Murine MDC CCL22, Source: E. Coli, Protein
- Known as:
- Murine MDC CCL22, Source: E. Coli, Protein
- Catalog number:
- W 1680.960.005
- Product Quantity:
- 5
- Category:
- -
- Supplier:
- Biochro
- Gene target:
- Murine MDC CCL22 Source: . Coli Protein
Related genes to: Murine MDC CCL22, Source: E. Coli, Protein
- 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: Murine MDC CCL22, Source: E. Coli, Protein
Related articles to: Murine MDC CCL22, Source: E. Coli, Protein
- 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 - Cutaneous gene therapy has the potential to treat a wide range of skin disorders, but effective delivery remains limited by the barrier properties and immune surveillance of the skin. Here, we identify AAVrh32.33 as a potent vector for targeting dermal stromal compartments. Following systemic administration in mice, AAVrh32.33 mediated robust and durable transgene expression, with preferential targeting of dermal fibroblasts and hair follicle bulge cells. Expression peaked at 1 month and persisted for up to 2 years, highlighting its suitability for chronic conditions. To reduce immunogenicity, a dominant CD8 T cell epitope was disrupted, generating the IDPΔ variant. This modification attenuated peptide-specific T cell responses while preserving stromal transduction. In human skin explants, IDPΔ achieved high levels of gene expression, primarily in dermal fibroblasts and precursors, confirming translational relevance. Finally, vectors encoding CCL17, CCL20, and CCL22 demonstrated localized targeted therapeutic gene delivery in both healthy and inflamed skin, underscoring the feasibility of using this platform to reshape local immune responses. Together, these findings establish AAVrh32.33 and IDPΔ as promising platforms for durable cutaneous gene therapy, with direct applications in diseases such as vitiligo, where long-term modulation of the dermal microenvironment is essential. - Source: PubMed
Publication date: 2026/05/01
Arjomandnejad MotaharehEssien KingsleySylvia KatelynBlackwood MeghanTutto AmandaKatz EricaTang QiushiHarris John EKeeler Allison M - This study explored the effect and dual-targeting mechanism of total lignans from flower buds of Magnolia biondii Pamp. (TLFM) against AD. - Source: PubMed
Publication date: 2026/04/22
Yan MengdanYu WenchaoCheng MeiyuWu LonglongHan LinhangChen KaixianLi YimingZhang QingguangZhang LiuqiangQian Fei