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The development of inducible Bronchus Associated Lymphoid Tissue (iBALT) is dependent on IL-17

Ectopic or tertiary lymphoid tissues, such as inducible bronchus-associated lymphoid tissue (iBALT), form in non-lymphoid organs after local infection or inflammation. However, the initial events that promote this process remain enigmatic. Here we show that iBALT formed in murine lungs as a conseque...

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Detalles Bibliográficos
Autores principales: Rangel-Moreno, Javier, Carragher, Damian M., Garcia-Hernandez, Maria de la Luz, Hwang, Ji Young, Kusser, Kim, Hartson, Louise, Kolls, Jay K., Khader, Shabaana A., Randall, Troy D.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3520063/
https://www.ncbi.nlm.nih.gov/pubmed/21666689
http://dx.doi.org/10.1038/ni.2053
Descripción
Sumario:Ectopic or tertiary lymphoid tissues, such as inducible bronchus-associated lymphoid tissue (iBALT), form in non-lymphoid organs after local infection or inflammation. However, the initial events that promote this process remain enigmatic. Here we show that iBALT formed in murine lungs as a consequence of pulmonary inflammation during the neonatal period. Although CD4(+)CD3(−) lymphoid tissue inducer (LTi) cells were found in neonatal lungs, particularly after inflammation, iBALT was formed in mice lacking LTi cells. Instead, we found that interleukin 17 (IL-17) produced by CD4(+) T cells was essential for iBALT formation. IL-17 acted by promoting the lymphotoxin-α-independent expression of CXCL13, which was important for follicle formation. These results suggest that IL-17-producing T cells are critical for the development of ectopic lymphoid tissues.