• CNS
• EAE
• IL-17A
• Interleukin-17
• Neuroinflammation
• Pertussis

• Mice
• Animals
• Interleukin-17
• T-Lymphocytes
• Encephalomyelitis, Autoimmune, Experimental
• Multiple Sclerosis
• Mice, Transgenic
• Granulocytes
• Mice, Inbred C57BL

• Rheinische Friedrich-Wilhelms-Universität Bonn
• Universitätsklinikum Bonn (8930)

• EAE
• Multiple sclerosis
• animal models
• cortical lesions
• cuprizone
• demyelinating
• disease progression
• ethidium bromide
• in vitro models
• lysolecithin
• neurodegeneration
• plaques
• transgenic animal models
• white matter lesions

• autoimmune disease
• immune metabolism
• innate immunity
• mitochondria
• therapeutic targets

• Humans
• Autoimmune Diseases
• Mitochondria/metabolism
• Immunity, Innate
• Lupus Erythematosus, Systemic
• Arthritis, Rheumatoid

• COVID-19
• SARS-CoV-2
• autoimmunity
• epitopes
• molecular mimicry
• network biology
• neurodegenerative diseases
• neurological diseases
• neuropsychiatric disorders
• systems bioinformatics

• Humans
• Computational Biology
• COVID-19
• Epitopes
• Glial Fibrillary Acidic Protein
• Microtubule-Associated Proteins
• Neurodegenerative Diseases/etiology
• Receptors, Cholinergic
• SARS-CoV-2

• NA Telethon

• adjuvant
• autoimmunity
• cell death
• cytokines
• genetic polymorphism
• tuberculosis
• vitamin D

• MHC
• TCR
• coinhibition
• costimulation
• cytokines

• Autoimmune Diseases
• Autoimmunity
• CD4-Positive T-Lymphocytes
• Humans
• Lymphocyte Activation
• T-Lymphocytes

• R01 NS030843 NINDS NIH HHS
• R01 NS045937 NINDS NIH HHS
• R01NS30843 NIH HHS
• T32 AR007530 NIAMS NIH HHS
• U19 AI133524 NIAID NIH HHS
• R01NS045937 NIH HHS
• P01AI039671 NIH HHS
• P01 AI073748 NIAID NIH HHS
• P01 AI056299 NIAID NIH HHS
• P01AI056299 NIH HHS
• P01 AI039671 NIAID NIH HHS
• P01AI073748 NIH HHS
• R01AI144166 NIH HHS
• R01 AI144166 NIAID NIH HHS

Multiple sclerosis is an autoimmune treatable but not curable disease. There are a multiplicity of medications for multiple sclerosis therapy, including a class entitled disease-modifying drugs that are mainly indicated to reduce the number and severity of disease relapses. Not all patients respond well to these therapies, and minor to severe adverse effects have been reported. Vitamin D, called sunshine vitamin, is being studied as a possible light at the end of the tunnel. In this review, we recapitulated the similar immunopathogenesis of multiple sclerosis and experimental autoimmune encephalomyelitis, the immunomodulatory and neuroprotective potential of vitamin D and the state-of-art concerning its supplementation to multiple sclerosis patients. Finally, based on our and other groups’ experimental findings, we analyzed the need to consider the relevance of the route and the different time-point administration aspects for a more rational indication of this vitamin to multiple sclerosis patients.

• central nervous system
• cytokines
• experimental autoimmune encephalomyelitis
• immunomodulation
• immunopathogenesis
• inflammation
• multiple sclerosis
• neuroprotection
• regulatory T cells
• vitamin D

• Guillain-Barré syndrome
• Myasthenia gravis
• inhibitors
• multiple sclerosis
• neuroimmune diseases
• neuromyelitis optica spectrum disorder
• toll-like receptors

• Animals
• Biomarkers
• Diagnosis, Differential
• Disease Management
• Disease Susceptibility
• Drug Development
• Gene Expression Regulation
• Humans
• Immune System Diseases/diagnosis
• Immune System Diseases/etiology
• Immune System Diseases/metabolism
• Immune System Diseases/therapy
• Molecular Targeted Therapy
• Multigene Family
• Nervous System Diseases/diagnosis
• Nervous System Diseases/etiology
• Nervous System Diseases/metabolism
• Nervous System Diseases/therapy
• Organ Specificity
• Signal Transduction
• Structure-Activity Relationship
• Theranostic Nanomedicine
• Toll-Like Receptors/chemistry
• Toll-Like Receptors/genetics
• Toll-Like Receptors/metabolism

