[Laquinimod Is an Oral Drug With a Marked Neuroprotective Effect for Pathogenetic Treatment of Multiple Sclerosis(review)].

[Laquinimod is an oral drug with a marked neuroprotective effect for pathogenetic treatment of multiple sclerosis(review)].

Zh Nevrol Psikhiatr Im S S Korsakova. 2013; 113(2 Pt 2): 93-9

New oral therapies of MS cause great attention. This review includes data on the II and III phase clinical studies of laquinimod (LAQ) – a new oral therapy for MS with immunoregulatory, anti inflammatory and neuroprotective action. LAQ has no immunosuppressive effects and has a very good safety and tolerability profile. Data of phase III studies including 2437 MS patients confirmed positive effect of LAQ on relapse rate and disability progression. These clinical results were supported by the MRI data, showing also a significant slowing of the brain atrophy. Russian neurological clinics actively participated in all LAQ clinical trials: 241 MS patients from 11 centers from Russia took part in the phase II trials. The data in this subgroup confirm all changes, registered in the whole group of patients. HubMed – drug


[Alemtuzumab is a new drug based on monoclonal antibodies for treatment multiple sclerosis: treatment possibilities and risks(review)].

Zh Nevrol Psikhiatr Im S S Korsakova. 2013; 113(2 Pt 2): 87-92

Recently published results of II and II phase clinical trials of alemtuzumab in relapsing-remitting multiple sclerosis (MS) are reviewed. This drug has an immunosuppressive mechanism of action with an anti-inflammatory effect higher than that of high-dose beta-interferon. Its neuroprotective activity and possible side-effects are discussed. HubMed – drug


Leishmania mexicana Infection Induces IgG to Parasite Surface Glycoinositol Phospholipids that Can Induce IL-10 in Mice and Humans.

PLoS Negl Trop Dis. 2013 May; 7(5): e2224
Buxbaum LU

Infection with the intracellular protozoan parasite Leishmania mexicana causes chronic disease in C57BL/6 mice, in which cutaneous lesions persist for many months with high parasite burdens (10(7)-10(8) parasites). This chronic disease process requires host IL-10 and Fc?RIII. When Leishmania amastigotes are released from cells, surface-bound IgG can induce IL-10 and suppress IL-12 production from macrophages. These changes decrease IFN-? from T cells and nitric oxide production in infected cells, which are both required for Leishmania control. However, antibodies targets and the kinetics of antibody production are unknown. Several groups have been unsuccessful in identifying amastigote surface proteins that bind IgG. We now show that glycoinositol phospholipids (GIPLs) of L. mexicana are recognized by mouse IgG1 by 6 weeks of infection, with a rapid increase between 12 and 16 weeks, consistent with the timing of chronic disease in C57BL/6 mice vs. healing in Fc?RIII-deficient mice. A single prominent spot on TLC is recognized by IgG, and the glycolipid is a glycosyl phosphatidylinositol containing a branched mannose structure. We show that the lipid structure of the GIPL (the sn-2 fatty acid) is required for antibody recognition. This GIPL is abundant in L. mexicana amastigotes, rare in stationary-phase promastigotes, and absent in L. major, consistent with a role for antibodies to GIPLs in chronic disease. A mouse monoclonal anti-GIPL IgG recognizes GIPLs on the parasite surface, and induces IL-10 from macrophages. The current work also extends this mouse analysis to humans, finding that L. mexicana-infected humans with localized and diffuse cutaneous leishmaniasis have antibodies that recognize GIPLs, can bind to the surface of amastigotes, and can induce IL-10 from human monocytes. Further characterization of the target glycolipids will have important implications for drug and vaccine development and will elucidate the poorly understood role of glycolipids in the immunology of infections. HubMed – drug