Interleukin-17 Enhances Germinal Center Formation and Immunoglobulin G1 Production in Mice
Journal of Rheumatic Diseases
;
: 271-278, 2017.
Artículo
en Inglés
| WPRIM
| ID: wpr-217324
ABSTRACT
OBJECTIVE:
Interleukin (IL)-17 is a pro-inflammatory cytokine that has pleiotropic effects on multiple target cells and thereby contributes to the development of immune-mediated inflammatory disorders. However, the role of IL-17 in the humoral immune response has not been clearly elucidated.METHODS:
Mice deficient in IL-17A (IL-17A knockout [KO] mice) and wild type (WT) C57BL/6 mice were compared. Distinct B cell (mature/precursor and marginal zone/follicular) and plasma cell populations were compared using fluorescence-activated cell sorting (FACS) and confocal immunostaining. Immunoglobulin production was assessed by enzyme-linked immunosorbent assay.RESULTS:
There was no difference in B cell and plasma cell populations between IL-17A KO and WT mice. However, after T cell-dependent antigen challenge, IL-17A KO mice produced lower levels of immunoglobulin (Ig)G1 than wild-type animals. IL-17A KO mice also showed reduced germinal center (GC) formation and lower expression of activation-induced cytidine deaminase, the essential enzyme for class switch recombination (CSR). IL-17 had no effect on the proliferation or survival of naïve B cells in in vitro functional studies. However, IL-17 treatment promoted naïve B cell differentiation into plasma cells in synergy with IL-4, although IL-17 alone had no effect.CONCLUSION:
Our findings suggest that IL-17 contributes to the humoral immune response by enhancing GC formation, CSR to IgG1, and plasma cell differentiation in synergy with IL-4.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Células Plasmáticas
/
Recombinación Genética
/
Técnicas In Vitro
/
Inmunoglobulina G
/
Inmunoglobulinas
/
Ensayo de Inmunoadsorción Enzimática
/
Linfocitos B
/
Diferenciación Celular
/
Interleucinas
/
Interleucina-4
Límite:
Animales
Idioma:
Inglés
Revista:
Journal of Rheumatic Diseases
Año:
2017
Tipo del documento:
Artículo
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