Some of our on-going projects are to investigate the following: (i) the expression pattern and role of the interleukin (IL)-12 p40 family of monokines in secondary progressive MS; (ii) the role of IL-12 and IL-23 in T cell homing to the CNS and epitope spreading during the course of EAE; (iii) CNS expression and functional significance of “lymphoid” chemokines, such as CXCL13 and CCL21, in driving the formation of organized inflammatory infiltrates during relapsing EAE and MS; (iv) the origin and biological activities of dendritic cells that accumulate in demyelinating lesions during EAE; (v) the importance of regulatory T cells for remission during relapsing autoimmune demyelination; (vi) the role of neutrophils and the chemokines that attract them in blood-brain-barrier breakdown during EAE; and (vii) the impact of b -IFN therapy on the immune system of patients with MS.
Segal, B.M. , Dwyer, B., Shevach, E.M. An IL-12/IL-10 Immunoregulatory Circuit Controls Susceptibility to Autoimmune Disease. Journal of Experimental Medicine 187: 537-546, 1998.
Chang, J.T., Shevach, E.M., Segal, B.M. Regulation of IL-12 Receptor ß2 Subunit Expression by Endogenous IL-12: A Critical Step in the Differentiation of Pathogenic Autoreactive T cells. Journal of Experimental Medicine 189: 969-978, 1999.
Segal, B.M., Chang, J.T., Shevach, E.M. CpG Oligonucleotides are Potent Adjuvants for the Activation of Autoreactive Encephalitogenic T Cells in Vivo. Journal of Immunology 164: 5683-5688, 2000.
Segal, B.M. , Glass, D. and Shevach, E.M. IL-10 Producing Tr1 Cells Mediate Tumor Rejection, Journal of Immunology (Cutting Edge) 168: 1-4, 2002.
Ichikawa , H., Williams, L.P. and Segal, B.M. Activation of Antigen Presenting Cells through CD40 or Toll-9 Receptors Overcomes Tolerance and Precipitates Autoimmune Disease. Journal of Immunology , 169:2781-2787 2002.
Segal, B.M. Experimental Autoimmune Encephalomyelitis: Cytokines, Antigen Presenting Cells and Immunoregulation. Current Allergy and Asthma Reports 3(1): 86-93, 2003.
Bagaeva, L., Williams, L.P. and Segal, B.M. IL-12 Dependent/ IFNg Independent Expression of CCR5 by Myelin Reactive T Cells Correlates with Encephalitogenicity. Journal of Neuroimmunology 137(1-2): 109-116, 2003.
Segal, B.M. CNS Chemokines, Cytokines, and Dendritic Cells in Autoimmune Demyelination. J Neurol Sci. 228(2):210-4, 2005.
King, I. and Segal, B.M. Cutting Edge: IL-12 induces CD4 + CD25 - T Cell Activation in the Presence of Regulatory T Cells. Journal of Immunology (Cutting Edge section) 175(2): 641-5, 2005.
Deshpande, P. and Segal, B.M. IL-12 Driven Upregulation of P-selectin Ligand on Myelin-Specific T Cells is a Critical Step in an Animal Model of Autoimmune Demyelination. Journal of Neuroimmunology 173(1-2):35-44, 2006.
Bagaeva, L.V., Rao, P., Powers, J.M. and Segal, B.M. CXCL13 Plays a Role in Experimental Autoimmune Encephalomyelitis. Journal of Immunology 176(12):7676-85, 2006.
Deshpande, P., King, I.L. and Segal, B.M. Cutting Edge: CNS CD11c + Cells from Mice with Encephalomyelitis Polarize Th17 Cells and Support CD25 + CD4 + Mediated Immunosuppression, Suggesting Dual Roles in the Disease Process. Journal of Immunology 178(11): 6695-99, 2007.
Carlson, T., Kroenke, M., Rao, P., Lane, T.E., Segal, B.M. The Th17-ELR+ CXC Chemokine Pathway is Essential for the Development of CNS Autoimmune Disease. Journal of Experimental Medicine,208; 205(4): 811-823, 2008.
Kroenke MA, Carlson TJ, Andjelkovic A, Segal BM. IL-12 and IL-23 modulated T cells induce distinct types of EAE based on histology, CNS chemokine profile, and response to cytokine inhibition. J Exp Med 2008;205(7): 1535-1541. PMCID: PMC2442630
Segal BM, Constantinescu CS, Raychaudhuri A, Kim L, Fidelus-Gort R, Kasper LH on behalf of the Ustekinumab MS Investigators. Repeated subcutaneous injections of IL12/23 p40 neutralising antibody, ustekinumab, in patients with relapsing-remitting multiple sclerosis: a phase II, double-blind, placebo-controlled, randomised, dose-ranging study. Lancet Neurol 2008;7(9): 796-804.
King IL, Dickendesher TL, Segal BM. Circulating Ly-6C+ myeloid precursors migrate to the CNS and play a pathogenic role during autoimmune demyelinating disease. Blood 2009;113(14): 3190-3197. PMCID: PMC2665891.
Segal BM. Getting to the crux of the matter: IL-23 and Th17 cell accumulation in the CNS. Eur J Immunol 2009; 39(7):1713-1715. PMCID: PMC2760599.