• National Natural Science Foundation of China
• Natural Science Foundation of Jilin Province

• Animals
• Autoantigens/immunology
• CD4-Positive T-Lymphocytes/cytology
• CD4-Positive T-Lymphocytes/immunology
• Cells, Cultured
• Dendritic Cells/cytology
• Dendritic Cells/immunology
• Encephalomyelitis, Autoimmune, Experimental/immunology
• Mice
• Mice, Inbred C57BL
• Mice, Transgenic
• Myelin Sheath/immunology

• The Barsumian Trust
• Penn State College of Medicine

• Autoimmune inner ear disease
• Selective immunoglobulin A deficiency

Multiple sclerosis (MS) is a neuro-autoimmune and neurodegenerative disorder leading to chronic inflammation, demyelination, axonal, and neuronal loss in the central nervous system (CNS). Despite intense research efforts, the pathogenesis of MS still remains unclear. Toll-like receptors (TLRs) are a family of type I transmembrane receptors that play a crucial role in the innate immune response. Myeloid differentiation factor 88 (MyD88) is the adaptor of major TLRs. It has been widely considered that the TLR-MyD88 signaling pathway plays an important role in the occurrence and development of autoimmune disease. Data have revealed that the TLR-MyD88 signaling may be involved in the pathogenesis of MS and experimental autoimmune encephalomyelitis (EAE), an animal model for MS, by regulating the antigen presentation of dendritic cells, the integrity of blood-brain barrier (BBB), and the activation of T cells and B cells. Here, we summarize the role of TLRs and MyD88 in MS and discuss the possible therapies that are based on these molecules.

• Toll-like receptors
• experimental autoimmune encephalomyelitis
• inflammation
• multiple sclerosis
• myeloid differentiation primary response protein 88

• Toll-like receptor 4 (TLR4)
• animal model
• autoimmune disease
• glucose metabolism
• insulin resistance
• islet
• microbiome
• mitochondrial metabolism
• type 1 diabetes

Toll-like receptor 4 (TLR4) is well known for activating the innate immune system; however, it is also highly expressed in adaptive immune cells, such as CD4⁺ T-helper 17 (Th17) cells, which play a key role in multiple sclerosis (MS) pathology. However, the function and governing mechanism of TLR4 in Th17 remain unclear.

The changes of TLR4 in CD4⁺ T cells from MS patients and experimental autoimmune encephalomyelitis (EAE) mice were tested. TLR4-deficient (TLR4^−/−) naïve T cells were induced in vitro and transferred into Rag1^−/− mice to measure Th17 differentiation and EAE pathology. DNA sequence analyses combining with deletion fragments and mutation analyses, chromatin immunoprecipitation (ChIP), and electrophoretic mobility shift assay (EMSA) were used to explore the mechanism of TLR4 signaling pathway in regulating Th17 differentiation.

The levels of TLR4 were increased in CD4⁺ Th17 cells both from MS patients and EAE mice, as well as during Th17 differentiation in vitro. TLR4^−/− CD4⁺ naïve T cells inhibited their differentiation into Th17, and transfer of TLR4^−/− CD4⁺ naïve T cells into Rag1^−/− mice was defective in promoting EAE, characterized by less demyelination and Th17 infiltration in the spinal cord. TLR4 signal enhanced Th17 differentiation by activating RelA, downregulating the expression of miR-30a, a negative regulator of Th17 differentiation. Inhibition of RelA activity increased miR-30a level, but decreased Th17 differentiation rate. Furthermore, RelA directly regulated the expression of miR-30a via specific binding to a conserved element of miR-30a gene.

TLR4^−/− CD4⁺ naïve T cells are inadequate in differentiating to Th17 cells both in vitro and in vivo. TLR4-RelA-miR-30a signal pathway regulates Th17 differentiation via direct binding of RelA to the regulatory element of miR-30a gene. Our results indicate modulating TLR4-RelA-miR-30a signal in Th17 may be a therapeutic target for Th17-mediated neurodegeneration in neuroinflammatory diseases.

