mProX™ Human CD40 Stable Cell Line

Product Information

Target Family

Target Protein Species

Human

Host Cell Type

HEK293;CHO-K1;U87;LN229;T98G

Target Classification

CD Cell Lines

Target Research Area

Immunology Research

Related Diseases

Immunodeficiency With Hyper-Igm, Type 3; Immunodeficiency With Hyper-Igm, Type 1

Gene ID

Human:958

UniProt ID

Human:P25942

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

CD40 agonism has potential therapeutic applications in enhancing immune-checkpoint blockade and activating effector T and NK cells to create a T cell-inflamed tumor microenvironment. It can stimulate dendritic cells, improve expansion of antigen-specific T cells, and exhibit antitumor efficacy in multiple solid tumor models. CD40-CD154 interaction is involved in the pathogenesis of inflammatory and autoimmune diseases, and the soluble CD40 receptor (sCD40) isoform may serve as a biomarker for chronic inflammatory diseases. Inflammation can induce Œ±(1)-adrenoceptor expression in peripheral blood mononuclear cells, contributing to the inflammatory state in complex regional pain syndrome. Overall, CD40 has potential applications in cancer immunotherapy, chronic inflammatory diseases, and pain management.

Protocols

Please visit our protocols page.

Customer Reviews

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FAQ

chat Alex Brown (Verified Customer)

How does CD40 influence T cell responses? Nov 09 2022

chat Patrick Liam (Creative Biolabs Scientific Support)

CD40-CD40L interactions are vital for T cell help in immune responses, particularly in activating antigen-presenting cells and generating cytotoxic T lymphocytes. Nov 09 2022

chat Taylor Smith (Verified Customer)

Can CD40 agonists alter tumor stroma? Apr 19 2021

chat Patrick Liam (Creative Biolabs Scientific Support)

CD40 agonists can modify tumor stroma, demonstrating efficacy against pancreatic carcinoma by altering the tumor microenvironment and enhancing antitumor immunity. Apr 19 2021

Published Data

Fig.1 The clonogenicity and invasiveness are influenced by CD40 expression status, which is dependent upon the v-control control cells.

The clonogenicity and invasiveness, depending on CD40 expression status, were depicted in the graphs in relation to the respective v-control control cells, with no change signified by the dotted lines. The mean value of three independent experiments was represented in the figures, and statistical significance was indicated (*p < 0.05, **p < 0.01). In CD40-positive U87MG cells, the silencing of CD40 resulted in an equalization of clonogenicity and invasiveness between v-control and LAPTM5 knockdown cells, mirroring the phenotypes of CD40-negative LN229 and T98G v-control and shLAPTM5 cells. A significant increase in clonogenicity and invasiveness of LAPTM5 knockdown in relation to the respective v-control control cells was observed upon exogenous overexpression of CD40 in CD40-negative LN229 and T98G cells, confirming the results observed in CD40-positive U87MG cells.

Ref: Berberich, Anne, et al. "LAPTM5-CD40 crosstalk in glioblastoma invasion and temozolomide resistance." Frontiers in oncology 10 (2020): 747.

Pubmed: 32582531

DOI: 10.3389/fonc.2020.00747

Research Highlights

C, Richard; J, Jason. "Uncovering the potential of CD40 agonism to enhance immune-checkpoint blockade." Clinical cancer research : an official journal of the American Association for Cancer Research, 2023.
This article examines the potential therapeutic effects of CD40 agonism in CCR Translations. CD40 agonism, by stimulating antigen-presenting cells, can activate T and NK cells. This process may promote the development of an interferon-activated and T cell-inflamed tumor microenvironment. Furthermore, CD40 agonism has the potential to improve long-term response when combined with immune-checkpoint blockade. These results suggest that CD40 agonism is a promising candidate for cancer therapy. Overall, this study highlights the potential benefits of targeting CD40 in the treatment of cancer.
C, Richard; J, Jason. "Uncovering the potential of CD40 agonism to enhance immune-checkpoint blockade." Clinical cancer research : an official journal of the American Association for Cancer Research, 2023.
Pubmed: 37870487 DOI: 10.1158/1078-0432.CCR-23-2437

Wang, Bochun. et al. "XFab-α4-1BB/CD40L fusion protein activates dendritic cells, improves expansion of antigen-specific T cells, and exhibits antitumour efficacy in multiple solid tumour models." Cancer immunology, immunotherapy : CII, 2023.
It has been observed that certain patients with refractory or relapsing cancers do not respond to checkpoint inhibitors and require additional immunotherapies. These treatments are particularly necessary for individuals with "cold" tumours lacking significant immune infiltration at the start of treatment. One such therapy is XFab-Œ±4-1BB/CD40L, a bispecific antibody designed to target both 4-1BB and CD40. This antibody aims to activate dendritic cells and prime tumour-reactive T cells, ultimately inhibiting the growth of tumours.
Wang, Bochun. et al. "XFab-α4-1BB/CD40L fusion protein activates dendritic cells, improves expansion of antigen-specific T cells, and exhibits antitumour efficacy in multiple solid tumour models." Cancer immunology, immunotherapy : CII, 2023.
Pubmed: 37863852 DOI: 10.1007/s00262-023-03535-y