title: Rituximab reduces B cells and T cells in cerebrospinal fluid of multiple sclerosis patients.
abstract: Effects of B cell depletion by rituximab, a monoclonal antibody to CD20, were studied in patients with relapsing MS that had not responded optimally to standard immunomodulatory therapies. Flow cytometry demonstrated reduced cerebrospinal fluid (CSF) B cells and T cells in most patients at 6 months post-treatment. ELISAs demonstrated modest reductions in serum antibodies to myelin oligodendrocyte glycoprotein and myelin basic protein in some subjects. Beta-interferon neutralizing antibodies were reduced in three subjects, but developed anew after treatment in three others, suggesting caution in considering rituximab as a means to eliminate NABs. In summary, rituximab depleted B cells from CSF at 24 weeks after initial treatment, and this B cell depletion was associated with a reduction in CSF T cells as well.
authors.affiliation: Box 8111, Department of Neurology, Washington University School of Medicine, 660 S. Euclid Avenue, Saint Louis, MO 63110, USA. crossa@neuro.wustl.edu
authors.forename: Anne H
authors.initials: AH
authors.lastname: Cross
authors.forename: Jennifer L
authors.initials: JL
authors.lastname: Stark
authors.forename: Joanne
authors.initials: J
authors.lastname: Lauber
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Ramsbottom
authors.forename: Jeri-Anne
authors.initials: JA
authors.lastname: Lyons
mesh_terms: D000328:Adult; D000911:Antibodies, Monoclonal / Q000276:immunology / Q000494:pharmacology* / Q000627:therapeutic use; D058846:Antibodies, Monoclonal, Murine-Derived; D000917:Antibody Formation / Q000187:drug effects / Q000276:immunology; D018951:Antigens, CD20 / Q000276:immunology; D001323:Autoantibodies / Q000032:analysis / Q000097:blood / Q000276:immunology; D001402:B-Lymphocytes / Q000187:drug effects* / Q000276:immunology; D002555:Cerebrospinal Fluid / Q000166:cytology* / Q000276:immunology; D015536:Down-Regulation / Q000187:drug effects / Q000276:immunology; D005260:Female; D005434:Flow Cytometry; D000068717:Glatiramer Acetate; D006801:Humans; D007111:Immunity, Cellular / Q000187:drug effects / Q000276:immunology; D007155:Immunologic Factors / Q000276:immunology / Q000494:pharmacology / Q000627:therapeutic use; D007165:Immunosuppression Therapy / Q000379:methods; D000068556:Interferon beta-1a; D000068576:Interferon beta-1b; D016899:Interferon-beta / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D020529:Multiple Sclerosis, Relapsing-Remitting / Q000134:cerebrospinal fluid / Q000188:drug therapy* / Q000276:immunology*; D009185:Myelin Proteins / Q000276:immunology; D010455:Peptides / Q000627:therapeutic use; D000069283:Rituximab; D013601:T-Lymphocytes / Q000187:drug effects* / Q000276:immunology; D016896:Treatment Outcome
chemical_list: D000911:Antibodies, Monoclonal; D058846:Antibodies, Monoclonal, Murine-Derived; D018951:Antigens, CD20; D001323:Autoantibodies; D007155:Immunologic Factors; D009185:Myelin Proteins; D010455:Peptides; D000068576:Interferon beta-1b; D000069283:Rituximab; D000068717:Glatiramer Acetate; D016899:Interferon-beta; D000068556:Interferon beta-1a