• Differentiation
• MiR-30a
• Multiple sclerosis
• Neuroinflammation
• RelA
• T helper cell
• TLR4

• CD95
• EAE
• Fas
• STAT1
• STAT3
• Th1 cells
• Th17 cells
• apoptosis
• autoimmunity
• death receptor

• Animals
• Apoptosis/immunology
• Biomarkers
• Caspases/metabolism
• Cell Differentiation/immunology
• Gene Expression Profiling
• Gene Knockout Techniques
• Lymphocyte Activation
• Mice
• Phenotype
• Phosphorylation
• Protein Binding
• Protein Transport
• STAT1 Transcription Factor/metabolism
• STAT3 Transcription Factor/metabolism
• Th1 Cells/immunology
• Th1 Cells/metabolism
• Th17 Cells/cytology
• Th17 Cells/immunology
• Th17 Cells/metabolism
• Transcriptome
• fas Receptor/genetics
• fas Receptor/metabolism

• Howard Hughes Medical Institute
• R01 NS030843 NINDS NIH HHS
• P01 NS076410 NINDS NIH HHS
• P01 AI039671 NIAID NIH HHS
• P01 AI045757 NIAID NIH HHS
• P01 AI073748 NIAID NIH HHS

Epigenetics defines the persistent modifications of gene expression in a manner that does not involve the corresponding alterations in DNA sequences. It includes modifications of DNA nucleotides, nucleosomal remodeling, and post-translational modifications (PTMs). It is becoming evident that PTMs which act singly or in combination to form “histone codes” orchestrate the chromatin structure and dynamic functions. PTMs of histone tails have been demonstrated to influence numerous biological developments, as well as disease onset and progression. Multiple sclerosis (MS) is an autoimmune inflammatory demyelinating and neurodegenerative disease of the central nervous system, of which the precise pathophysiological mechanisms remain to be fully elucidated. There is a wealth of emerging evidence that epigenetic modifications may confer risk for MS, which provides new insights into MS. Histone PTMs, one of the key events that regulate gene activation, seem to play a prominent role in the epigenetic mechanism of MS. In this review, we summarize recent studies in our understanding of the epigenetic language encompassing histone, with special emphasis on histone acetylation and histone lysine methylation, two of the best characterized histone modifications. We also discuss how the current studies address histone acetylation and histone lysine methylation influencing pathophysiology of MS and how future studies could be designed to establish optimized therapeutic strategies for MS.

• Histone modifications
• Immune-mediated injury
• Multiple sclerosis
• Myelin destruction
• Neurodegeneration

• EAE
• ethidium bromide
• glial cells
• lysolecithin toxin and virus-induced demyelination
• multiple sclerosis

• aging
• complement
• dysbiosis
• immune tolerance
• multiple sclerosis

• experimental autoimmune encephalomyelitis
• immune cell surveillance
• multiple sclerosis
• neuroinflammation
• upper-respiratory viral infection

• Animals
• Cerebellum/immunology
• Cerebellum/metabolism
• Chemokine CXCL5/immunology
• Chemokine CXCL5/metabolism
• Encephalomyelitis, Autoimmune, Experimental/complications
• Encephalomyelitis, Autoimmune, Experimental/genetics
• Immunologic Surveillance
• Alphainfluenzavirus
• Mice
• Mice, Inbred C57BL
• Mice, Transgenic
• Orthomyxoviridae Infections/complications
• Spinal Cord/immunology
• Spinal Cord/metabolism
• Transcriptome

Eosinophils are multifunctional granulocytes that contribute to initiation and modulation of inflammation. Their role in asthma and parasitic infections has long been recognized. Growing evidence now reveals a role for eosinophils in autoimmune diseases. In this review, we summarize the function of eosinophils in inflammatory bowel diseases, neuromyelitis optica, bullous pemphigoid, autoimmune myocarditis, primary biliary cirrhosis, eosinophilic granulomatosis with polyangiitis, and other autoimmune diseases. Clinical studies, eosinophil-targeted therapies, and experimental models have contributed to our understanding of the regulation and function of eosinophils in these diseases. By examining the role of eosinophils in autoimmune diseases of different organs, we can identify common pathogenic mechanisms. These include degranulation of cytotoxic granule proteins, induction of antibody-dependent cell-mediated cytotoxicity, release of proteases degrading extracellular matrix, immune modulation through cytokines, antigen presentation, and prothrombotic functions. The association of eosinophilic diseases with autoimmune diseases is also examined, showing a possible increase in autoimmune diseases in patients with eosinophilic esophagitis, hypereosinophilic syndrome, and non-allergic asthma. Finally, we summarize key future research needs.

