CD80 Specific Neutra™ Antibody Products

CD80 is a co-stimulatory molecule, also known as B7-1. It is selectively expressed in antigen-presenting cells, including dendritic cells, macrophages, and B cells. It plays a very important role in activating T cells, one of the important effector arms of the adaptive immune system. CD80 interacts with two receptors present in T cells, CD28 and CTLA-4 (cytotoxic T-lymphocyte-associated protein 4). When CD80 binds to CD28, it provides a co-stimulatory signal necessary for the full activation and proliferation of T cells upon encountering an antigen. It allows T cell survival, cytokine production, and effector functions. Conversely, the binding of CD80 with CTLA-4 delivers an inhibitory signal to tune down T cell activation that might be responsible for immune hyperactivity. Therefore, T cell activation is down-regulated since CTLA-4 binds to CD80 by competitive inhibition with CD28 in the binding to CD80, leading to immune tolerance. There is a reason to understand involvement and regulation of CD80 in designing strategies of immunotherapy and therapeutic treatment of autoimmune diseases, cancer, and infectious diseases.

Its Gene ID: 941, UniProtKB ID: P33681, OMIM ID: 112203

The Structure of CD80

CD80 is a type I transmembrane protein belonging to the immunoglobulin superfamily. Structurally, this molecule is well characterized by several recognizable domains that permit it to perform its indispensable role in immune regulation. There are two important Ig-like domains in CD80, located in its extracellular region: an IgV-like and IgC-like domain. Adjacent to the IgC-like domain is a stalk region that connects the extracellular domain to the cell membrane. This region facilitates proper positioning of CD80 for receptor engagement and signaling. The CD80 cytoplasmic tail contains signaling motifs, responsible for the signaling cascades taking place in the cell when a receptor is engaged. The same motifs are involved in cytokine control and T-cell activation. In general, CD80 has a structure that fits well with its function as a co-stimulatory molecule in the immune system.

The Signal Pathway of CD80 Molecule

CD80 is usually expressed on dendritic cells, activated B cells and monocytes, which provides necessary costimulatory signals for T cell activation and survival. When antigen-presenting cells (APCs) encounter pathogens or foreign antigens, they upregulate the expression of CD80 on their surface. CD80 then interacts with two receptors on T cells: CD28 and CTLA-4.

• CD80 and CD28 Interaction

Upon interaction with CD28, CD80 initiates a co-stimulatory signal essential for T cell activation. This interaction triggers downstream signaling cascades that promote T cell proliferation, cytokine production, and effector functions, bolstering the adaptive immune response. The primary signaling pathways activated by CD80-CD28 engagement include the phosphatidylinositol-3 kinase (PI3K) pathway and the mitogen-activated protein kinase (MAPK) pathway. Activation of PI3K leads to the phosphorylation of Akt, promoting cell survival and metabolism. Meanwhile, MAPK pathway activation results in the phosphorylation of ERK, JNK, and p38, regulating gene expression and cell proliferation. Additionally, CD28 engagement enhances calcium influx and NF-κB activation, further augmenting T cell activation and effector functions. Overall, the CD80-CD28 interaction provides a critical co-stimulatory signal that amplifies T cell responses against pathogens and promotes immune defense.

• CD80 and CTLA-4 Interaction

In contrast, interaction of CD80 with CTLA-4 initiates an inhibitory signal that regulates T cell activation and promotes immune tolerance. CTLA-4 competes with CD28 for binding to CD80, leading to the attenuation of downstream signaling events associated with T cell activation. The inhibitory signaling pathways induced by CD80-CTLA-4 engagement include the dephosphorylation of signaling molecules such as Akt and ERK, resulting in the inhibition of T cell proliferation and cytokine production. Additionally, CTLA-4 engagement promotes the recruitment of phosphatases, such as SHP-2, to the immunological synapse, further dampening T cell activation. Moreover, CTLA-4 engagement inhibits CD28-mediated co-stimulatory signals by inducing the downregulation of CD80 and CD86 expression on APCs, thereby limiting T cell activation. Overall, the CD80-CTLA-4 interaction plays a crucial role in maintaining immune homeostasis by dampening excessive T cell responses and promoting immune tolerance.

Fig.1 Interactions between CD80, CD86, CD28 and CD152.¹

Related Diseases of CD80 Molecule

CD80 is implicated in a wide range of diseases due to its critical role in regulating immune responses and T cell activation. Understanding the mechanisms underlying CD80 involvement in these diseases is essential for developing targeted therapies and interventions.

• Autoimmune diseases: CD80 dysregulation is associated with autoimmune disorders such as rheumatoid arthritis, systemic lupus erythematosus (SLE), multiple sclerosis, and inflammatory bowel disease (IBD). In these conditions, aberrant CD80 expression or signaling can lead to excessive T cell activation and autoimmunity.
• Cancer: CD80 expression on tumor cells can influence tumor immune evasion and anti-tumor immune responses. Strategies targeting the CD80 pathway, such as immune checkpoint blockade, are being explored for cancer treatment.
• Infectious diseases: CD80 is involved in the immune response to infectious agents such as viruses, bacteria, and parasites. Its dysregulation or modulation by pathogens can impact the outcome of infection and the host immune response.
• Transplant rejection: CD80 plays a role in alloimmune responses and transplant rejection by facilitating T cell activation against foreign antigens presented by transplanted tissues or organs.
• Allergic diseases: CD80 expression on antigen-presenting cells can contribute to T cell activation and the development of allergic responses in conditions such as asthma and allergic rhinitis.

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REFERENCE

1. Sansom, David M., Claire N. Manzotti, and Yong Zheng. "What's the difference between CD80 and CD86?." Trends in immunology 24.6 (2003): 313-318.