B cells in multiple sclerosis

Abstract

The most common laboratory abnormality in multiple sclerosis (MS) is an increased amount of cerebrospinal fluid IgG and the presence of oligoclonal bands. Despite studies of the humoral response that suggest the involvement of an infectious agent or autoantigen in disease, the major targets of the oligoclonal response are still unknown. Identification of these targets will reveal valuable insights into the cause and pathogenesis of MS and is likely to lead to effective treatment.

Vorinostat, a histone deacetylase inhibitor, suppresses dendritic cell function and ameliorates experimental autoimmune encephalomyelitis

“…Our results thus suggest that vorinostat ameliorates autoimmunity diseases by reducing these proinflammatory cytokines. These data support previously reports that the HDAC inhibitors trichostatin A (TSA) and sodium valproate (VPA) blocked secretion of proinflammatory cytokines, such as TNF-α, IL-1β, IL-6 and IL-12 (Burgoon et al, 2004;Dangond et al, , 1999Lucchinetti et al, 2000).…”

Catalytic autoantibodies in multiple sclerosis: Pathogenetic and clinical aspects

“…3). Activity towards MBP [7,9] was completely suppressed after preincubation with immobilized antispecies AB (data not presented), which confirms catalytic nature of detected activity and rules out the risk of enzyme contamination. IgG isotype AB from donor sera (Fig.…”

“…Autoantibodies presented by a heterogeneous group of immunoglobulins were detected in the liquor and peripheral blood proteins of MS patients [7,9,13,14].…”

Laser-capture microdissection of plasma cells from subacute sclerosing panencephalitis brain reveals intrathecal disease-relevant antibodies

“…These studies have led to the hypothesis that the oligoclonal IgG in the brain and CSF of patients with a chronic inflammatory CNS disease of unknown etiology, such as multiple sclerosis (MS), sarcoidosis, and Behcet's disease, is antibody directed against the agent that causes disease. Although OGBs are found in 88-100% of CSF from MS patients (9), the corresponding antigens remain unknown (10,11). Such unanswered questions point to the need for improved techniques to identify disease-relevant antibodies and their cognate antigens and suggest the promise of such techniques in revealing the causes of inflammatory diseases with unknown etiologies.…”