• autoimmune diseases
• bullous pemphigoid
• eosinophilia
• eosinophilic granulomatosis with polyangiitis
• inflammatory bowel disease
• innate immune system
• myocarditis
• neuromyelitis optica

Multipotent mesenchymal stromal cells (MSCs) have emerged as a promising therapy for autoimmune diseases, including multiple sclerosis (MS). Administration of MSCs to MS patients has proven safe with signs of immunomodulation but their therapeutic efficacy remains low. The aim of the current study has been to further characterize the immunomodulatory mechanisms of adipose tissue-derived MSCs (ASCs) in vitro and in vivo using the EAE model of chronic brain inflammation in mice. We found that murine ASCs (mASCs) suppress T cell proliferation in vitro via inducible nitric oxide synthase (iNOS) and cyclooxygenase- (COX-) 1/2 activities. mASCs also prevented the lipopolysaccharide- (LPS-) induced maturation of dendritic cells (DCs) in vitro. The addition of the COX-1/2 inhibitor indomethacin, but not the iNOS inhibitor L-NAME, reversed the block in DC maturation implicating prostaglandin (PG) E₂ in this process. In vivo, early administration of murine and human ASCs (hASCs) ameliorated myelin oligodendrocyte protein- (MOG_35-55-) induced EAE in C57Bl/6 mice. Mechanistic studies showed that mASCs suppressed the function of autoantigen-specific T cells and also decreased the frequency of activated (CD11c⁺CD40^high and CD11c⁺TNF-α⁺) DCs in draining lymph nodes (DLNs). In summary, these data suggest that mASCs reduce EAE severity, in part, through the impairment of DC and T cell function.

• Autoimmune disease
• Immune response
• Therapeutic application
• Toll-like receptor

• Autoimmune diseases
• Campylobacter jejuni
• Innate immunity
• Receptor

Over the past several decades, significant advances have been made in identifying factors that contribute to the pathogenesis of multiple sclerosis (MS) and have culminated in the approval of some effective therapeutic strategies for disease intervention. However, the mechanisms by which environmental factors, such as infection, contribute to the pathogenesis and/or symptom exacerbation remain to be fully elucidated. Relapse frequency in MS patients contributes to neurological impairment and, in the initial phases of disease, serves as a predictor of poor disease prognosis. The purpose of this review is to examine the evidence that supports a role for peripheral infection in modulating the natural history of this disease. Evidence supporting a role for infection in promoting exacerbation in animal models of MS is also reviewed. Finally, a few mechanisms by which infection may exacerbate symptoms of MS and other neurological diseases are discussed. Those who comprise the majority of MS patients acquire approximately two upper-respiratory infections per year; furthermore, this type of infection doubles the risk for MS relapse, underscoring the contribution of this relationship as being potentially important and particularly detrimental.

• multiple sclerosis
• natural history
• neuroinflammation
• relapse
• viral infection

• Acanthamoeba spp.
• Dental units water lines
• Ozone
• PCR

Antigen presentation is in the center of the immune system, both in host defense against pathogens, but also when the system is unbalanced and autoimmune diseases like multiple sclerosis (MS) develop. It is not just by chance that a major histocompatibility complex gene is the major genetic susceptibility locus in MS; a feature that MS shares with other autoimmune diseases. The exact etiology of the disease, however, has not been fully understood yet. T cells are regarded as the major players in the disease, but most probably a complex interplay of altered central and peripheral tolerance mechanisms, T-cell and B-cell functions, characteristics of putative autoantigens, and a possible interference of environmental factors like microorganisms are at work. In this review, new data on all these different aspects of antigen presentation and their role in MS will be discussed, probable autoantigens will be summarized, and comparisons to other autoimmune diseases will be drawn.

