Anti_Mouse, mab CCR3 Source Rat
- Known as:
- Anti_Mouse, mab CCR3 Source Rat
- Catalog number:
- 103-M339
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Mouse mab CCR3 Source Rat
Related genes to: Anti_Mouse, mab CCR3 Source Rat
- Gene:
- CCR3 NIH gene
- Name:
- C-C motif chemokine receptor 3
- Previous symbol:
- CMKBR3
- Synonyms:
- CC-CKR-3, CKR3, CD193
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-30
- Date modifiied:
- 2016-10-05
Related products to: Anti_Mouse, mab CCR3 Source Rat
Related articles to: Anti_Mouse, mab CCR3 Source Rat
- [This corrects the article DOI: 10.1002/ccr3.72681.]. - Source: PubMed
Publication date: 2026/06/28
- Osteoporosis weakens the skeleton by lowering bone mass and damaging bone microarchitecture. A growing body of evidence points to disruptions in osteoimmune homeostasis as a key driver of this disease. In particular, apoptosis of bone cells and immune cells appears to be a critical contributing mechanism. Within the bone marrow, CD8 T cells display a surprising functional duality: whether they protect bone or promote its loss depends heavily on local signals. Under healthy conditions or after mechanical loading, activated CD8 T cells help maintain bone mass. They do so mainly by secreting interferon‑γ (IFN‑γ), which blocks osteoclast formation through interference with NF‑κB and MAPK signaling. However, this protective role is not fixed. Pathological cues such as estrogen deficiency can flip CD8 T cells into a bone‑destroying phenotype. For example, when estrogen drops, muscle‑derived IL‑33 decreases. That drop prompts bone marrow CD8 T cells to release large amounts of CCL5. CCL5 then binds to CCR3 on osteoclast precursors and activates the ERK pathway, thereby accelerating bone loss in postmenopausal osteoporosis. Aging and chronic inflammation add another layer of complexity. They drive the accumulation of senescent CD28 CD8 T cells. These aged cells no longer produce enough IFN‑γ to protect bone; instead, they adopt a senescence‑associated secretory phenotype (SASP) that suppresses osteoblast differentiation and reduces mesenchymal stromal cell viability. Moreover, apoptosis of osteoblasts and osteocytes-triggered by TNF‑α, IFN‑γ, or glucocorticoids-worsens bone loss. New findings suggest that CD8 T cells may fuel this apoptotic process through Fas/FasL interactions and the granzyme/perforin pathway. This review brings together these context‑dependent mechanisms. We place special emphasis on how hormonal shifts, metabolic changes, and inflammatory mediators converge to decide whether CD8 T cells support skeletal integrity or drive bone resorption. - Source: PubMed
Publication date: 2026/06/12
Chen ZiChaoHu HaoHu DieDu QinChuanYang HuanZhiXu RongHuaYu PengHu XingBoHu Jun - Eosinophilic colitis (EC) is a rare eosinophilic gastrointestinal disorder with increasing frequency in recent years. Although normal eosinophil density varies substantially by colonic segment, several proposed eosinophil thresholds have been used in the literature to support the diagnosis in the appropriate clinical context. However, some patients with clinical features suggestive of eosinophilic colitis (EC) do not demonstrate increased tissue eosinophil counts on histopathologic examination. - Source: PubMed
Publication date: 2026/06/28
Khatami SaghiEbrahimi SabaMahjoub Fatemeh ElhamYousefi AzizollahHosseini AmirhosseinKhoshmirsafa MajidMousavinasab FatemehsadatMansouri MahboubehShabani MahdiMesdaghi Mehrnaz - Allergic rhinitis (AR) is a common Th2-mediated inflammatory disease of the nasal mucosa, in which eosinophils serve as pivotal effector cells. The CCR3 receptor, specific for eotaxin, plays a critical role in allergic inflammation. However, the role of CCR3 in the differentiation of bone marrow CD34 ⁺ progenitor cells into eosinophils and its contribution to AR pathogenesis remains incompletely defined. - Source: PubMed
Publication date: 2026/06/22
Zhang Zhi-QiangWei Meng-YiBei Jia-leLi Jing-YangDai Mei-NaJiang Yin-LiXiao Ya-TingZhang YingZhu Xinhua - BPA exposure is known to be correlated with asthma incidence. This study aimed to investigate the molecular mechanisms underlying bisphenol A (BPA)-induced asthma. - Source: PubMed
Publication date: 2026/06/03
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