| Literature DB >> 32573493 |
Erin Janssen1, Mira Tohme1, Jordan Butts1, Sophie Giguere2, Peter T Sage3, Francisco E Velázquez4, Christy Kam1, Elena Milin1, Mrinmoy Das1, Ali Sobh5, Salem Al-Tamemi6, Francis W Luscinskas4, Facundo Batista2, Raif S Geha1.
Abstract
T follicular helper (Tfh) cell migration into germinal centers (GCs) is essential for the generation of GC B cells and antibody responses to T cell-dependent (TD) antigens. This process requires interactions between lymphocyte function-associated antigen 1 (LFA-1) on Tfh cells and ICAMs on B cells. The mechanisms underlying defective antibody responses to TD antigens in DOCK8 deficiency are incompletely understood. We show that mice selectively lacking DOCK8 in T cells had impaired IgG antibody responses to TD antigens, decreased GC size, and reduced numbers of GC B cells. However, they developed normal numbers of Tfh cells with intact capacity for driving B cell differentiation into a GC phenotype in vitro. Notably, migration of DOCK8-deficient T cells into GCs was defective. Following T cell receptor (TCR)/CD3 ligation, DOCK8-deficient T cells had impaired LFA-1 activation and reduced binding to ICAM-1. Our results therefore indicate that DOCK8 is important for LFA-1-dependent positioning of Tfh cells in GCs, and thereby the generation of GC B cells and IgG antibody responses to TD antigen.Entities:
Keywords: Adaptive immunity; Immunology; T cells
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Year: 2020 PMID: 32573493 PMCID: PMC7455063 DOI: 10.1172/jci.insight.134508
Source DB: PubMed Journal: JCI Insight ISSN: 2379-3708