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Your search keyword '"Parker Harp, Chelsea R."' showing total 8 results
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8 results on '"Parker Harp, Chelsea R."'

1. Discovery and Preclinical Characterization of BIIB129, a Covalent, Selective, and Brain-Penetrant BTK Inhibitor for the Treatment of Multiple Sclerosis

Author

Himmelbauer, Martin K., primary, Bajrami, Bekim, additional, Basile, Rebecca, additional, Capacci, Andrew, additional, Chen, TeYu, additional, Choi, Colin K., additional, Gilfillan, Rab, additional, Gonzalez-Lopez de Turiso, Felix, additional, Gu, Chungang, additional, Hoemberger, Marc, additional, Johnson, Douglas S., additional, Jones, J. Howard, additional, Kadakia, Ekta, additional, Kirkland, Melissa, additional, Lin, Edward Y., additional, Liu, Ying, additional, Ma, Bin, additional, Magee, Tom, additional, Mantena, Srinivasa, additional, Marx, Isaac E., additional, Metrick, Claire M., additional, Mingueneau, Michael, additional, Murugan, Paramasivam, additional, Muste, Cathy A., additional, Nadella, Prasad, additional, Nevalainen, Marta, additional, Parker Harp, Chelsea R., additional, Pattaropong, Vatee, additional, Pietrasiewicz, Alicia, additional, Prince, Robin J., additional, Purgett, Thomas J., additional, Santoro, Joseph C., additional, Schulz, Jurgen, additional, Sciabola, Simone, additional, Tang, Hao, additional, Vandeveer, H. George, additional, Wang, Ti, additional, Yousaf, Zain, additional, Helal, Christopher J., additional, and Hopkins, Brian T., additional

Published
2024
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2. Preclinical Analysis of Candidate Anti-Human CD79 Therapeutic Antibodies Using a Humanized CD79 Mouse Model

Author

Wemlinger, Scott M., primary, Parker Harp, Chelsea R., additional, Yu, Bo, additional, Hardy, Ian R., additional, Seefeldt, Matthew, additional, Matsuda, Jennifer, additional, Mingueneau, Michael, additional, Spilker, Kerri A., additional, Cameron, Thomas O., additional, Larrick, James W., additional, Getahun, Andrew, additional, and Cambier, John C., additional

Published
2022
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3. Neutrophils promote VLA-4–dependent B cell antigen presentation and accumulation within the meninges during neuroinflammation

Author

Parker Harp, Chelsea R., primary, Archambault, Angela S., additional, Cheung, Matthew, additional, Williams, Jesse W., additional, Czepielewski, Rafael S., additional, Duncker, Patrick C., additional, Kilgore, Aaron J., additional, Miller, Aidan T., additional, Segal, Benjamin M., additional, Kim, Alfred H. J., additional, Randolph, Gwendalyn J., additional, and Wu, Gregory F., additional

Published
2019
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6. B cell antigen presentation is sufficient to drive neuro-inflammation in an animal model of multiple sclerosis1

Author

Parker Harp, Chelsea R., Archambault, Angela S., Sim, Julia, Ferris, Stephen T., Mikesell, Robert J., Koni, Pandelakis A., Shimoda, Michiko, Linington, Christopher, Russell, John H., and Wu, Gregory F.

Subjects
CD4-Positive T-Lymphocytes, Antigen Presentation, B-Lymphocytes, Encephalomyelitis, Autoimmune, Experimental, Multiple Sclerosis, Histocompatibility Antigens Class II, Dendritic Cells, Article, Mice, Inbred C57BL, Mice, immune system diseases, Animals, Myelin-Oligodendrocyte Glycoprotein, Neurogenic Inflammation
Abstract

B cells are increasingly regarded as integral to the pathogenesis of multiple sclerosis (MS) in part due to the success of B cell depletion therapy. Multiple B cell-dependent mechanisms contributing to inflammatory demyelination of the central nervous system (CNS) have been explored using experimental autoimmune encephalomyelitis (EAE), a CD4 T cell-dependent animal model for multiple sclerosis (MS). While B cell antigen presentation has been suggested to regulate CNS inflammation during EAE, direct evidence that B cells can independently support antigen-specific autoimmune responses by CD4 T cells in EAE is lacking. Using a newly developed murine model of in vivo conditional expression of MHCII, we previously reported that encephalitogenic CD4 T cells are incapable of inducing EAE when B cells are the sole antigen presenting cell. Herein we find that B cells cooperate with dendritic cells to enhance EAE severity resulting from myelin oligodendrocyte glycoprotein (MOG) immunization. Further, increasing the precursor frequency of MOG-specific B cells, but not addition of soluble MOG-specific antibody, is sufficient to drive EAE in mice expressing MHCII by B cells alone. These data support a model in which expansion of antigen-specific B cells during CNS autoimmunity amplifies cognate interactions between B and CD4 T cells and have the capacity to independently drive neuro-inflammation at later stages of disease.

Published
2015

8. Optic Neuritis: A Model for the Immuno-pathogenesis of Central Nervous System Inflammatory Demyelinating Diseases.

Author

Wu GF, Parker Harp CR, and Shindler KS

Abstract

Evidence for the tenuous regulation between the immune system and central nervous system (CNS) can be found with examples of interaction between these organ systems gone awry. Multiple sclerosis (MS) is the prototypical inflammatory disease of the CNS and is characterized by widely distributed inflammatory demyelinating plaques that can involve the brain, spinal cord and/or optic nerves. Optic neuritis (ON), inflammatory injury of the optic nerve that frequently occurs in patients with MS, has been the focus of intense study in part given the readily accessible nature of clinical outcome measures. Exploring the clinical and pathological features of ON in relation to other inflammatory demyelinating conditions of the CNS, namely MS and neuromyelitis optica, provides an opportunity to glean common and distinct mechanisms of disease. Emerging data from clinical studies along with various animal models involving ON implicate innate and adaptive immune responses directed at glial targets, including myelin oligodendrocyte glycoprotein and aquaporin 4. Resolution of inflammation in ON is commonly observed both clinically and experimentally, but persistent nerve injury is also one emerging hallmark of ON. One hypothesis seeking evaluation is that, in comparison to other sites targeted in MS, the optic nerve is a highly specialized target within the CNS predisposing to unique immunologic processes that generate ON. Overall, ON serves as a highly relevant entity for understanding the pathogenesis of other CNS demyelinating conditions, most notably MS., Competing Interests: CONFLICT OF INTEREST The authors confirm that this article content has no conflict of interest.

Published
2015
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