Cargando…
Tuning of in vivo cognate B-T cell interactions by Intersectin 2 is required for effective anti-viral B cell immunity
Wiskott-Aldrich syndrome (WAS) is an immune pathology associated with mutations in WAS protein (WASp) or in WASp interacting protein (WIP). Together with the small GTPase Cdc42 and other effectors, these proteins participate in the remodelling of the actin network downstream of BCR engagement. Here...
Autores principales: | Burbage, Marianne, Gasparrini, Francesca, Aggarwal, Shweta, Gaya, Mauro, Arnold, Johan, Nair, Usha, Way, Michael, Bruckbauer, Andreas, Batista, Facundo D |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
eLife Sciences Publications, Ltd
2018
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5770159/ https://www.ncbi.nlm.nih.gov/pubmed/29337666 http://dx.doi.org/10.7554/eLife.26556 |
Ejemplares similares
-
Wiskott-Aldrich Syndrome Interacting Protein Deficiency Uncovers the Role of the Co-receptor CD19 as a Generic Hub for PI3 Kinase Signaling in B Cells
por: Keppler, Selina Jessica, et al.
Publicado: (2015) -
The Lack of WIP Binding to Actin Results in Impaired B Cell Migration and Altered Humoral Immune Responses
por: Keppler, Selina Jessica, et al.
Publicado: (2018) -
Cdc42 is a key regulator of B cell differentiation and is required for antiviral humoral immunity
por: Burbage, Marianne, et al.
Publicado: (2015) -
Initiation of Antiviral B Cell Immunity Relies on Innate Signals from Spatially Positioned NKT Cells
por: Gaya, Mauro, et al.
Publicado: (2018) -
The Small Rho GTPase TC10 Modulates B Cell Immune Responses
por: Burbage, Marianne, et al.
Publicado: (2017)