Sökning: onr:"swepub:oai:DiVA.org:uu-453396" >
Means, Motive, and ...
-
Rodriguez-Calvo, TeresaGerman Res Ctr Environm Hlth, Inst Diabet Res, Helmholtz Zentrum Munchen, Munich, Germany; German Ctr Diabet Res DZD, Neuherberg, Germany
(författare)
Means, Motive, and Opportunity : Do Non-Islet-Reactive Infiltrating T Cells Contribute to Autoimmunity in Type 1 Diabetes?
- Artikel/kapitelEngelska2021
Förlag, utgivningsår, omfång ...
-
2021-06-16
-
Frontiers Media S.A.2021
-
electronicrdacarrier
Nummerbeteckningar
-
LIBRIS-ID:oai:DiVA.org:uu-453396
-
https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-453396URI
-
https://doi.org/10.3389/fimmu.2021.683091DOI
Kompletterande språkuppgifter
-
Språk:engelska
-
Sammanfattning på:engelska
Ingår i deldatabas
Klassifikation
-
Ämneskategori:ref swepub-contenttype
-
Ämneskategori:for swepub-publicationtype
Anmärkningar
-
In human type 1 diabetes and animal models of the disease, a diverse assortment of immune cells infiltrates the pancreatic islets. CD8+ T cells are well represented within infiltrates and HLA multimer staining of pancreas sections provides clear evidence that islet epitope reactive T cells are present within autoimmune lesions. These bona fide effectors have been a key research focus because these cells represent an intellectually attractive culprit for β cell destruction. However, T cell receptors are highly diverse in human insulitis. This suggests correspondingly broad antigen specificity, which includes a majority of T cells for which there is no evidence of islet-specific reactivity. The presence of “non-cognate” T cells in insulitis raises suspicion that their role could be beyond that of an innocent bystander. In this perspective, we consider the potential pathogenic contribution of non-islet-reactive T cells. Our intellectual framework will be that of a criminal investigation. Having arraigned islet-specific CD8+ T cells for the murder of pancreatic β cells, we then turn our attention to the non-target immune cells present in human insulitis and consider the possible regulatory, benign, or effector roles that they may play in disease. Considering available evidence, we overview the case that can be made that non-islet-reactive infiltrating T cells should be suspected as co-conspirators or accessories to the crime and suggest some possible routes forward for reaching a better understanding of their role in disease.
Ämnesord och genrebeteckningar
Biuppslag (personer, institutioner, konferenser, titlar ...)
-
Christoffersson, GustafUppsala universitet,Institutionen för medicinsk cellbiologi,Science for Life Laboratory, SciLifeLab(Swepub:uu)guchr179
(författare)
-
Bender, ChristineLa Jolla Inst Immunol, Type Diabet Ctr 1, Ctr Autoimmun & Inflammat, La Jolla, CA USA
(författare)
-
von Herrath, Matthias G.La Jolla Inst Immunol, Type Diabet Ctr 1, Ctr Autoimmun & Inflammat, La Jolla, CA USA
(författare)
-
Mallone, RobertoUniv Paris, CNRS, Inst Cochin, INSERM, Paris, France; Cochin Hosp, AP HP, Serv Diabetol & Immunol Clin, Paris, France
(författare)
-
Kent, Sally C.Univ Massachusetts, Med Sch, Dept Med, Div Diabet, Diabet Ctr Excellence, Worcester, MA 01605 USA
(författare)
-
James, Eddie A.Benaroya Res Inst, Translatonal Res Program, Seattle, WA USA
(författare)
-
German Res Ctr Environm Hlth, Inst Diabet Res, Helmholtz Zentrum Munchen, Munich, Germany; German Ctr Diabet Res DZD, Neuherberg, GermanyInstitutionen för medicinsk cellbiologi
(creator_code:org_t)
Sammanhörande titlar
-
Ingår i:Frontiers in Immunology: Frontiers Media S.A.121664-3224
Internetlänk
Hitta via bibliotek
Till lärosätets databas