• B cell
• HLA
• MHC
• T cell
• antigen presentation
• autoantigen
• autoimmune disease
• multiple sclerosis

• Dietary supplements
• Experimental autoimmune encephalomyelitis
• Multiple sclerosis
• Nutricals
• Therapeutics

• Infectious disease
• Innate immunity
• TLR
• Toll-like receptors
• Zebrafish

• Animals
• Fishes/immunology
• Humans
• Immunity, Innate
• Infections/immunology
• Infections/veterinary
• Mammals/immunology
• Signal Transduction
• Toll-Like Receptors/immunology
• Zebrafish/immunology
• Zebrafish Proteins/immunology

• Antigen-based immune-specific therapy
• Experimental autoimmune encephlalomyelitis (EAE)
• HLA-II transgenic mice
• Humanized EAE models
• Multiple sclerosis (MS)
• Spontaneous EAE models

Autoimmune inner ear disease (AIED) represents a very fertile research field and the advancements in the understanding of this disease have a direct application not only in patients affected with this condition but also in other inner ear disorders that share the same injury mechanism, damage to the inner ear hair cells. AIED also presents many challenges that have still to be overcome. Firstly, access to the inner ear is limited, as many interventions such as biopsies can result in great irreversible damage. Secondly, there are no completely specific markers for AIED. Lack of a definitive diagnosis can result in the treatment of patients not affected with the disease and, therefore, no response. Finally, some patients become refractory to glucocorticoids and new therapies are needed. This review offers an overview of the animal models that have contributed to the understanding of AIED pathophysiology, the value of currently available diagnostic tests, and therapeutic options, with a special focus on new therapies for non responders or patients refractory to glucocorticoids. Among these new options for therapy, biological agents have been tested recently, whereas gene and stem cell therapy may have a role in the future. The intratympanic route of administration avoids the systemic side effects associated with currently used drugs, and may become a more frequent approach in the future.

• Autoimmune inner ear disease
• Diagnostic tests
• Biologic therapy agents
• Gene therapy
• Stem cells

We recently reported that Acanthamoeba castellanii (ACA), an opportunistic pathogen of the central nervous system (CNS) possesses mimicry epitopes for proteolipid protein (PLP) 139–151 and myelin basic protein 89–101, and that the epitopes induce experimental autoimmune encephalomyelitis (EAE) in SJL mice reminiscent of the diseases induced with their corresponding cognate peptides. We now demonstrate that mice infected with ACA also show the generation of cross-reactive T cells, predominantly for PLP 139–151, as evaluated by T cell proliferation and IA^s/dextramer staining. We verified that PLP 139–151-sensitized lymphocytes generated in infected mice contained a high proportion of T helper 1 cytokine-producing cells, and they can transfer disease to naïve animals. Likewise, the animals first primed with suboptimal dose of PLP 139–151 and later infected with ACA, developed EAE, suggesting that ACA infection can trigger CNS autoimmunity in the presence of preexisting repertoire of autoreactive T cells. Taken together, the data provide novel insights into the pathogenesis of Acanthamoeba infections, and the potential role of infectious agents with mimicry epitopes to self-antigens in the pathogenesis of CNS diseases such as multiple sclerosis.

• Acanthamoeba castellanii/immunology
• Amebiasis/immunology
• Animals
• Antigens/immunology
• Autoimmunity/immunology
• Central Nervous System/immunology
• Cross Reactions/immunology
• Encephalomyelitis, Autoimmune, Experimental/immunology
• Epitopes/immunology
• Female
• Lymphocyte Activation/immunology
• Mice
• Mice, Inbred Strains
• Multiple Sclerosis/immunology
• Myelin Proteolipid Protein/immunology
• Myelin Sheath/immunology
• Peptide Fragments/immunology
• T-Lymphocytes/immunology

• 5R01-GM065494 NIGMS NIH HHS
• P50-HG002790 NHGRI NIH HHS

• Autoimmunity
• Central nervous system
• Gut microbiota
• Multiple sclerosis

Myelin-specific, pro-inflammatory T_H17 cells are widely regarded as the drivers of experimental autoimmune encephalomyelitis (EAE), an animal model for Multiple sclerosis (MS). The factors, responsible for the generation and maintenance of T_H17 cells as well as their participation in the pathogenic cascade leading to the demyelinating disease, have been studied extensively. However, how these harmful autoreactive cells are controlled in vivo remains unclear. By comparing TCR transgenic mice on a disease susceptible and a disease resistant genetic background, we show here that pathogenic T_H17 cells are sequestered within the intestine of spontaneous EAE resistant B10.S mice. Disease resistant B10.S mice harbored higher frequencies of T_H17 cells in the intestine compared to EAE susceptible SJL/J mice. Moreover, transferred T_H17 cells selectively migrated to intestinal lymphoid organs of B10.S mice. The sequestration of T_H17 cells in the gut was partially dependent on the gut homing receptor α4β7-mediated adhesion to the intestine. Administration of α4β7 blocking-antibodies increased the peripheral availability of T_H17 cells, resulting in increased EAE severity after immunization in B10.S mice. Together, these results support the concept that the intestine is a check-point for controlling pathogenic, organ-specific T cells.

