B cells are required for sunlight protection of mice from a CNS-targeted autoimmune attack.
- Publisher:
- ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
- Publication Type:
- Journal Article
- Citation:
- J Autoimmun, 2016, 73, pp. 10-23
- Issue Date:
- 2016-09
Closed Access
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1-s2.0-S0896841116300774-main.pdf | Published version | 3.77 MB | Adobe PDF |
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Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author | Kok, LF | |
dc.contributor.author | Marsh-Wakefield, F | |
dc.contributor.author | Marshall, JE | |
dc.contributor.author |
Gillis, C https://orcid.org/0000-0001-9892-206X |
|
dc.contributor.author | Halliday, GM | |
dc.contributor.author | Byrne, SN | |
dc.date.accessioned | 2022-08-11T20:27:20Z | |
dc.date.available | 2016-05-31 | |
dc.date.available | 2022-08-11T20:27:20Z | |
dc.date.issued | 2016-09 | |
dc.identifier.citation | J Autoimmun, 2016, 73, pp. 10-23 | |
dc.identifier.issn | 0896-8411 | |
dc.identifier.issn | 1095-9157 | |
dc.identifier.uri | http://hdl.handle.net/10453/159971 | |
dc.description.abstract | The ultraviolet (UV) radiation contained in sunlight is a powerful immune suppressant. While exposure to UV is associated with protection from the development of autoimmune diseases, particularly multiple sclerosis, the precise mechanism by which UV achieves this protection is not currently well understood. Regulatory B cells play an important role in preventing autoimmunity and activation of B cells is a major way in which UV suppresses adaptive immune responses. Whether UV-protection from autoimmunity is mediated by the activation of regulatory B cells has never been considered before. When C57BL/6 mice were exposed to low, physiologically relevant doses of UV, a unique population of B cells was activated in the skin draining lymph nodes. As determined by flow cytometry, CD1d(low)CD5(-)MHC-II(hi)B220(hi) UV-activated B cells expressed significantly higher levels of CD19, CD21/35, CD25, CD210 and CD268 as well as the co-stimulatory molecules CD80, CD86, CD274 and CD275. Experimental autoimmune encephalomyelitis (EAE) in mice immunized with MOG/CFA was reduced by exposure to UV. UV significantly inhibited demyelination and infiltration of inflammatory cells into the spinal cord. Consequently, UV-exposed groups showed elevated IL-10 levels in secondary lymphoid organs, delayed EAE onset, reduced peak EAE score and significantly suppressed overall disease incidence and burden. Importantly, protection from EAE could be adoptively transferred using B cells isolated from UV-exposed, but not unirradiated hosts. Indeed, UV-protection from EAE was dependent on UV activation of lymph node B cells because UV could not protect mice from EAE who were pharmacologically depleted of B cells using antibodies. Thus, UV maintenance of a pool of unique regulatory B cells in peripheral lymph nodes appears to be essential to prevent an autoimmune attack on the central nervous system. | |
dc.format | Print-Electronic | |
dc.language | eng | |
dc.publisher | ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD | |
dc.relation.ispartof | J Autoimmun | |
dc.relation.isbasedon | 10.1016/j.jaut.2016.05.016 | |
dc.rights | info:eu-repo/semantics/closedAccess | |
dc.subject | 1107 Immunology | |
dc.subject.classification | Immunology | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Antibodies, Monoclonal | |
dc.subject.mesh | Antigens, CD | |
dc.subject.mesh | Autoimmunity | |
dc.subject.mesh | B-Lymphocytes, Regulatory | |
dc.subject.mesh | Central Nervous System | |
dc.subject.mesh | Encephalomyelitis, Autoimmune, Experimental | |
dc.subject.mesh | Enzyme-Linked Immunosorbent Assay | |
dc.subject.mesh | Female | |
dc.subject.mesh | Flow Cytometry | |
dc.subject.mesh | Histocompatibility Antigens Class II | |
dc.subject.mesh | Injections, Intraperitoneal | |
dc.subject.mesh | Interleukin-10 | |
dc.subject.mesh | Lymph Nodes | |
dc.subject.mesh | Lymphocyte Activation | |
dc.subject.mesh | Mice | |
dc.subject.mesh | Mice, Inbred C57BL | |
dc.subject.mesh | Myelin-Oligodendrocyte Glycoprotein | |
dc.subject.mesh | Sunlight | |
dc.subject.mesh | Central Nervous System | |
dc.subject.mesh | Lymph Nodes | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Mice, Inbred C57BL | |
dc.subject.mesh | Mice | |
dc.subject.mesh | Encephalomyelitis, Autoimmune, Experimental | |
dc.subject.mesh | Antigens, CD | |
dc.subject.mesh | Interleukin-10 | |
dc.subject.mesh | Antibodies, Monoclonal | |
dc.subject.mesh | Histocompatibility Antigens Class II | |
dc.subject.mesh | Enzyme-Linked Immunosorbent Assay | |
dc.subject.mesh | Flow Cytometry | |
dc.subject.mesh | Injections, Intraperitoneal | |
dc.subject.mesh | Lymphocyte Activation | |
dc.subject.mesh | Sunlight | |
dc.subject.mesh | Autoimmunity | |
dc.subject.mesh | Female | |
dc.subject.mesh | B-Lymphocytes, Regulatory | |
dc.subject.mesh | Myelin-Oligodendrocyte Glycoprotein | |
dc.title | B cells are required for sunlight protection of mice from a CNS-targeted autoimmune attack. | |
dc.type | Journal Article | |
utslib.citation.volume | 73 | |
utslib.location.activity | England | |
utslib.for | 1107 Immunology | |
pubs.organisational-group | /University of Technology Sydney | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science/School of Life Sciences | |
utslib.copyright.status | closed_access | * |
dc.date.updated | 2022-08-11T20:27:18Z | |
pubs.publication-status | Published | |
pubs.volume | 73 |
Abstract:
The ultraviolet (UV) radiation contained in sunlight is a powerful immune suppressant. While exposure to UV is associated with protection from the development of autoimmune diseases, particularly multiple sclerosis, the precise mechanism by which UV achieves this protection is not currently well understood. Regulatory B cells play an important role in preventing autoimmunity and activation of B cells is a major way in which UV suppresses adaptive immune responses. Whether UV-protection from autoimmunity is mediated by the activation of regulatory B cells has never been considered before. When C57BL/6 mice were exposed to low, physiologically relevant doses of UV, a unique population of B cells was activated in the skin draining lymph nodes. As determined by flow cytometry, CD1d(low)CD5(-)MHC-II(hi)B220(hi) UV-activated B cells expressed significantly higher levels of CD19, CD21/35, CD25, CD210 and CD268 as well as the co-stimulatory molecules CD80, CD86, CD274 and CD275. Experimental autoimmune encephalomyelitis (EAE) in mice immunized with MOG/CFA was reduced by exposure to UV. UV significantly inhibited demyelination and infiltration of inflammatory cells into the spinal cord. Consequently, UV-exposed groups showed elevated IL-10 levels in secondary lymphoid organs, delayed EAE onset, reduced peak EAE score and significantly suppressed overall disease incidence and burden. Importantly, protection from EAE could be adoptively transferred using B cells isolated from UV-exposed, but not unirradiated hosts. Indeed, UV-protection from EAE was dependent on UV activation of lymph node B cells because UV could not protect mice from EAE who were pharmacologically depleted of B cells using antibodies. Thus, UV maintenance of a pool of unique regulatory B cells in peripheral lymph nodes appears to be essential to prevent an autoimmune attack on the central nervous system.
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