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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

B and T lymphocyte associated

BTLA, B and T lymphocyte attenuator
This gene encodes a member of the immunoglobulin superfamily. The encoded protein contains a single immunoglobulin (Ig) domain and is a receptor that relays inhibitory signals to suppress the immune response. Alternative splicing results in multiple transcript variants. Polymorphisms in this gene have been associated with an increased risk of rheumatoid arthritis. [provided by RefSeq, Aug 2011] (from NCBI)
Top mentioned proteins: HVEM, CAN, CTLA-4, CD4, CD28
Papers on BTLA
Assessment of costimulation and coinhibition in a triple parameter T cell reporter line: Simultaneous measurement of NF-κB, NFAT and AP-1.
Steinberger et al., Vienna, Austria. In J Immunol Methods, Feb 2016
In these experiments we could show that engagement of the costimulatory molecule 4-1BB enhances NF-κB and AP-1 activity, whereas coinhibition via PD-1 or BTLA strongly reduced the activation of NF-κB and NFAT.
Enhanced Innate Inflammation Induced by Anti-BTLA Antibody in Dual Insult Model of Hemorrhagic Shock/Sepsis.
Ayala et al., Shanghai, China. In Shock, Jan 2016
B and T lymphocyte attenuator (BTLA) is an immune-regulatory coinhibitory receptor expressed not only on adaptive, but also on innate immune cells.
Amyloid fibrils activate B-1a lymphocytes to ameliorate inflammatory brain disease.
Rothbard et al., 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.
CD40 controls CXCR5-induced recruitment of myeloid-derived suppressor cells to gastric cancer.
Chen et al., Suzhou, China. In Oncotarget, Dec 2015
Microarray analyses comparing CD40high and CD40low MDSC revealed 1872 differentially expressed genes, including CD83, CXCR5, BTLA, CXCL9, TLR1, FLT3, NOD2 and CXCL10.
BTLA marks a less-differentiated tumor-infiltrating lymphocyte subset in melanoma with enhanced survival properties.
Radvanyi et al., Houston, United States. In Oncoimmunology, Aug 2015
UNASSIGNED: In a recent adoptive cell therapy (ACT) clinical trial using autologous tumor-infiltrating lymphocytes (TILs) in patients with metastatic melanoma, we found an association between CD8(+) T cells expressing the inhibitory receptor B- and T-lymphocyte attenuator (BTLA) and clinical response.
Immune checkpoint protein inhibition for cancer: preclinical justification for CTLA-4 and PD-1 blockade and new combinations.
Weber et al., Tampa, United States. In Semin Oncol, Jun 2015
In addition, we review herein the preclinical data surrounding emerging immune checkpoint proteins, including BTLA, VISTA, CD160, LAG3, TIM3, and CD244 as potential targets for inhibition.
Tumor necrosis factor superfamily in innate immunity and inflammation.
Ware et al., 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.
Silva-Santos et al., 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.
Kronenberg et al., 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.
The inhibitory receptor BTLA controls γδ T cell homeostasis and inflammatory responses.
Ware et al., Los Angeles, United States. In Immunity, 2014
We found that retinoid-related orphan receptor gamma-t (RORγt) and interleukin-7 (IL-7) influence γδ T cell homeostasis and function by regulating expression of the inhibitory receptor, B and T lymphocyte attenuator (BTLA).
Mixing Signals: Molecular Turn Ons and Turn Offs for Innate γδ T-Cells.
Ware et al., 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.
BTLA expression contributes to septic morbidity and mortality by inducing innate inflammatory cell dysfunction.
Ayala et al., Providence, United States. In J Leukoc Biol, 2012
These findings support role for BTLA and/or HVEM as potential, novel diagnostic markers of innate immune response/status and as therapeutic targets of sepsis.
B and T lymphocyte attenuator mediates inhibition of tumor-reactive CD8+ T cells in patients after allogeneic stem cell transplantation.
Dolstra et al., Nijmegen, Netherlands. In J Immunol, 2012
BTLA-HVEM interactions impair minor histocompatibiility antigen-specific T cell functionality, providing a rationale for BTLA signaling blockade in post-stem cell transplantation.
The expression and anatomical distribution of BTLA and its ligand HVEM in rheumatoid synovium.
Chen et al., Chifeng, China. In Inflammation, 2012
study described the expression and spatial distribution of HVEM and BTLA in rheumatoid arthritis synovial tissues, and results indicated that HVEM/BTLA may be involved in regulating the progress of joint inflammation
Selective blockade of herpesvirus entry mediator-B and T lymphocyte attenuator pathway ameliorates acute graft-versus-host reaction.
Rodriguez-Barbosa et al., León, Spain. In J Immunol, 2012
Combined blockade of BTLA and herpesvirus entry mediator (HVEM) does not inhibit donor T cell infiltration into graft-versus-host reaction organs; instead, it decreases the functional activity of the alloreactive T cells.
CD8(+) T cells specific for tumor antigens can be rendered dysfunctional by the tumor microenvironment through upregulation of the inhibitory receptors BTLA and PD-1.
Zarour et al., Pittsburgh, United States. In Cancer Res, 2012
Added with PD-1 and Tim-3 blockades, BTLA blockade enhanced the expansion, proliferation, and cytokine production of NY-ESO-1-specific CD8(+) T cells.
Slow down and survive: Enigmatic immunoregulation by BTLA and HVEM.
Murphy et al., Saint Louis, United States. In Annu Rev Immunol, 2009
B and T lymphocyte associated (BTLA) is an Ig domain superfamily protein with cytoplasmic immunoreceptor tyrosine-based inhibitory motifs.
Targeting of antigen to the herpesvirus entry mediator augments primary adaptive immune responses.
Ertl et al., Philadelphia, United States. In Nat Med, 2008
Interactions between the herpesvirus entry mediator (HVEM) and the B- and T-lymphocyte attenuator (BTLA) inhibit B and T cell activation.
CD160 inhibits activation of human CD4+ T cells through interaction with herpesvirus entry mediator.
Freeman et al., Boston, United States. In Nat Immunol, 2008
We found that herpesvirus entry mediator (HVEM) was a ligand of CD160 that acted as a 'bidirectional switch' for T cell activation, producing a positive or negative outcome depending on the engagement of HVEM by CD160 and known HVEM ligands such as B and T lymphocyte attenuator (BTLA) and the T lymphocyte receptor LIGHT.
B and T lymphocyte attenuator regulates CD8+ T cell-intrinsic homeostasis and memory cell generation.
Kaye et al., Los Angeles, United States. In Nat Immunol, 2007
mice deficient in full-length BTLA or its ligand, herpesvirus entry mediator, had increased number of memory CD8(+) T cells
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