Honors & Awards

  • T32 Postdoctoral Fellow, Stanford University School of Medicine, Department of Immunology (2015-2016)
  • T32 Postdoctoral Fellow, Stanford University School of Medicine, Department of Immunology (2014-2015)

Boards, Advisory Committees, Professional Organizations

  • Stanford Immunology Postdoctoral Committee Member, Stanford University, Department of Immunology (2015 - Present)

Professional Education

  • Doctor of Philosophy, University of California Davis, Immunology (2014)
  • Master of Science, California State Univ, Los Angeles (2009)
  • Bachelor of Science, California State Univ, Los Angeles (2007)

Stanford Advisors

  • May Han, Postdoctoral Faculty Sponsor

Community and International Work

  • Stanford Immunology Postdoctoral Committee Member, Stanford University


    Bay Area

    Ongoing Project


    Opportunities for Student Involvement


Research & Scholarship

Current Research and Scholarly Interests

I am interested in investigating the effects of S1P-mediated signaling in immune-mediated CNS inflammation, microglial activation and oligodendrocyte differentiation.


All Publications

  • Effects of sphingosine-1-phosphate receptor 1 phosphorylation in response to FTY720 during neuroinflammation. JCI insight Tsai, H., Huang, Y., Garris, C. S., Moreno, M. A., Griffin, C. W., Han, M. H. 2016; 1 (9)


    Fingolimod (FTY720, Gilenya), a sphingosine-1-phosphate receptor (S1PR) modulator, is one of the first-line immunomodulatory therapies for treatment of relapsing-remitting multiple sclerosis (MS). Human S1PR1 variants have been reported to have functional heterogeneity in vitro, suggesting that S1PR1 function may influence FTY720 efficacy. In this study, we examined the influence of S1PR1 phosphorylation on response to FTY720 in neuroinflammation. We found that mice carrying a phosphorylation-defective S1pr1 gene [S1PR1(S5A) mice] were refractory to FTY720 treatment in MOG35-55-immunized and Th17-mediated experimental autoimmune encephalomyelitis (EAE) models. Long-term treatment with FTY720 induced significant lymphopenia and suppressed Th17 response in the peripheral immune system via downregulating STAT3 phosphorylation in both WT and S1PR1(S5A) mice. However, FTY720 did not effectively prevent neuroinflammation in the S1PR1(S5A) EAE mice as a result of encephalitogenic cells expressing C-C chemokine receptor 6 (CCR6). Combined treatment with FTY720 and anti-CCR6 delayed disease progression in S1PR1(S5A) EAE mice, suggesting that CCR6-mediated cell trafficking can overcome the effects of FTY720. This work may have translational relevance regarding FTY720 efficacy in MS patients and suggests that cell type-specific therapies may enhance therapeutic efficacy in MS.

    View details for PubMedID 27699272

  • Therapeutic depletion of monocyte-derived cells protects from long-term axonal loss in experimental autoimmune encephalomyelitis JOURNAL OF NEUROIMMUNOLOGY Moreno, M. A., Burns, T., Yao, P., Miers, L., Pleasure, D., Soulika, A. M. 2016; 290: 36-46


    Studies in multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE) suggest that peripheral monocyte-derived cells (MDCs) are instrumental for disease initiation. MDCs, however, are plastic, and may exert various functions once in the central nervous system (CNS) for prolonged periods. Furthermore, the long-term effect of MDC depletion on continuing axon loss is not known. We show that long-lasting depletion of MDCs, after onset of EAE clinical deficits, is accompanied by decreased CNS infiltration by pathogenic T lymphocytes. Although this treatment does not reverse clinical disease, it prevents worsening of neurological deficits and long-term axonal loss.

