dc.contributor.author |
Lupsa, Nikolett |
|
dc.contributor.author |
Molnár-Érsek, Barbara |
|
dc.contributor.author |
Horváth, Andor |
|
dc.contributor.author |
Bencsik, András |
|
dc.contributor.author |
Lajkó, Eszter |
|
dc.contributor.author |
Silló, Pálma |
|
dc.contributor.author |
Oszvald, Ádám |
|
dc.contributor.author |
Wiener, Zoltán |
|
dc.contributor.author |
Reményi, Péter |
|
dc.contributor.author |
Mikala, Gábor |
|
dc.contributor.author |
Masszi, Tamás |
|
dc.contributor.author |
Buzás, Edit Irén |
|
dc.contributor.author |
Pós, Zoltán |
|
dc.date.accessioned |
2021-08-31T07:43:28Z |
|
dc.date.available |
2021-08-31T07:43:28Z |
|
dc.date.issued |
2018 |
|
dc.identifier.citation |
journalVolume=48;journalIssueNumber=12;journalTitle=EUROPEAN JOURNAL OF IMMUNOLOGY;pagerange=1944-1957;journalAbbreviatedTitle=EUR J IMMUNOL; |
|
dc.identifier.uri |
http://repo.lib.semmelweis.hu//handle/123456789/6707 |
|
dc.identifier.uri |
doi:10.1002/eji.201847552 |
|
dc.description.abstract |
This study sought to identify novel CD8+ T cell homing markers by studying acute graft versus host disease (aGvHD), typically involving increased T cell homing to the skin and gut. FACS-sorted skin-homing (CD8β+ /CLA+ ), gut-homing (CD8β+ /integrinβ7+ ), and reference (CD8β+ /CLA- /integrinβ7- ) T cells were compared in patients affected by cutaneous and/or gastrointestinal aGVHD. Microarray analysis, qPCR, and flow cytometry revealed increased expression of peptidase inhibitor 16 (PI16) in skin-homing CD8+ T cells. Robust association of PI16 with skin homing was confirmed in all types of aGvHD and in healthy controls, too. PI16 was not observed on CLA+ leukocytes other than T cells. Induction of PI16 expression on skin-homing T cells occurred independently of vitamin D3. Among skin-homing T cells, PI16 expression was most pronounced in memory-like CD45RO+ /CD127+ /CD25+ /CD69- /granzyme B- cells. PI16 was confined to the plasma membrane, was GPI-anchored, and was lost upon restimulation of memory CD8+ T cells. Loss of PI16 occurred by downregulation of PI16 transcription, and not by Phospholipase C (PLC)- or Angiotensin-converting enzyme (ACE)-mediated shedding, or by protein recycling. Inhibitor screening and pull-down experiments confirmed that PI16 inhibits cathepsin K, but may not bind to other skin proteases. These data link PI16 to skin-homing CD8+ T cells, and raise the possibility that PI16 may regulate cutaneous cathepsin K. |
|
dc.relation.ispartof |
urn:issn:0014-2980 |
|
dc.title |
Skin-homing CD8+ T cells preferentially express GPI-anchored peptidase inhibitor 16, an inhibitor of cathepsin K |
|
dc.type |
Journal Article |
|
dc.date.updated |
2019-01-29T14:58:27Z |
|
dc.language.rfc3066 |
en |
|
dc.rights.holder |
NULL |
|
dc.identifier.mtmt |
30336199 |
|
dc.identifier.wos |
000452047500004 |
|
dc.identifier.pubmed |
30365157 |
|
dc.contributor.department |
SE/AOK/I/Genetikai, Sejt- és Immunbiológiai Intézet |
|
dc.contributor.department |
SE/AOK/I/GSII/MTA-SE Immun-proteogenomikai Extracelluláris Vezikula Kutatócsoport |
|
dc.contributor.department |
SE/AOK/K/Bőr-, Nemikórtani és Bőronkológiai Klinika |
|
dc.contributor.department |
SE/AOK/K/III. Sz. Belgyógyászati Klinika |
|
dc.contributor.institution |
Semmelweis Egyetem |
|