Ask about this productRelated genes to: CD80 antibody
- Gene:
- CD80 NIH gene
- Name:
- CD80 molecule
- Previous symbol:
- CD28LG, CD28LG1
- Synonyms:
- B7.1, B7-1
- Chromosome:
- 3q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-14
- Date modifiied:
- 2016-10-05
Related products to: CD80 antibody
Related articles to: CD80 antibody
- Intradermal delivery of the Toll-like receptor (TLR)-9 agonist agatolimod/CPG7909, prior to sentinel lymph node (SLN) biopsy was previously shown to induce locoregional and systemic immunity, reduce tumor-involved SLN rates, and improve recurrence-free survival in patients with early-stage melanoma. Remarkably, men exhibited superior dendritic cell (DC) maturation. Here, we report on further sex-based differences in the immune response after intradermal administration of CPG7909, which included higher CD80/CD83 expression levels in conventional (c) DC subsets in men's as compared to women's SLN, as well as higher release levels of IL-1β, TNF, and IL-6 (all contributors to cDC activation) and Th1/Th2 cytokines. In an effort to identify a more effective DC-activating therapy for women, we compared the in-vitro effects of CPG7909 with those of the TLR7/8 agonist resiquimod/R848 on SLN single cells from female patients. R848 induced superior cDC subset activation and TNF, IL-6, IL-10, IL-12, IFNγ, and CXCL10 release. Correlation analyses suggested that IFNα, TNF, and IL-6 were key for CPG7909-induced LNR-cDC activation, whereas R848's effect appeared more cytokine-independent. We conclude that combining locally delivered CPG7909 and R848 in early-stage melanoma will ensure full-range DC subset activation and robust pro-inflammatory T-cell responses in melanoma SLN, independent of sex. - Source: PubMed
Publication date: 2026/05/07
Notohardjo Jessica C LToffoli Elisa CMuijlwijk Taravan den Hout Mari F C MKandiah VinithaLabots Mariettevan de Ven Rienekevan den Eertwegh Alfons J Mde Gruijl Tanja D - Emerging evidence from lupus-prone mice and patients with systemic lupus erythematosus implicates enhanced glycolysis in lymphocytes as a driver of disease. We previously showed that the pharmacologic blockade of glycolysis reduced the production of autoantibodies without affecting antibodies induced by immunization to a foreign protein. Here we used CRISPR/Cas9 to reduce the expression of glucose transporter GLUT1 in B cells from autoreactive AM14 Vk8R (AM14) and antigen-specific B1-8 Jκ (B1-8) transgenic mice, comparing intrinsic glycolytic requirements across disease-relevant contexts. Following adoptive transfer into BALB/c recipients, Glut1 knockdown (Glut1KD) decreased the persistence of AM14 B cells, their differentiation into plasmablasts, and production of antibodies upon immunization with the PL2-3 hybridoma that activates both their B-cell receptor and endosomal TLR. In addition, PL2-3-stimulated Glut1KD AM14 B cells selectively reduced their CD80 expression both in vivo and in vitro, as well as ATP production and mammalian target of rapamycin (mTOR) signaling in vitro. In contrast, Glut1KD B1-8 B cells retained persistence, plasmablast output, and nitrophenyl (NP)-specific IgM production after NP-OVA immunization, with a selective reduction in the proliferation of naive B cells. Bioenergetic output was preserved despite Glut1KD in both clones stimulated with TLR7 agonist R848, but CD80 and mTOR signaling were differentially affected. Thus, GLUT1-dependent glycolysis is essential for immune complex-driven autoreactive B-cell activation yet largely dispensable for antigen-specific responses, identifying metabolic checkpoints that may selectively restrain pathogenic B cells while sparing protective humoral immunity. - Source: PubMed
Zhu YananChoi Seung ChulShlomchik Mark JMorel Laurence - Although culturing cells in serum-free or low-serum media may lead to reduced cell proliferation, it is crucial to minimise the presence of foreign proteins and other impurities that could compromise the validity of experimental findings on immunomodulation. The study aimed to investigate the immunomodulatory effects of the secretome derived from the serum-free media (SFM) of stem cells obtained from human exfoliated deciduous teeth on THP-1-derived macrophage polarisation and the assessment of inflammatory and oxidative stress mediators. THP-1 cells were polarised into M0 and M1 macrophages, and their differentiation was confirmed using flow cytometry to analyse specific markers of M0 (CD14 and CD68) and M1 (CD80 and CD86). The secretome was collected from SHED-MSCs cultured for 48 h in serum-free DMEM/F12 media. After treating THP-1-derived M0/M1 macrophages with SFM-secretome from SHED-MSCs, cells and supernatants were evaluated for immunosuppressive (anti-inflammatory and antioxidant) and immunostimulatory (pro-inflammatory and pro-oxidant) indicators. Secretome treatment decreased the population of M1 macrophages, along with the expression of pro-inflammatory and pro-oxidative markers, including CD80, CD86, TNF-α, IL-12, NO, MDA and IL-6R. The immunomodulatory effect of the secretome produced by SFM, which may help reduce inflammation, is demonstrated by an increase in M2 macrophages and anti-inflammatory and antioxidant markers, including CD206, TGFβ-2, IL-10, TAC, CAT, SOD and ARG1. The secretome produced by SFM-derived SHED-MSCs may reduce the risk of introducing foreign proteins and other potentially hazardous chemicals and enhance the efficacy of cellular secretions for applications such as immunotherapy or regenerative medicine by modulating the immune system. - Source: PubMed
Mohammad-Hasani AzadehMohammadi SaeedSaeidi MohsenFallah AliKhosravi Ayyoob - Chronic immune activation and systemic inflammation persist in people living with HIV (PWH) despite effective antiretroviral therapy, contributing to increased cardiovascular and cancer risk. Monocytes play a central role in this process, partly through type I interferon (IFN-I) signaling. As Toll-like receptor (TLR) 3 and 7 are key inducers of endogenous IFN-I in response to viral RNA, we investigated how TLR3 and TLR7 stimulation contributes to IFN-I-driven monocyte activation, and whether this response-potentially involving both direct TLR signaling and IFN-I mediated amplification- can be modulated by JAK-STAT inhibition. - Source: PubMed
Publication date: 2026/05/04
Camard MarionPlaçais LéoBitu MarieMouanga ChristelliahBourdic KatiaRick-Ryan MagagiPaoletti AudreyBourgeois ChristineLambotte OlivierNoel Nicolas - Human papillomavirus (HPV) infection is strongly associated with multiple malignancies, primarily driven by the viral oncoproteins E6 and E7, which play a central role in HPV-induced malignant transformation. Although current prophylactic HPV vaccines have shown remarkable efficacy in preventing initial infections, there remains an urgent need for therapeutic vaccines targeting pre-existing HPV infections and HPV-associated malignancies. - Source: PubMed
Publication date: 2026/04/17
Li QiLiu YongzhuangWang YiLi Zhigang