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K DiSano Dissertation.pdf (3.83 MB)

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Factors promoting B cell activation and accumulation in the inflamed CNS

DiSano, Krista D
http://rave.ohiolink.edu/etdc/view?acc_num=kent1489666546396967

Abstract Details

2017, PHD, Kent State University, College of Arts and Sciences / School of Biomedical Sciences.
Central nervous system (CNS) inflammation results in the accumulation of various B cell subsets, including naive, activated, memory B cells (Bmem), and antibody secreting cells (ASC). While ASC are well studied, signals driving recruitment of B cells, their relationship to peripheral activation, and role within the CNS remain largely unknown. Using the murine neurotropic coronavirus JHMV infection model, our studies established a critical role for draining lymph node germinal center formation in driving accumulation of isotype-switched ASC/Bmem in the CNS. Divergent accumulation of isotype-unswitched B cells to perivascular/meningeal space and isotype-switched B cells to the CNS parenchyma indicated B cell differentiation state regulates localization. Multiple lymphoid chemokines guiding B cell migration are induced following CNS infection. Differing chemokine receptor expression profiles on infiltrating B cell subsets implied receptors in combination or alone regulate their migration to and within the CNS. Interestingly, B cell accumulation occurred independent of ectopic follicles during JHMV infection. A sustained CD4 T cell “helped” phenotype during both JHMV infection and autoimmune mediated inflammation indicated B cell activation in the CNS occurred independent of follicle formation. Moreover, isotype-switched B cell accumulation and activation was unaltered in the absence of CXCL13, a chemokine critical in organizing follicles. CD4 T cells supported isotype-unswitched B cell CNS accumulation, indicating a role in facilitating B cell survival and undefined effector functions in the CNS. The identification of virus-specific Bmem during persistent JHMV infection implied Bmem contribute to local Ab production. In contrast, early accumulating B cells were not virus specific, implying non-specific bystander recruitment and functions not related to antigen presentation. Nonetheless, the recruitment of isotype-unswitched B cells in multiple CNS inflammation models suggests an important, yet to be defined role in the inflamed CNS.
Cornelia Bergmann, PhD (Committee Chair)
William Lynch, PhD (Committee Member)
Jennifer McDonough, PhD (Committee Member)
Booki Min, PhD (Committee Member)
John Johnson, PhD (Committee Member)
203 p.
Immunology; Neurosciences
B cell; CNS; Ectopic follicle; Neuroimmunology; T cell; Viral encephalomyelitis; Neuroinflammation; Chemokines; Coronavirus

Recommended Citations

Citations

  • DiSano, K. D. (2017). Factors promoting B cell activation and accumulation in the inflamed CNS [Doctoral dissertation, Kent State University]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=kent1489666546396967

    APA Style (7th edition)

  • DiSano, Krista . Factors promoting B cell activation and accumulation in the inflamed CNS. 2017. Kent State University, Doctoral dissertation. OhioLINK Electronic Theses and Dissertations Center, http://rave.ohiolink.edu/etdc/view?acc_num=kent1489666546396967.

    MLA Style (8th edition)

  • DiSano, Krista . "Factors promoting B cell activation and accumulation in the inflamed CNS." Doctoral dissertation, Kent State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=kent1489666546396967

    Chicago Manual of Style (17th edition)

kent1489666546396967
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© 2017, all rights reserved.
This open access ETD is published by Kent State University and OhioLINK.
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