Corrigendum: Akt2 Regulates the Differentiation and Function of NKT17 Cells via FoxO-1-ICOS Axis.

[This corrects the article DOI: 10.3389/fimmu.2018.

AKT2 deficiency impairs formation of the BCR signalosome.

Background: AKT2 is one of the key molecules that involves in the insulin-induced signaling and the development of cancer. In B cells, the function of AKT2 is unclear.

Methods: In this study, we used AKT2 knockout mice model to study the role of AKT2 in BCR signaling and B cell differentiation.

Dock5 controls the peripheral B cell differentiation via regulating BCR signaling and actin reorganization.

As an atypical guanine nucleotide exchange factor (GEF), Dock5 has been extensively studied in cellular functions. However, the role of Dock5 on B-cell immunity still remain elusive. In this study, we generated a Dock5 knockout mouse model to study the effect of Dock5 deficiency on B cell development, differentiation and BCR signaling.

Akt2 Regulates the Differentiation and Function of NKT17 Cells via FoxO-1-ICOS Axis.

As a critical linker between mTORC1 and mTORC2, Akt is important for the cell metabolism. The role of Akt in the function and development of B and T cells is well characterized, however, the role of Akt for development and function of iNKT cells is unknown. iNKT cells bridge the adaptive and innate immunity, and in this study, we found that the differentiation of NKT17 cells and IL17 production of NKT17 cells were disrupted in Akt2 KO mice.

Dock8 regulates BCR signaling and activation of memory B cells via WASP and CD19.

Dock8 deficiency leads to immunodeficiency, and the role of Dock8 in B-cell development and function has been revealed; however, the role of DocK8 on B-cell receptor (BCR) signaling and function of memory B cells remains elusive. In this study, we generated a Dock8 knockout mouse model and collected peripheral blood mononuclear cells from Dock8 patients to study the effect of Dock8 deficiency on the BCR signaling and activation of memory B cells with confocal microscopy and total internal reflection fluorescence microscopy. The activation of key, positive upstream BCR signaling molecules, pCD19 and phosphorylated Brutons tyrosine kinase (pBtk), is reduced.

Rictor positively regulates B cell receptor signaling by modulating actin reorganization via ezrin.

As the central hub of the metabolism machinery, the mammalian target of rapamycin complex 2 (mTORC2) has been well studied in lymphocytes. As an obligatory component of mTORC2, the role of Rictor in T cells is well established. However, the role of Rictor in B cells still remains elusive.