Amyloid fibrils activate B-1a lymphocytes to ameliorate inflammatory brain disease.
Stanford, United States. In Proc Natl Acad Sci U S A, Jan 2016
Analysis of gene expression indicated that the fibrils activated the CD40/B-cell receptor pathway in B-1a cells and induced a set of immune-suppressive cell-surface proteins, including BTLA, IRF4, and Siglec G. Collectively, these data indicate that the fibrils activate B-1a cells and F4/80(+) MΦs, resulting in their migration to the lymph nodes, where IL-10 and cell-surface receptors associated with immune-suppression limit antigen presentation and T-cell activation.
Tumor necrosis factor superfamily in innate immunity and inflammation.
Los Angeles, United States. In Cold Spring Harb Perspect Biol, Apr 2015
Recent results illustrate how the communication networks formed among these cytokines and the coreceptors B and T lymphocyte attenuator (BTLA) and CD160 both inhibit and activate innate lymphoid cells (ILCs), innate γδ T cells, and natural killer (NK) cells.
Five Layers of Receptor Signaling in γδ T-Cell Differentiation and Activation.
Lisbon, Portugal. In Front Immunol, 2014
Some of the key players are the costimulatory receptors CD27 and CD28, which differentially impact on pro-inflammatory subsets of γδ T-cells; the cytokine receptors IL-2R, IL-7R, and IL-15R, which drive functional differentiation and expansion of γδ T-cells; the NK receptor NKG2D and its contribution to γδ T-cell cytotoxicity; and the inhibitory receptors PD-1 and BTLA that control γδ T-cell homeostasis.
HVEM is a TNF Receptor with Multiple Regulatory Roles in the Mucosal Immune System.
Los Angeles, United States. In Immune Netw, 2014
HVEM is an unusual TNF receptor because of its high expression levels in the gut epithelium, its capacity to bind ligands that are not members of the TNF super family, including immunoglobulin (Ig) superfamily members BTLA and CD160, and its bi-directional functionality, acting as a signaling receptor or as a ligand for the receptor BTLA.
Mixing Signals: Molecular Turn Ons and Turn Offs for Innate γδ T-Cells.
Los Angeles, United States. In Front Immunol, 2013
Here, we discuss some of the key mechanisms that regulate the development, activation, and inhibition of innate γδ T-cells in light of recent evidence that the inhibitory immunoglobulin-superfamily member B and T lymphocyte attenuator restricts their differentiation and effector function.