Anti-Mouse CD69 PE 100 ug
- Known as:
- Antibody toMouse CD69 PE 100 ug
- Catalog number:
- 12-0691-82
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD69 100
Related genes to: Anti-Mouse CD69 PE 100 ug
- Gene:
- CD69 NIH gene
- Name:
- CD69 molecule
- Previous symbol:
- -
- Synonyms:
- CLEC2C
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1992-08-06
- Date modifiied:
- 2016-10-05
Related products to: Anti-Mouse CD69 PE 100 ug
Related articles to: Anti-Mouse CD69 PE 100 ug
- The precise mechanisms underlying the pathogenesis of idiopathic inflammatory myopathy (IIM) remain undefined. However, there has been increasing recognition that tissue-resident memory cells (TRMs) play an important role in the pathogenesis of systemic autoimmune disease. In IIM, TRM-associated transcriptional signatures have been reported, but on a very limited basis. By using multimodal single-cell RNA sequencing analysis in our established murine model of histidyl-tRNA synthetase (HRS)-induced myositis, we identified a prominent population of CD4+ TRMs in inflamed skeletal muscle. Muscle CD4+ TRMs exhibited high expression of genes encoding Cd69, Cxcr6, Runx3, and Prdm1, alongside low expression of Klf2, Ccr7, Sell, S1pr1, and Tcf7 - a profile that is generally consistent with previous reports of TRM gene signature and that we validate through comparison to transcriptomic profiles of human muscle tissue. Detailed pathway analysis in our model indicates that muscle CD4+ TRMs contribute to innate immune regulatory pathways enriched for TNF and IFN-γ signaling. Furthermore, analysis of TCR clonotype distribution and CDR3 sequence similarity revealed pronounced clonal expansion of CD4+ TRMs relative to other T-cell subsets - a pattern that remained stable from 2 to 6 weeks post-immunization. Collectively, these results suggest a potential role for CD4+ TRMs in the pathogenesis of autoimmune myositis. - Source: PubMed
Publication date: 2026/07/23
Li DechengReay Daniel PPinal-Fernandez IagoCasal-Dominguez MariaMammen Andrew LGaffen Sarah LOriss Timothy BAscherman Dana P - The biophysical microenvironment critically shapes T cell activation, yet how nanoscale geometry regulates signaling remains poorly understood. Here, we demonstrate that microvilli insertion into nanopores robustly activates primary human T cells in the absence of TCR ligands, in a pore-size-dependent manner. Nanopores of ∼240 nm in diameter elicit strong ERK phosphorylation, Ca influx, and NFAT nuclear translocation, reaching levels comparable to biochemical stimulation using antibodies against the TCR complex and CD28. Although TCR knockdown attenuates responses, residual CD69 expression upon nanopore engagement indicates that nanoscale confinement lowers the activation threshold. Perturbation of membrane mechanics with GsMTx4 or methyl-β-cyclodextrin, as well as disruption of extracellular Ca-dependent interactions by EDTA, markedly impaired signaling, implicating extracellular calcium and membrane organization as key regulators of signaling. Together, these findings support a model in which ∼240 nm-sized nanopores promote stable close-contact patches that seed TCR signaling. Finally, we show that nanoporous stimulation combined with CD28 costimulation activates patient-derived T cells comparably to conventional methods, highlighting a strategy with translational potential for immunotherapy. - Source: PubMed
Publication date: 2026/07/22
Zünd TamaraLickert SebastianWeber WilliSaxer RafaelWenk MariusZünd JaninaKovalchuk TatianaBaldi LucreziaAghaizu Nozie DDaskalakis MichaelVogel ViolaKlotzsch Enrico - Genetic and preclinical data highlight CD6 as a promising target for multiple sclerosis (MS), yet the impact of clinically available CD6-targeting treatments on MS immunopathogenesis remains insufficiently defined. Itolizumab, a humanized anti-CD6 antibody with established safety and clinical efficacy in other autoimmune disorders, represents a potential candidate to interrogate this pathway in MS. - Source: PubMed
Publication date: 2026/07/21
