevus] can still mount vaccine responses, it's not nearly as strong as prior to treatment," Bar-Or said in a press release. "While antibody responses were reduced in the ocrelizumab treated patients, they still responded to a certain level," he said. "This is valuable information in terms of seasonal vaccines such as the flu — it appears safe for patients taking ocrelizumab to get vaccinated and vaccination is likely to provide them with at least some protection from such infections." These findings correlate with standard guidelines that advise patients to undergo vaccinations six weeks before they start treatment with Ocrevus.

March 27, 2018 News by Patricia Inacio, PhD

Smoking Increases Relapses in RRMS Patients Receiving Interferon-beta, Study Suggests

Cigarette smoking increases the relapse rate in patients with relapsing-remitting multiple sclerosis who are being treated with interferon-beta, a study suggests. The findings suggest that RRMS patients who smoke may have fewer relapses if they quit. An article on the results, “Smoking affects the interferon beta treatment response in multiple sclerosis,” appeared in the journal Neurology. A number of studies have looked at the link between environmental and lifestyle factors and the risk of developing MS. These factors include how much sunlight and vitamin D patients get and whether they have an Epstein-Barr virus infection. Cigarette smoking is a well-documented risk factor in MS, but most of the studies on it have focused on the link between smoking and MS, or the link between smoking and the  disease's progression. “Studies that addressed the relationship between smoking and disease activity in RRMS are rarer,” the researchers wrote. The team decided to investigate whether smoking during interferon-beta treatment would affect relapse rates. Previous research had set the stage for the study by showing a link between smoking and gene mutations that make people more susceptible to developing MS. The mutations were in the HLA and NAT1 genes. The team looked at DNA from 834 RRMS patients in the Danish Multiple Sclerosis Biobank who were treated with interferon-beta. Well-known brand names of the treatment include Rebif, Avonex, and Plegridy. There are also other brand names and biosimilar drugs. Researchers also looked at patients’ medical records two years before they started on interferon-beta. Before making any conclusions on possible links between smoking and patients' relapse rate, the team adjusted for patients’ sex, age at the start of treatment, and number of relapses in the two years before treatment began. Their key conclusion was that smoking increased by more than a quarter the number of relapses in patients on interferon-beta therapy. “Each pack of cigarettes more per day during IFN-β [interferon-beta] treatment increased the number of relapses by 27%,” the team wrote. The researchers found no association among smoking, relapses, and mutations of the HLA or NAT1 genes. “Our results confirm that lifestyle factors are important in MS, suggesting that smoking cessation may be associated with a reduction in disease activity,” they wrote. “Although not formally proving that smoking cessation will decrease disease activity in RRMS, the results should encourage physicians to inform patients with MS about the harmful effect of smoking and increase focus on smoking cessation,” they observed.

March 8, 2018 News by Patricia Inacio, PhD

Increase in Blood-Brain Barrier Protein May Protect Against MS, Study Finds

One way the body may protect itself from nerve cell inflammation is to have cells in the blood-brain barrier increase their production of a protein that keeps immune cells from entering the brain, researchers in Germany and Canada report. The finding suggests that scientists could develop a multiple sclerosis therapy around the protein, known as EGFL7. It would work by preventing as many inflammation-generating immune cells from entering the brain. The underlying trigger for MS is immune cells crossing the blood-brain barrier to invade the central nervous system (CNS). The barrier is a selective membrane that shields the CNS from general blood circulation. Therapies that prevent immune cells from entering the brain can help control the disease, studies have shown. They include Tysabri (natalizumab, marketed by Biogen). But “as with other highly effective disease-modifying therapies which influence a broad range of peripheral immune cells, potential devastating adverse events limit the use of this therapy as a first-line agent,” the researchers wrote. The team at Mainz University Medical Center in Germany and the University of Montreal wondered if epidermal growth factor-like protein 7 (EGFL7) could prevent the brain inflammation in MS.  Although scientists had not previously linked it to MS, it was shown to regulate the migration of immune cells into breast cancer tumors. The CNS response to the chronic inflammation seen in MS patients and a mouse model of the disease was to increase EGFL7 in the blood-brain barrier, the researchers found. Researchers said the increase prevented pro-inflammatory immune cells from crossing into the CNS. Endothelial cells that line blood capillaries in the blood-brain barrier are the ones that secrete EGFL7. “We postulate that EGFL7 upregulation by BBB-ECs [brain blood barrier-endothelial cells] is induced as a compensatory mechanism to promote survival and recovery of BBB function in neuroinflammatory conditions,” the team wrote. Researchers then tested what happened in mice that lacked EGFL7. They found that the mice developed MS earlier and that their blood-brain barrier membrane was less efficient at keeping immune cells out. Treatment with EGFL7 improved the disease severity in the MS mice and tightened the blood-brain barrier, they said. “In light of our findings, smaller EGFL7 agonists, in development for other diseases, could therefore constitute an appealing therapeutic avenue for MS,” the team concluded.

February 27, 2018 News by Patricia Inacio, PhD

Transforming Skin Cells Into Nerve Stem Cells Could Be a Way to Treat MS, Study Suggests

Reprogramming skin cells into brain stem cells, then transplanting them into the central nervous system may reduce inflammation and reverse the nerve cell damage in progressive multiple sclerosis, a mouse study shows. Scientists have dubbed macrophages the immune system's big eaters because they engulf abnormal cells like cancer in addition to invaders like viruses and bacteria. Special classes of macrophages live in a number of organs, including the brain and spinal cord, where they’re called microglia. Although they protect the body, microglia can participate in the development of progressive forms of MS by attacking the central nervous system, causing nerve cell damage. MS is an autoimmune disease, or one in which the immune system can attack healthy tissue besides invaders. Recent studies have suggested that neural stem cells, which have the capacity to differentiate into any type of nerve cell, can regulate immune response and inflammation in the central nervous system. At one point, researchers obtained neural stem cells from embryos. But this technique generated only a fraction of the cells needed for treatments. Meanwhile, doctors have tried to avoid collecting stem cells from someone with a different genetic profile than the patient because this increases the risk that the immune system will attack them once they're transplanted. University of Cambridge scientists decided to try reprogramming skin cells into neural stem cells. The idea behind the mouse study was that using skin cells from the same person who will receive the stem cells will reduce the chance that the immune system will attack the stem cells. In the mouse study, the team discovered a link between higher than normal levels of a small metabolite, called succinate, and chronic MS. The metabolite prompts macrophages and microglia to generate inflammation in the cerebrospinal fluid that bathes the brain and spinal cord. Transplanting neural stem cells and progenitors of these stem cells into the cerebrospinal fluid of mice improved the animals' chronic nerve cell inflammation. The stem cells reduced the animals' succinate levels and switched their macrophages and microglia from a pro- to an anti-inflammatory state. This led to a decrease in inflammation and less damage to the central nervous system. “Our mouse study suggests that using a patient’s reprogrammed cells could provide a route to personalized treatment of chronic inflammatory diseases, including progressive forms of MS,” Stefano Pluchino, a principal researcher in Cambridge's Department of Clinical Neurosciences, said in a press release. “This is particularly promising as these cells should be more readily obtainable than conventional neural stem cells and would not carry the risk of an adverse immune response,” said Pluchino, the study's lead author. Luca Peruzzotti-Jametti, a Wellcome Trust research training fellow, said the discovery would not have been possible without a multidisciplinary collaboration. “We made this discovery by bringing together researchers from diverse fields, including regenerative medicine, cancer, mitochondrial biology, inflammation and stroke, and cellular reprogramming."