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June 15, 2015
Editor: Andrew H. Lichtman, MD, PhD, Brigham & Women's Hospital
Editorial Board: Abul K. Abbas, MD, University of California, San Francisco | Carla J. Greenbaum, MD, Benaroya Research Institute | Andrew H. Lichtman, MD, PhD, Brigham & Women's Hospital
|Highlights from Recent Literature|
Regulating the Regulators: Shutting Down Regulatory T Cells with GARP-TGFβ1 Antibodies
Research paper: Julia Cuende et al. Monoclonal antibodies against GARP/TGFβ-1 complexes inhibit the immunosuppressive activity of human regulatory T cells in vivo. Science Translational Medicine (2015) 7, 274ra18
Regulatory T cells (Treg) play critical roles in initiating and maintaining self tolerance but they can also interfere with tumor immunity and permit the persistence of chronic infections. One of the mechanisms by which Treg suppress other T cells is by presenting inactive TGFβ1 on the cell surface that becomes activated to immunosuppressive active TGFβ1 by unknown mechanisms. The authors demonstrate that the protein GARP plays a key role in TGFβ1 activation and that a monoclonal antibody that blocks this conversion inhibits Treg function.
|Highlights from Clinical Immunology, Official Journal of FOCIS|
B Cells and GCs in EAE
A review of Batoulis H. et al. “Central nervous system infiltrates are characterized by features of ongoing B cell-related immune activity in MP4-induced experimental autoimmune encephalomyelitis.” Clinical Immunology. (2015) 158, 47–58
B cell aggregates and perhaps tertiary lymphoid organs (TLOs) form in the meninges of multiple sclerosis (MS) patients, and these have been correlated with more aggressive disease. Nonetheless, the contribution of B cells, antibodies, and TLOs to MS is poorly understood. Experimental autoimmune encephalomyelitis (EAE) is a demyelinating disease of mice that is widely used as model of human MS. EAE is induced by immunization with myelin proteins and strong adjuvant, but the disease is usually helper T cell dependent. The authors have previously described a B cell-dependent variation of the EAE model, induced by immunization of C57BL/6 mice with MP4, a fusion protein of myelin basic protein (MBP) and parts of proteolipid protein (PLP). In this report, the authors' goal was to determine the function and disease impact of B ell infiltrates in the CNS in MP4-EAE.
|Human Immunophenotyping Update|
Immunophenotyping of Human NK Cells
Catherine A. Blish, MD, PhD, Stanford University School of Medicine
Natural killer (NK) cells are innate lymphocytes that can rapidly respond to tumor or infected cells by killing (cytolysis) or by secreting cytokines. Unlike adaptive T and B lymphocytes that somatically rearrange antigen-specific receptors, NK cells express a variety of germline-encoded activating and inhibitory receptors on their cell surface. These receptors include the killer immunoglobulin-like receptors (KIR), C-type-lectin-like receptors (for example, NKG2A, NKG2C, and NKG2D), leukocyte immunoglobulin-like receptor subfamily b member 1 (LILRB1, also known as ILT-2 and CD85j), natural cytotoxicity receptors (NCRs, including NKp30, NKp44, NKp46, and NKp80), and signaling lymphocyte activation molecule (SLAM) family receptors (for example, 2B4, NTB-A). NK cells also express a variety of adhesion molecules such as CD2 and DNAM-1 that influence their function. These receptors allow NK cells to recognize ‘altered self’ on virus-infected, malignant or stressed cells.
|Developments in Basic Immunology and Novel Therapies|
B Cell Depletion Therapy For Autoimmune and Inflammatory Diseases
Shiv Pillai, PhD, Ragon Institute of MGH, MIT and Harvard; Harvard Medical School
B cell depletion using a monoclonal antibody to CD20, a B cell surface protein whose function remains poorly defined, was first conceived of as a therapeutic strategy to treat B cell lymphomas and chronic lymphocytic leukemia. Although this approach is still utilized for the treatment of B cell malignancies, B cell depletion has since emerged as a powerful way to treat a number of autoimmune and inflammatory conditions, including certain disorders that are generally believed to be caused by T cells. The initial anti-CD20 antibody used for therapy was a chimeric antibody called Rituximab. Rituximab remains the major B cell depleting reagent in clinical use today. The success of Rituximab therapy has spawned the generation of a number of newer therapeutics that also target B cells.
|Selected Recent Clinical Trial Results|
Thank you to the 2013 FOCIS Corporate Council: