Ccl22 polyclonal antibody
- Known as:
- Ccl22 pab (anti-)
- Catalog number:
- PAB8827
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- Ccl22 polyclonal antibody
Related genes to: Ccl22 polyclonal antibody
- Gene:
- CCL22 NIH gene
- Name:
- C-C motif chemokine ligand 22
- Previous symbol:
- SCYA22
- Synonyms:
- MDC, STCP-1, ABCD-1, DC/B-CK, A-152E5.1, MGC34554
- Chromosome:
- 16q21
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-22
- Date modifiied:
- 2016-10-05
Related products to: Ccl22 polyclonal antibody
Related articles to: Ccl22 polyclonal antibody
- serovar Dublin ( Dublin) is a host-adapted pathogen that causes severe systemic disease in cattle and presents a zoonotic risk to humans. While macrophages play a pivotal role in host defense against they are also an intracellular niche for bacterial persistence. However, the mechanism underlying the early transcriptional response of macrophages to Dublin infection is poorly understood. This study used high-throughput sequencing to profile mRNA and miRNA expression in RAW 264.7 mouse macrophages 2 h after infection with Dublin compared to uninfected control cells. A total of 1,080 differentially expressed (DE) mRNAs were identified, of which 492 were up-regulated and 588 were down-regulated. In addition, 23 DE miRNAs, 18 up-regulated and 5 down-regulated, were identified. Meanwhile, KEGG enrichment analysis indicated significant enrichment of the DE mRNAs and miRNAs in signaling pathways associated with macrophage immune activation, including the TNF, HIF-1, and MAPK signaling pathways, as well as those involved in responses to infection. The accuracy of the mRNA sequencing results was verified using RT-qPCR. In conclusion, the findings showed significant up-regulation of , , , , and the early stages of Dublin infection of mouse macrophages, suggesting the involvement of these molecules in regulating the host immune response. - Source: PubMed
Publication date: 2026/05/04
Wang ZiSun MiaoZhang ZipengWang YongqiangTong ShengjieMeng LinghaoHan DongxuGe XinranChen HengliYang DahanLiu Kai - Skeletal muscle injuries are a common consequence of physical activity, repetitive movements, and trauma. Regulatory T cells (Treg) act as critical mediators of immune repair response after injury. Thus, treatments effectively targeting Treg may accelerate injury resolution. CCL22 is a chemokine that recruits CCR4-expressing cells, particularly Treg, to sites of inflammation or immune regulation, such as tumor microenvironments. When an immunomodulatory, sustained release formulation of polymeric microparticles (MP) delivering CCL22 (CCL22MP), was administered after cardiotoxin (CTx)-mediated muscle injury, significantly improved limb function was observed on days 3 and 5 post injury. Histologic evaluation of the injured limbs showed reduced injury and enhanced myofiber cross-sectional area in CCL22MP treated limbs. Analysis of the local immune populations revealed augmented Treg concentrations, as well as altered infiltrating myeloid populations towards pro-repair subsets. These findings reveal that amplifying local Treg to damaged areas improves outcomes, thus offering a translationally promising approach after muscle injury. - Source: PubMed
Publication date: 2026/05/19
Borrelli Matthew AWarunek Jordan J PAnn Varghese BetsyTurner NeillLittle Steven RTurnquist Hēth R - Here we determined whether myeloid Mir34a has a tumor suppressive function in Apc mice, a model for intestinal and colon cancer. Myeloid cell-specific deletion of Mir34a in Apc mice increased tumor initiation and allowed progression towards invasive carcinomas, which are generally not observed in Apc mice. Loss of Mir34a facilitated the polarization of tumor-associated macrophages (TAMs) towards a pro-tumorigenic M2-like state, implying that Mir34a is required to maintain TAMs in a tumor-suppressive state. Also, Mir34a-deficient, bone-marrow-derived macrophages (BMDMs) from Apc mice were polarized towards a pro-tumorigenic, M2-like state and displayed enhanced migration when compared to Mir34a-proficient BMDMs. Intestinal tumors in myeloid Mir34a-deficient mice showed elevated expression of several known Mir34a target mRNAs, including Csf1r, Pd-l1, Mmp9, Ccl22, and c-Myc. In addition, the number of immuno-suppressive, pro-tumorigenic CD4Foxp3 T cells increased in myeloid Mir34a-deficient intestinal tumors. Moreover, Apc mice with myeloid-specific deletion of Mir34a had a significantly diminished survival rate. Following the induction of inflammatory colitis, these mice showed enhanced colon cancer initiation and progression towards invasive carcinomas with an increase in M2-like TAMs, N2-like neutrophils and T cells. These findings imply that myeloid Mir34a suppresses tumor formation and progression by maintaining myeloid and T-cells in an anti-tumorigenic state. Therefore, the p53-miR-34a axis has a central role in non-tumor cell mediated suppression of intestinal and colon cancers. - Source: PubMed
