Journal article icon

Journal article

CD1a promotes systemic manifestations of skin inflammation.

Abstract:

Inflammatory skin conditions are increasingly recognised as being associated with systemic inflammation. The mechanisms connecting the cutaneous and systemic disease are not well understood. CD1a is a virtually monomorphic major histocompatibility complex (MHC) class I-like molecule, highly expressed by skin and mucosal Langerhans cells, and presents lipid antigens to T-cells. Here we show an important role for CD1a in linking cutaneous and systemic inflammation in two experimental disease models. In human CD1a transgenic mice, the toll-like receptor (TLR)7 agonist imiquimod induces more pronounced splenomegaly, expansion of the peripheral blood and spleen T cell compartments, and enhanced neutrophil and eosinophil responses compared to the wild-type, accompanied by elevated skin and plasma cytokine levels, including IL-23, IL-1α, IL-1β, MCP-1 and IL-17A. Similar systemic escalation is shown in MC903-induced skin inflammation. The exacerbated inflammation could be counter-acted by CD1a-blocking antibodies, developed and screened in our laboratories. The beneficial effect is epitope dependent, and we further characterise the five best-performing antibodies for their capacity to modulate CD1a-expressing cells and ameliorate CD1a-dependent systemic inflammatory responses. In summary, we show that a therapeutically targetable CD1a-dependent pathway may play a role in the systemic spread of cutaneous inflammation.

Publication status:
Published
Peer review status:
Peer reviewed

Actions


Access Document


Publisher copy:
10.1038/s41467-022-35071-1

Authors


More by this author
Institution:
University of Oxford
Division:
MSD
Department:
RDM
Role:
Author
ORCID:
0000-0002-1127-6446
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
RDM
Role:
Author
ORCID:
0000-0003-3758-0638
More by this author
Role:
Author
ORCID:
0000-0002-3275-9850
More by this author
Institution:
University of Oxford
Role:
Author
ORCID:
0000-0002-9867-6353


Publisher:
Springer Nature
Journal:
Nature Communications More from this journal
Volume:
13
Issue:
1
Article number:
7535
Publication date:
2022-12-07
Acceptance date:
2022-11-17
DOI:
EISSN:
2041-1723
Pmid:
36477177


Language:
English
Keywords:
Pubs id:
1312394
Local pid:
pubs:1312394
Deposit date:
2022-12-16

Terms of use



Views and Downloads






If you are the owner of this record, you can report an update to it here: Report update to this record

TO TOP