• Animals
• Antigen-Presenting Cells/immunology
• Demyelinating Autoimmune Diseases, CNS/genetics
• Demyelinating Autoimmune Diseases, CNS/immunology
• Disease Models, Animal
• Disease Resistance/genetics
• Disease Resistance/immunology
• Encephalomyelitis, Autoimmune, Experimental/immunology
• Histocompatibility Antigens Class II/immunology
• Integrins/metabolism
• Intestinal Mucosa/metabolism
• Intestines/immunology
• Lymphocyte Activation/immunology
• Lymphoid Tissue/immunology
• Mice
• Mice, Transgenic
• Myelin-Oligodendrocyte Glycoprotein/immunology
• Receptors, Antigen, T-Cell/genetics
• T-Cell Antigen Receptor Specificity/immunology
• T-Lymphocyte Subsets/immunology
• T-Lymphocyte Subsets/metabolism
• Th17 Cells/immunology

• t cells
• autoimmunity
• inflammation
• transgenic/knockout mice

• Animals
• Autoimmune Diseases/immunology
• Autoimmune Diseases/metabolism
• Autoimmune Diseases/pathology
• Chickens
• Ligands
• Lipopolysaccharides/metabolism
• Mice
• Mice, Inbred C57BL
• Mice, Transgenic
• Muramidase/genetics
• Peptidoglycan/metabolism
• Poly I-C/metabolism
• Th1 Cells/immunology
• Th1 Cells/metabolism
• Th1 Cells/pathology
• Th17 Cells/immunology
• Th17 Cells/metabolism
• Th17 Cells/pathology
• Toll-Like Receptor 2/metabolism
• Toll-Like Receptor 3/metabolism
• Toll-Like Receptor 4/metabolism
• Toll-Like Receptor 9/metabolism
• Toll-Like Receptors/metabolism
• Toll-Like Receptors/physiology

• ZIA EY000069-35 Intramural NIH HHS

• Animals
• Cell Differentiation/drug effects
• Cell Proliferation/drug effects
• Coumarins/pharmacology
• Coumarins/therapeutic use
• Dendritic Cells/drug effects
• Dendritic Cells/immunology
• Diabetes Mellitus, Type 1/immunology
• Diabetes Mellitus, Type 1/metabolism
• Diabetes Mellitus, Type 1/prevention & control
• Female
• Forkhead Transcription Factors/genetics
• Immunologic Factors/pharmacology
• Immunologic Factors/therapeutic use
• Mice
• Mice, Inbred NOD
• Pancreas/drug effects
• Pancreas/metabolism
• RNA, Messenger/metabolism
• Signal Transduction/drug effects
• Spleen/cytology
• Spleen/drug effects
• Spleen/metabolism
• T-Lymphocytes/cytology
• T-Lymphocytes/drug effects
• T-Lymphocytes/immunology
• Thymus Gland/drug effects
• Thymus Gland/metabolism
• Toll-Like Receptor 4/antagonists & inhibitors
• Toll-Like Receptor 4/physiology
• Urticaceae

• Multiple sclerosis
• TLR1
• TLR10
• TLR2
• TLR3
• TLR4
• TLR5
• TLR6
• TLR7
• TLR8
• TLR9
• autoimmunity
• gene/environment interactions
• hygiene hypothesis
• microbial flora
• toll-like receptors

• experimental autoimmune encephalomyelitis
• ifn-γ
• immunomodulation
• inflammation
• mesenchymal stromal cell
• multiple sclerosis
• th17 cell
• toll-like receptor
• transplantation

• Animals
• Cell- and Tissue-Based Therapy
• Central Nervous System/physiology
• Central Nervous System/physiopathology
• Humans
• Immunomodulation
• Mesenchymal Stem Cell Transplantation
• Multiple Sclerosis/physiopathology
• Multiple Sclerosis/therapy
• Regeneration
• Translational Research, Biomedical

• R01 NS074787 NINDS NIH HHS
• NS074787 NINDS NIH HHS
• K08 AI057801 NIAID NIH HHS
• P01 AI089556 NIAID NIH HHS
• AI089556 NIAID NIH HHS
• AI57801 NIAID NIH HHS