Human

4-1BB is a member of the tumor necrosis factor (TNF) receptor family. Its alternative names are tumor necrosis factor receptor superfamily member 9 (TNFRSF9), CD137 and induced by lymphocyte activation (ILA). It is currently of interest to immunologists as a co-stimulatory immune checkpoint molecule. 4-1BB can be expressed by activated T cells, but to a larger extent on CD8 than on CD4 T cells. In addition, CD137 expression is found on dendritic cells, follicular dendritic cells, natural killer cells, granulocytes and cells of blood vessel walls at sites of inflammation. The best characterized activity of 4-1BB is its costimulatory activity for activated T cells. Crosslinking of 4-1BB enhances T cell proliferation, IL-2 secretion, survival and cytolytic activity. Further, it can enhance immune activity to eliminate tumors in mice.

Human

BDCA-2 is a novel type II C-type lectin, which shows 50.7% sequence identity at the amino acid level to its putative murine ortholog, the murine dendritic cell–associated C-type lectin 2. In addition to its antigen capturing function, BDCA-2 can mediate potent inhibition of induction of IFN-α/β expression in PDCs. Production of IFN-α/β in response to several different types of viruses, bacteria, CpG-DNA, dsRNA, and SLE serum is by far the most prominent feature of PDCs.

Cyno

BDCA-2 is a novel type II C-type lectin, which shows 50.7% sequence identity at the amino acid level to its putative murine ortholog, the murine dendritic cell–associated C-type lectin 2. In addition to its antigen capturing function, BDCA-2 can mediate potent inhibition of induction of IFN-α/β expression in PDCs. Production of IFN-α/β in response to several different types of viruses, bacteria, CpG-DNA, dsRNA, and SLE serum is by far the most prominent feature of PDCs.

Human

B7-H3, a new member of the B7 family of immune-regulatory molecules, was identified in 2001 by database searches of a human dendritic cell-derived cDNA library. It is a type I transmembrane protein, which expresses in certain normal cells and tissues, such as dendritic cells, as well as the liver, lung, breast, placenta, and prostate. Aberrant expression of B7-H3 has been reported in a wide range of solid cancers, including brain, lung, pancreatic, colorectal, liver, and breast cancers, as well as in hematologic malignancies, such as acute leukemia and multiple myeloma, and it is associated with more advanced disease and poor prognosis.

Human

CTLA4 or CTLA-4 (cytotoxic T-lymphocyte-associated protein 4), also known as CD152 (cluster of differentiation 152), is a protein receptor that functions as an immune checkpoint and downregulates immune responses. CTLA4 is constitutively expressed in regulatory T cells but only upregulated in conventional T cells after activation – a phenomenon which is particularly notable in cancers. It acts as an "off" switch when bound to CD80 or CD86 on the surface of antigen-presenting cells. The CTLA-4 protein is encoded by the Ctla4 gene in mice and the CTLA4 gene in humans.

Human

Integrin, alpha E (ITGAE) also known as CD103 (cluster of differentiation 103) is an integrin protein that in human. ITGAE is expressed widely on intraepithelial lymphocyte (IEL) T cells (both αβ T cells and γδ T cells) and on some peripheral regulatory T cells (Tregs). It has also been reported on lamina propria T cells. A subset of dendritic cells in the gut mucosa and mesenteric lymph nodes, known as CD103 dendritic cells, also expresses this marker.

Cyno

BDCA-2 is a novel type II C-type lectin, which shows 50.7% sequence identity at the amino acid level to its putative murine ortholog, the murine dendritic cell–associated C-type lectin 2. In addition to its antigen capturing function, BDCA-2 can mediate potent inhibition of induction of IFN-α/β expression in PDCs. Production of IFN-α/β in response to several different types of viruses, bacteria, CpG-DNA, dsRNA, and SLE serum is by far the most prominent feature of PDCs.

Cyno

V-domain Ig suppressor of T cell activation (VISTA) is a potent negative regulator of T-cell function that is expressed on hematopoietic cells. VISTA levels are heightened within the tumor microenvironment, in which its blockade can enhance antitumor immune responses in mice. In humans, blockade of the related programmed cell death 1 (PD-1) pathway has shown great potential in clinical immunotherapy trials.

Human

Lymphocyte-activation gene 3, also known as LAG-3, is a protein which in humans is encoded by the LAG3 gene.[1] LAG3, which was discovered in 1990[2] and was designated CD223 (cluster of differentiation 223) after the Seventh Human Leucocyte Differentiation Antigen Workshop in 2000[3]. LAG-3 is a cell surface molecule with diverse biologic effects on T cell function. It is an immune checkpoint receptor and as such is the target of various drug development programs by pharmaceutical companies seeking to develop new treatments for cancer and autoimmune disorders.

cyno

Programmed death-ligand 1 (PD-L1) also known as cluster of differentiation 274 (CD274) or B7 homolog 1 (B7-H1) is a protein that in humans is encoded by the CD274 gene. The formation of PD-1 receptor / PD-L1 or B7.1 receptor /PD-L1 ligand complex transmits an inhibitory signal which reduces the proliferation of these CD8+ T cells at the lymph nodes. Supplementary to that PD-1 is also able to control the accumulation of foreign antigen specific T cells in the lymph nodes through apoptosis which is further mediated by a lower regulation of the gene Bcl-2.