B-cell anergy induces a Th17 shift in a novel B lymphocyte transgenic NOD mouse model, the 116C-NOD mouse
Issue date
2016Author
Carrascal, Jorge
Carrillo, Jorge
Arpa i Puigdemont, Berta
Pujol Autonell, Irma
Planas, Raquel
Ampudia, Rosa Maria
Vives Pi, Marta
Suggested citation
Carrascal, Jorge;
Carrillo, Jorge;
Arpa i Puigdemont, Berta;
Egia-Mendikute, Leire;
Rosell Mases, Estela;
Pujol Autonell, Irma;
...
Verdaguer Autonell, Joan.
(2016)
.
B-cell anergy induces a Th17 shift in a novel B lymphocyte transgenic NOD mouse model, the 116C-NOD mouse.
European Journal of Immunology, 2016, vol. 46, núm. 3, p. 593-608.
https://doi.org/10.1002/eji.201445376.
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Show full item recordAbstract
Autoreactive B lymphocytes play a key role as APCs in diaebetogenesis. However, it
remains unclear whether B-cell tolerance is compromised in NOD mice. Here, we describe
a new B lymphocyte transgenic NOD mouse model, the 116C-NOD mouse, where the
transgenes derive from an islet-infiltrating B lymphocyte of a (8.3-NODxNOR) F1 mouse.
The 116C-NOD mouse produces clonal B lymphocytes with pancreatic islet beta cell specificity.
The incidence of T1D in 116C-NOD mice is decreased in both genders when compared
with NOD mice.Moreover, several immune selectionmechanisms (including clonal
deletion and anergy) acting on the development, phenotype, and function of autoreactive
B lymphocytes during T1D development have been identified in the 116C-NOD
mouse. Surprisingly, a more accurate analysis revealed that, despite their anergic phenotype, 116C B cells express some costimulatory molecules after activation, and induce a T-cell shift toward a Th17 phenotype. Furthermore, this shift on T lymphocytes seems to occur not only when both T and B cells contact, but also when helper T (Th) lineage is established. The 116C-NOD mouse model could be useful to elucidate the mechanisms involved in the generation of Th-cell lineages.