González-Muñoz CynthiaBaeten PaulienHermans DoryssaHoeks CindyDe Bondt MirreDuran GayelWijmeersch Bart VanSchroten HorstIshikawa HiroshiCrombet-Ramos TaniaLabrada-Mon MayrelBroux BiekeHellings Niels - The reservoir of persistently latently infected cells is a major barrier to a cure for HIV infection. Protein kinase C (PKC) modulators can reverse HIV latency and could thus be useful "Kick" components in "Kick and Kill" approaches to a cure. However, PKC modulators also affect immune cell function, potentially limiting their clinical safety and utility. Here, using PKC isoform inhibitors in models of HIV latency and HIV-negative mononuclear cells, we determined the PKC isoforms involved in PKC modulator-mediated HIV latency reversal and immunomodulation (CD69 and CD4 expression, and inflammatory cytokine production). We found that inhibition of PKC α, β, γ, δ, or θ limited PKC-mediated HIV latency reversal to varying degrees. We also found that combinatorial PKC isoform inhibition significantly limited robust PKC modulator-mediated immune cell surface expression of CD69 and cytokine production. None of the pharmacologic PKC inhibitors affected PKC modulator-mediated downmodulation of T-cell surface CD4 expression. These results provide important insight into the isoforms involved in the various PKC modulator-mediated activities, including HIV latency reversal. Design of next-generation PKC modulators that are more selective for PKC α, β, and θ may allow for the partial functional decoupling of HIV latency reversal from immunomodulatory effects, and lead to safer and more effective PKC modulator-based latency-reversing regimens.IMPORTANCEHIV persists in long-lived, latently infected cellular reservoirs, which prevents the cure of the infection using currently available antiretroviral therapy alone. The "Kick and Kill" strategy proposes the use of latency-reversing agents (LRAs) to induce viral reactivation leading to reservoir elimination. Protein kinase C (PKC) modulators are one of the most potent classes of LRAs and operate through the activation of several PKC isoforms. Here, we demonstrate the contribution of various PKC isoforms to PKC modulator-mediated HIV latency reversal and immunomodulation. We identified PKC α, β, and θ as the isoforms important for latency reversal, while other isoforms, especially broad PKC isoform activation, had greater relative effects on immune cell activation and cytokine release. Together, these results define the pathways required for PKC-mediated HIV latency reversal and other important immunomodulatory effects and will thus inform the development of next-generation isoform-selective PKC modulator LRAs. - Source: PubMed
Publication date: 2026/07/20
Zaikos Thomas DPham VictorChou Tessa CMoran Jose ATurner Shireen RYu Brian HHourani RamiRanjan AlokZack Jerome AWender Paul AMarsden Matthew D - Tissue-resident memory T cells (TRMs) are a distinct memory T-cell subset that permanently reside in tissues such as the skin. In chronic immune-mediated dermatoses, including psoriasis, atopic dermatitis, and vitiligo, TRMs are implicated in site-specific "disease memory," contributing to persistence and relapse at previously affected sites. This review synthesizes emerging concepts on TRMs in chronic inflammatory skin diseases and discusses clinical and translational implications, including TRM-targeted therapies. Original human, animal, or in vitro studies evaluating TRMs in the pathogenesis or persistence of dermatologic diseases were included. In psoriasis, CD8 TRMs (CD69CD103) persisted in clinically healed skin. For atopic dermatitis, both CD4 and CD8 TRMs are implicated in maintaining Th2/Th22 inflammation. In vitiligo, autoreactive CD8 TRMs at lesional margins mediate melanocyte destruction. Across dermatological diseases, TRMs share three core features: persistence in previously affected skin after clinical resolution, rapid reactivation by diverse triggers (stress, autoantigens, allergens, or cytokines) leading to site-specific recurrence, and relative resistance to conventional therapies. Together, these properties provide a unifying framework linking tissue immune memory to the chronic, relapsing nature of inflammatory skin diseases. However, the dominant TRM pathways vary by disease, reflecting differences in immune polarization and antigen specificity. Targeting TRMs represents a promising strategy for disease control and serves as a biomarker of residual disease or flare. - Source: PubMed
Publication date: 2026/07/20
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