    View details for DOI 10.1016/j.jneuroim.2015.11.004

    View details for Web of Science ID 000368955000007

    View details for PubMedID 26711567

  • Conditional Ablation of Astroglial CCL2 Suppresses CNS Accumulation of M1 Macrophages and Preserves Axons in Mice with MOG Peptide EAE. journal of neuroscience Moreno, M., Bannerman, P., Ma, J., Guo, F., Miers, L., Soulika, A. M., Pleasure, D. 2014; 34 (24): 8175-8185


    Current multiple sclerosis (MS) therapies only partially prevent chronically worsening neurological deficits, which are largely attributable to progressive loss of CNS axons. Prior studies of experimental autoimmune encephalomyelitis (EAE) induced in C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein peptide 35-55 (MOG peptide), a model of MS, documented continued axon loss for months after acute CNS inflammatory infiltrates had subsided, and massive astroglial induction of CCL2 (MCP-1), a chemokine for CCR2(+) monocytes. We now report that conditional deletion of astroglial CCL2 significantly decreases CNS accumulation of classically activated (M1) monocyte-derived macrophages and microglial expression of M1 markers during the initial CNS inflammatory phase of MOG peptide EAE, reduces the acute and long-term severity of clinical deficits and slows the progression of spinal cord axon loss. In addition, lack of astroglial-derived CCL2 results in increased accumulation of Th17 cells within the CNS in these mice, but also in greater confinement of CD4(+) lymphocytes to CNS perivascular spaces. These findings suggest that therapies designed to inhibit astroglial CCL2-driven trafficking of monocyte-derived macrophages to the CNS during acute MS exacerbations have the potential to significantly reduce CNS axon loss and slow progression of neurological deficits.

    View details for DOI 10.1523/JNEUROSCI.1137-14.2014

    View details for PubMedID 24920622

  • Neuronopathy in the Motor Neocortex in a Chronic Model of Multiple Sclerosis JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY Burns, T., Miers, L., Xu, J., Man, A., Moreno, M., Pleasure, D., Bannerman, P. 2014; 73 (4): 335-344


    We provide evidence of cortical neuronopathy in myelin oligodendrocyte glycoprotein peptide-induced experimental autoimmune encephalomyelitis, an established model of chronic multiple sclerosis. To investigate phenotypic perturbations in neurons in this model, we used apoptotic markers and immunohistochemistry with antibodies to NeuN and other surrogate markers known to be expressed by adult pyramidal Layer V somas, including annexin V, encephalopsin, and Emx1. We found no consistent evidence of chronic loss of Layer V neurons but detected both reversible and chronic decreases in the expression of these markers in conjunction with evidence of cortical demyelination and presynaptic loss. These phenotypic perturbations were present in, but not restricted to, the neocortical Layer V. We also investigated inflammatory responses in the cortex and subcortical white matter of the corpus callosum and spinal dorsal funiculus and found that those in the cortex and corpus callosum were delayed compared with those in the spinal cord. Inflammatory infiltrates initially included T cells, neutrophils, and Iba1-positive microglia/macrophages in the corpus callosum, whereas only Iba1-positive cells were present in the cortex. These data indicate that we have identified a new temporal pattern of subtle phenotypic perturbations in neocortical neurons in this chronic multiple sclerosis model.

    View details for DOI 10.1097/NEN.0000000000000058

    View details for Web of Science ID 000333471100006

    View details for PubMedID 24607968

  • Origins and significance of astrogliosis in the multiple sclerosis model, MOG peptide EAE. Journal of the neurological sciences Moreno, M., Guo, F., Mills Ko, E., Bannerman, P., Soulika, A., Pleasure, D. 2013; 333 (1-2): 55-59


    Astroglia, the most abundant cells in the human CNS, and even more prominent in multiple sclerosis patients, participate in CNS innate and adaptive immunity, and have been hypothesized to play an important role in multiple sclerosis progression. Experimental autoimmune encephalomyelitis elicited in mice by immunization with myelin oligodendrocyte glycoprotein peptide 35-55 provides a means by which to explore the genesis and disease significance of astrogliosis during a chronic immune-mediated CNS inflammatory/demyelinative disorder that, in its' pathological features, strongly resembles multiple sclerosis.

