Ask about this productRelated genes to: SIGLEC6 antibody
- Gene:
- SIGLEC6 NIH gene
- Name:
- sialic acid binding Ig like lectin 6
- Previous symbol:
- CD33L, CD33L1
- Synonyms:
- OB-BP1, SIGLEC-6, CD327
- Chromosome:
- 19q13.41
- Locus Type:
- gene with protein product
- Date approved:
- 1996-12-17
- Date modifiied:
- 2016-10-05
Related products to: SIGLEC6 antibody
Related articles to: SIGLEC6 antibody
- Chronic urticaria (CU) is a skin disease characterized by recurrent episodes of vascular dilation and increased permeability of the cutaneous and mucosal microvasculature. Although antihistamines and omalizumab remain first-line and second-line therapies, respectively, a significant proportion of patients develop recalcitrant disease phenotypes, highlighting critical unmet needs for innovative therapeutic paradigms. In recent years, emerging insights into Mas-related G protein-coupled receptor X2 (MRGPRX2) have revealed transformative perspectives for elucidating the pathobiology of refractory CU. As a class A G protein-coupled receptor (GPCR) that is predominantly localized to mast cells, MRGPRX2 orchestrates non-IgE-mediated mast cell degranulation through its pluripotent ligand recognition capacity, engaging diverse exogenous cationic compounds, neuropeptides, and certain pharmacological agents. This comprehensive review evaluates recent advancements in deciphering the mechanistic contributions of MRGPRX2 to CU pathogenesis, with the ultimate aim of informing the development of precision diagnostic and therapeutic frameworks for CU management. - Source: PubMed
Publication date: 2026/04/23
Wu KunLiu Junlin - - Source: PubMed
Publication date: 2026/04/25
Wang LipingWang YufeiWang XinyeDai YuanyuanDeng YanbingHuang TiantuoWen ChaoJin XiaoliTong ShoufangSun WeiyueWeng Wenwen - Cutaneous antigen-presenting cells (APCs), particularly dendritic cells (DCs) and Langerhans cells (LCs), are a diverse population of cells that play a vital role in immune surveillance by initiating and shaping skin immune responses. They link innate and adaptive immunity by presenting antigens, migrating, and activating T lymphocytes, thereby acting as orchestrators of tissue immunity. This review provides an updated overview of the morphofunctional diversity of cutaneous APCs, ranging from epidermal LCs and DCs, to dermal conventional DCs (DC1/DC2), plasmacytoid DCs (pDCs), including newly defined subsets such as DC3, AxlSiglec-6 DCs (ASDCs) and LAMP3 mature regulatory DCs (mRegDCs). Dynamic differences in APC composition and function between homeostatic and inflamed skin are discussed, with particular emphasis on inflammatory and autoimmune conditions such as psoriasis, lupus erythematosus and chronic atopic dermatitis, in which distinct DC subsets contribute to Th1 and Th17 immune circuits. This review is the first skin-related approach that extensively discusses the cutaneous role of APCs in the neuro-immune-cutaneous axis, as well as their interactions with the local microenvironment. Ongoing controversies regarding the classification and stability of certain DC populations are discussed. A better understanding of the diversity, migration mechanisms and microenvironmental interactions of cutaneous APCs could lead to the identification of new biomarkers and therapeutic targets for inflammatory, autoimmune, and oncological skin diseases. - Source: PubMed
Publication date: 2026/02/19
Alexandru Ioana CristinaGrigore MarianaSimionescu Olga - Preterm birth remains a leading cause of neonatal morbidity and mortality. It is classified as spontaneous, characterized by the unexpected onset of labor, or medically indicated, resulting from obstetric intervention due to pregnancy complications. The mechanisms underlying each subtype are incompletely understood, and obesity further modulates preterm birth risk through unclear biological pathways. This study aims to identify second trimester maternal plasma proteomic signatures distinguishing spontaneous and medically-indicated preterm birth and to determine how body mass index modifies these profiles. - Source: PubMed
Publication date: 2026/02/12
Lopez Zapana Paola ADeBolt Chelsea AKarginov LukaRiis ValerieNcube LiqhwaEdlow Andrea GElovitz Michal ALauffenburger Douglas A - Chronic urticaria, which is divided into chronic spontaneous urticaria (CSU) and chronic inducible urticaria (CIndU), affects a significant percentage of the global population and carries a high burden of unmet medical need. Current standard of care includes nonsedating H1-antihistamines and omalizumab, which targets peripheral blood IgE and downregulates mast cell and basophil IgE receptors. However, omalizumab provides complete hive resolution in approximately 45% of patients and does not produce lasting remission. This review examines the clinical data for newly approved and emerging systemic therapies spanning IgE-based and non-IgE-based targeting strategies. The therapeutic landscape has expanded rapidly, and multiple mechanisms are under investigation. IgE-targeted approaches include omalizumab biosimilars, with CT-P39 having received Food and Drug Administration (FDA) approval. Dupilumab received FDA approval for H1-antihistamine-refractory CSU, supporting targeting type 2 cytokines, IL-4 and IL-13. Most recently, a Bruton's tyrosine kinase inhibitor (BTKi), remibrutinib, demonstrated significant reductions in Urticaria Activity Score over 7 days in phase 3 trials, leading to FDA approval. Newer c-Kit (cKit or KIT) inhibitors have also shown efficacy in CSU and CIndU, with barzolvolimab showing sustained efficacy post-treatment. Finally, other BTKi, Janus kinase (JAK) inhibitors, tyrosine kinase 2/JAK inhibitors, MRGPRX2 antagonists, and other novel mechanisms are advancing through clinical trials. Some drugs have been halted in development because of safety concerns, such as fenebrutinib (BTKi), THB001 (Larvol; c-Kit inhibitor), and EP262 (MRGPRX2 antagonist), whereas others, targeting the alarmin thymic stromal lymphopoietin (tezepelumab), the Th2 cytokine IL-5 (mepolizumab) and its receptor IL-5R (benralizumab), as well as lirentelimab (sialic acid-binding immunoglobulin-like lectin 8 [Siglec-8]) and AK006 (Siglec-6), were halted because of lack of efficacy. However, these failed trials have provided informed insights into the relevant pathways for CSU pathogenesis and treatment. In summary, systemic therapies for CSU are maturing with multiple phase 3 programs targeting the IgE pathway and Th2 cytokines leading to recent approvals. This review will provide an overview of these recently completed and ongoing clinical studies investigating emerging IgE and non-IgE therapeutic options for CSU. - Source: PubMed
Hsu Florence IdaBernstein Jonathan AChhiba Krishan DSaini Sarbjit S