Cat.No. : CSC-RO0007 Host Cell: CHO-K1
| Cat. No. | CSC-RO0007 |
| Description | This cell line is engineered to stably overexpress the human CD86 in CHO-K1 cells. |
| Background | This gene encodes a type I membrane protein that is a member of the immunoglobulin superfamily. This protein is expressed by antigen-presenting cells, and it is the ligand for two proteins at the cell surface of T cells, CD28 antigen and cytotoxic T-lymphocyte-associated protein 4. Binding of this protein with CD28 antigen is a costimulatory signal for activation of the T-cell. Binding of this protein with cytotoxic T-lymphocyte-associated protein 4 negatively regulates T-cell activation and diminishes the immune response. Alternative splicing results in several transcript variants encoding different isoforms. |
| Gene | CD86 |
| Gene Species | Homo sapiens (Human) |
| Host Cell | CHO-K1 |
| Host Cell Species | Cricetulus griseus (Chinese hamster) |
| Stability | Validated for at least 10 passages |
| Application | 1. Studying the interactions between immune cells and cancer cells 2. Studying the mechanisms of resistance to immune checkpoint blockade 3. High-throughput screening 4. Drug target validation |
| Quality Control | Negative for bacteria, yeast, fungi and mycoplasma. |
| Shipping | Dry ice |
| Storage | Liquid nitrogen |
| Revival | Rapidly thaw cells in a 37°C water bath. Transfer contents into a tube containing pre-warmed media. Centrifuge cells and seed into a 25 cm2 flask containing pre-warmed media. |
| Gene Name | CD86 CD86 molecule [ Homo sapiens ] |
| Gene Symbol | CD86 |
| Synonyms | CD86; CD86 molecule; CD28LG2, CD86 antigen (CD28 antigen ligand 2, B7 2 antigen); T-lymphocyte activation antigen CD86; B lymphocyte antigen B7 2; B7 2; B7.2; BU63; FUN-1; CTLA-4 counter-receptor B7.2; B-lymphocyte activation antigen B7-2; CD86 antigen (CD28 antigen ligand 2, B7-2 antigen); B70; B7-2; LAB72; CD28LG2; MGC34413; |
| Gene ID | 942 |
| UniProt ID | P42081 |
| mRNA Refseq | BC040261 |
| Chromosome Location | 3q21 |
| Function | coreceptor activity; protein binding; receptor activity; |
| Pathway | Adaptive Immune System, organism-specific biosystem; Allograft rejection, organism-specific biosystem; Allograft rejection, conserved biosystem; Autoimmune thyroid disease, organism-specific biosystem; Autoimmune thyroid disease, conserved biosystem; CD28 co-stimulation, organism-specific biosystem; CD28 dependent PI3K/Akt signaling, organism-specific biosystem; |
| MIM | 601020 |
| Mycoplasma | Negative |
| Format | One frozen vial containing millions of cells |
| Storage | Liquid nitrogen |
| Safety Considerations |
The following safety precautions should be observed. 1. Use pipette aids to prevent ingestion and keep aerosols down to a minimum. 2. No eating, drinking or smoking while handling the stable line. 3. Wash hands after handling the stable line and before leaving the lab. 4. Decontaminate work surface with disinfectant or 70% ethanol before and after working with stable cells. 5. All waste should be considered hazardous. 6. Dispose of all liquid waste after each experiment and treat with bleach. |
| Ship | Dry ice |
Recently, a novel subset of human regulatory B cells has been described. They are derived from a transitional B cell subset and are characterized by the production of IL-10. They appear to play an important role in regulating T cell immunity in vivo. Despite this important function, the molecular mechanisms by which they control T cell activation are not fully understood. This study showed that transitional B cells produced more IL-10 and expressed higher levels of IL-10 receptors after CD40 ligation compared with other B cell subsets. In addition, under this stimulation condition, CD86 expressed by transitional B cells was downregulated and T cell proliferation was reduced. The evidence here suggests that the downregulation of CD86 expression by transitional B cells is due to the autocrine effect of IL-10, which in turn leads to reduced T cell proliferation and TNF-α production. This analysis was further extended to peripheral B cells from renal transplant recipients. B cells from patients who were tolerant to the transplanted organ maintained higher IL-10 production after CD40 ligation, which was associated with lower CD86 expression in patients with chronic rejection. Therefore, these findings reveal a new alternative mechanism by which transitional B cells inhibit T cell proliferation and cytokine production.
Here, to confirm the role of CD86 in CD4+T cell proliferation, researchers added CD86-expressing CHO cells to T cell-B cell co-cultures. The researchers observed that T cell proliferation was restored when CD86-expressing CHO cells were added to T cell co-cultures together with transitional B cells (Figure 1). Notably, although it has been reported that inhibition of TNF-α production by CD4+T cells induced by transitional B cells was reversed in the presence of CD80 and CD86 neutralizing antibodies, it was demonstrated here that the expression level of CD86 on transitional B cells correlated with the amount of TNF-α produced by CD4+T cells.
Figure 1. Histograms and total percentages of T-cell proliferation were measured in cocultures of 1X105 anti-CD3-activated CD4+T cells with 1X105 B-cell subsets in the presence of CD86-expressing and control CHO cells (5X103) after 72 h. (Nova-Lamperti E, et al., 2016)
A: The Human CD86 Stable Cell Line-CHO, due to its stable expression of the CD86 molecule, has significant potential in studying antigen presentation and immune activation processes. CD86, as a co-stimulatory molecule, is crucial for T cell activation and the regulation of immune responses. This cell line can be used to investigate the interaction between CD86 and T cell receptors and its impact on immune responses.
A: By using the Human CD86 Stable Cell Line-CHO, the role of CD86 in regulating immune tolerance can be studied. Techniques like co-immunoprecipitation and immunofluorescence can be used to analyze the interaction of CD86 with other immunosuppressive molecules and assess its impact on T cell subsets, such as regulatory T cells.
A: When conducting drug screening with the Human CD86 Stable Cell Line-CHO, experiments should be designed to evaluate the impact of candidate drugs on the expression and function of CD86. Techniques like flow cytometry and ELISA can be used to assess drug modulation of CD86 expression and its effects on T cell activation and differentiation.
A: The Human CD86 Stable Cell Line-CHO has potential applications in studying autoimmune diseases. CD86 plays a significant role in autoimmune responses, and this cell line can be used to investigate the regulatory mechanisms of CD86 in autoimmune diseases, such as multiple sclerosis and rheumatoid arthritis, and potential therapeutic targets.
A: When conducting gene editing experiments with the Human CD86 Stable Cell Line-CHO, it is important to maintain the expression and function of the CD86 protein. The choice and design of gene editing tools, such as CRISPR/Cas9, should ensure specificity to the target gene and accurate validation of the editing effects.
A: The Human CD86 Stable Cell Line-CHO has promising prospects in tumor immunotherapy research. Due to the co-stimulatory role of CD86 in the tumor microenvironment, this cell line can be used to study immunotherapeutic strategies targeting CD86, including immune checkpoint inhibitors and immune activators.
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