Publication date: 2026/05/15
Chen YunLiu FangtengKönig JanineBouznad NassimHermeking Heiko - Radiotherapy (RT) is increasingly recognized as a system‑level immunomodulator capable of reshaping cytokine networks across spatial, temporal and dosimetric dimensions. This review synthesizes existing evidence on RT parameters, key signaling axes, major effector cells, organ‑specific contexts and clinical translation. It describes how the cyclic GMP‑AMP synthase/stimulator of interferon genes (STING)/IFN‑I, NF‑κB and TGF‑β pathways coordinate immune activation and immune suppression after irradiation. It then summarizes macrophage‑centered regulatory circuits and chemokine axes, including C‑C motif chemokine ligand (CCL)2/CCR2 and CCL22/CCR4 that govern T‑cell trafficking and functional states. A map of organ‑specific cytokine programs that link therapeutic benefit and toxicity in the brain, lung, gastrointestinal tract, oral mucosa and liver is then provided, and actionable targets within inflammasome‑associated pyroptosis and fibrogenic cascades are highlighted. RT technical parameters, including fractionation, treatment volume, stereotactic body RT, Fast Linear Accelerator‑based Scanning Hybrid ultra‑high dose-rate delivery and proton therapy can differentially shape cytokine dynamics and modify the therapeutic window. The DNA damage response network with poly (ADP‑ribose) polymerase (PARP)1 as a central node represents a second hub that interfaces with antigen presentation and IFN signaling, supporting rational combinations with PARP inhibitors and immune checkpoint blockade. Finally, a translational algorithm with three pillars is proposed. The first pillar uses IFN‑related gene signatures and circulating cytokine profiles to stratify tumors by baseline IFN activity. The second pillar aligns RT timing with endogenous STING or IFN pulses and incorporates CCR2, CCR4 or colony stimulating factor 1 receptor blockade to counter myeloid cell‑mediated immunosuppression. The third pillar co‑manages treatment‑related toxicities by targeting the NLR family pyrin domain containing 3/gasdermin D axis or by using fibrosis‑modulating interventions. Furthermore, ongoing clinical trials of cytokine-directed agents combined with RT are summarized. This framework positions cytokines as measurable and modifiable variables for individualizing combined RT and immunotherapy. - Source: PubMed
Publication date: 2026/05/08
Zhou SiyuanJiang YurongFan JixuGuo MinjieWen YiDai Chunhua - Differentiating between infectious and non-infectious etiologies in systemic inflammatory disorders may be challenging due to overlapping clinical presentations and the lack of reliable discriminating biomarkers. Regulatory T-cells (Tregs) modulate immune responses. Their functionality is governed by specific chemokines, including CCL1 and CCL22. We investigated whether these Treg-attracting chemokines are differentially regulated in infectious versus sterile inflammation. This prospective, single-center biomarker study enrolled patients with sepsis, acute pancreatitis, and hospitalized controls without infectious diseases. Serum samples were collected on days 1, 3, 5, and 7, measuring CRP, IL-6, PCT, CCL1, and CCL22. Between March 2019 and October 2022, 159 patients were enrolled, comprising 45 patients suffering from acute pancreatitis, 15 patients with confirmed sepsis as well as 99 hospitalized controls. Established inflammatory parameters CRP, IL-6 and PCT showed typical kinetics. Decreased CCL1 levels, but not CCL22, distinguished acute pancreatitis from sepsis at all time points. Additionally, CCL1 levels inversely correlated with organ failure severity in sepsis patients. CCL1 shows potential to serve as a biomarker to differentiate sterile and non-sterile inflammation in sepsis and acute pancreatitis. This may support clinical decision-making and allow a more precise use of antibiotics in these patient cohorts. - Source: PubMed
Publication date: 2026/05/06
Vornhülz MarliesMüller JenniferTakken Lara LouisaLayritz PatrickPerleberg CarolinGärtig JanBeimert AntoniaWeber PatrickEndres StefanMayerle JuliaHoldt LescaPiseddu IgnazioAnz David