RT Journal Article
SR Electronic
T1 Contribution of DOCK11 to the Expansion of Antigen-Specific Populations among Germinal Center B Cells
JF ImmunoHorizons
FD American Association of Immunologists
SP 520
OP 529
DO 10.4049/immunohorizons.2000048
VO 4
IS 9
A1 Sakamoto, Akihiko
A1 Maruyama, Mitsuo
YR 2020
UL http://www.immunohorizons.org/content/4/9/520.abstract
AB Germinal centers (GCs) are a structure in which B cell populations are clonally expanded, depending on their affinities to Ag. Although we previously isolated a characteristic protein called dedicator of cytokinesis 11 (DOCK11) from GC B cells, limited information is available on the roles of DOCK11 in GC B cells. In this study, we demonstrate that DOCK11 may contribute to the expansion of Ag-specific populations among GC B cells upon immunization of mice. The lack of DOCK11 in B cells resulted in the lower frequency of Ag-specific GC B cells along with enhanced apoptosis upon immunization. Under competitive conditions, DOCK11-deficient B cells were dramatically prevented from participating in GCs, in contrast to DOCK11-sufficient B cells. However, minor impacts of the DOCK11 deficiency were identified on somatic hypermutations. Mechanistically, the DOCK11 deficiency resulted in the suppression of B cell–intrinsic signaling in vitro and in vivo. Although DOCK11 expression by B cells was required for the induction of T follicular helper cells at the early stages of immune responses, minor impacts were identified on the expansion of Ag-specific populations among GC B cells. Thus, DOCK11 appears to contribute to the expansion of Ag-specific populations among GC B cells through the stimulation of B cell–intrinsic signaling.