    View details for DOI 10.1016/j.jns.2012.12.014

    View details for PubMedID 23294494

  • Endocannabinoid Signaling Alters Internal Programming of Neuronal Fate Specification JOURNAL OF NEUROSCIENCE Sequerra, E. B., Cates, S., Moreno, M., Lang, J., Orosco, L. A., Spencer, K. 2013; 33 (13): 5437-5438
  • Disruption of NMDA Receptors in Oligodendroglial Lineage Cells Does Not Alter Their Susceptibility to Experimental Autoimmune Encephalomyelitis or Their Normal Development JOURNAL OF NEUROSCIENCE Guo, F., Maeda, Y., Ko, E. M., Delgado, M., Horiuchi, M., Soulika, A., Miers, L., Burns, T., Itoh, T., Shen, H., Lee, E., Sohn, J., Pleasure, D. 2012; 32 (2): 639-645


    Pharmacological studies have suggested that oligodendroglial NMDA glutamate receptors (NMDARs) mediate white matter injury in a variety of CNS diseases, including multiple sclerosis (MS). We tested this hypothesis in experimental autoimmune encephalomyelitis (EAE), a model of human MS, by timed conditional disruption of oligodendroglial NR1, an essential subunit of functional NMDARs, using an inducible proteolipid protein (Plp) promoter-driven Cre-loxP recombination system. We found that selective ablation of oligodendroglial NR1 did not alter the clinical severity of EAE elicited in C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein peptide 35-55 (MOG-peptide), nor were there significant differences between the oligodendroglial NR1 KO and non-KO mice in numbers of axons lost in spinal cord dorsal funiculi or severity of spinal cord demyelination. Similarly, constitutive deletion of NR3A, a modulatory subunit of oligodendroglial NMDARs, did not alter the course of MOG-peptide EAE. Furthermore, conditional and constitutive ablation of NR1 in neonatal oligodendrocyte progenitor cells did not interrupt their normal maturation and differentiation. Collectively, our data suggest that oligodendroglial lineage NMDARs are neither required for timely postnatal development of the oligodendroglial lineage, nor significant participants in the pathophysiology of MOG-peptide EAE.

    View details for DOI 10.1523/JNEUROSCI.4073-11.2012

    View details for Web of Science ID 000299121800025

    View details for PubMedID 22238099

  • Macroglial Plasticity and the Origins of Reactive Astroglia in Experimental Autoimmune Encephalomyelitis JOURNAL OF NEUROSCIENCE Guo, F., Maeda, Y., Ma, J., Delgado, M., Sohn, J., Miers, L., Ko, E. M., Bannerman, P., Xu, J., Wang, Y., Zhou, C., Takebayashi, H., Pleasure, D. 2011; 31 (33): 11914-11928


    Accumulations of hypertrophic, intensely glial fibrillary acidic protein-positive (GFAP(+)) astroglia, which also express immunoreactive nestin and vimentin, are prominent features of multiple sclerosis lesions. The issues of the cellular origin of hypertrophic GFAP(+)/vimentin(+)/nestin(+) "reactive" astroglia and also the plasticities and lineage relationships among three macroglial progenitor populations-oligodendrocyte progenitor cells (OPCs), astrocytes and ependymal cells-during multiple sclerosis and other CNS diseases remain controversial. We used genetic fate-mappings with a battery of inducible Cre drivers (Olig2-Cre-ER(T2), GFAP-Cre-ER(T2), FoxJ1-Cre-ER(T2) and Nestin-Cre-ER(T2)) to explore these issues in adult mice with myelin oligodendrocyte glycoprotein peptide-induced experimental autoimmune encephalomyelitis (EAE). The proliferative rate of spinal cord OPCs rose fivefold above control levels during EAE, and numbers of oligodendroglia increased as well, but astrogenesis from OPCs was rare. Spinal cord ependymal cells, previously reported to be multipotent, did not augment their low proliferative rate, nor give rise to astroglia or OPCs. Instead, the hypertrophic, vimentin(+)/nestin(+), reactive astroglia that accumulated in spinal cord in this multiple sclerosis model were derived by proliferation and phenotypic transformation of fibrous astroglia in white matter, and solely by phenotypic transformation of protoplasmic astroglia in gray matter. This comprehensive analysis of macroglial plasticity in EAE helps to clarify the origins of astrogliosis in CNS inflammatory demyelinative disorders.

    View details for DOI 10.1523/JNEUROSCI.1759-11.2011

    View details for Web of Science ID 000293950300019

    View details for PubMedID 21849552

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