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Brain Behav Immun. 2016 May;54:128-139. doi: 10.1016/j.bbi.2016.01.016. Epub 2016 Jan 18.

CXCL13 promotes isotype-switched B cell accumulation to the central nervous system during viral encephalomyelitis.

Author information

1
Department of Neurosciences NC30, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH, USA. Electronic address: pharest@ccf.org.
2
Department of Neurosciences NC30, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH, USA; School of Biomedical Sciences, Kent State University, Kent, OH, USA. Electronic address: disanok@ccf.org.
3
Department of Neurosciences NC30, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH, USA. Electronic address: stohlms2@ccf.org.
4
Department of Neurology, University of Michigan Medical School, Ann Arbor, MI, USA. Electronic address: bmsegal@med.umich.edu.
5
Department of Neurosciences NC30, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH, USA. Electronic address: bergmac@ccf.org.

Abstract

Elevated CXCL13 within the central nervous system (CNS) correlates with humoral responses in several neuroinflammatory diseases, yet its role is controversial. During coronavirus encephalomyelitis CXCL13 deficiency impaired CNS accumulation of memory B cells and antibody-secreting cells (ASC) but not naïve/early-activated B cells. However, despite diminished germinal center B cells and follicular helper T cells in draining lymph nodes, ASC in bone marrow and antiviral serum antibody were intact in the absence of CXCL13. The data demonstrate that CXCL13 is not essential in mounting effective peripheral humoral responses, but specifically promotes CNS accumulation of differentiated B cells.

KEYWORDS:

Antibody secreting cells; B cells; CXCL13; Central nervous system; Memory B cells; Neuroimmunology

PMID:
26795429
PMCID:
PMC4828287
DOI:
10.1016/j.bbi.2016.01.016
[Indexed for MEDLINE]
Free PMC Article

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