Ask about this productRelated genes to: IGHA1 antibody
- Gene:
- IGHA1 NIH gene
- Name:
- immunoglobulin heavy constant alpha 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 14q32.33
- Locus Type:
- immunoglobulin gene
- Date approved:
- 2001-06-22
- Date modifiied:
- 2014-11-19
Related products to: IGHA1 antibody
Related articles to: IGHA1 antibody
- Given the high incidence of epidural‑related maternal fever (ERMF) among women with epidural analgesia and the key roles of glycoproteins, an efficient nanoplatform is needed for N‑glycoproteomic analysis to better understand ERMF. Herein, we constructed an ultra-hydrophilic magnetic MXene-based nanoplatform (MMX-Cys) for efficient N-glycopeptide enrichment. By integrating the high surface area of MXene, the hydrophilicity of L-cysteine, MMX-Cys demonstrated ultra-hydrophilicity with a water contact angle of ~ 0°. It exhibits high sensitivity (1 fmol·µL⁻¹), excellent selectivity (HRP: BSA = 1:100), and good reproducibility in enriching glycopeptides from standard protein digests. Applied to plasma samples from ERMF patients and healthy controls, the MMX-Cys based nanoplatform enabled the identification of 1195 N-glycopeptides corresponding to 91 glycoproteins. Differential expression analysis revealed 18 significantly altered glycopeptides from 10 glycoproteins, predominantly involved in humoral immunity and complement activation, including immunoglobulin heavy chains (IGHG1, IGHG2, IGHA1, IGHA2) and complement component C2. This study presents an effective tool for N-glycopeptide determination and provides glycoproteomic evidence supporting the inflammatory pathogenesis of ERMF. The MMX-Cys based nanoplatform holds great potential in offering a foundation for future biomarker discovery and mechanistic studies. - Source: PubMed
Publication date: 2026/06/11
Xia ZiyeLi NingLiu ZhiqiangHu XufangDeng Chunhui - Class-switch recombination (CSR) allows B cells to produce antibodies with distinct effector functions, but its dynamics during a primary human response remain poorly understood. We sampled COVID-19-naive healthy volunteers every other day during the first 3 weeks after SARS-CoV-2 vaccination, combining bulk and single-cell B cell receptor repertoires, single-cell transcriptomics, immunophenotyping, and IGHC sterile transcript analysis. Vaccine-specific B cells show sterile transcription across all IGHC genes up to IGHG2, contradicting the prevailing idea of single-gene sterile transcription. Clonal tracking confirms that sequential CSR exists: e.g., IGHG3 to IGHG1 and IGHG1 to IGHA1 and IGHG2, with sparse switching beyond IGHG2. VDJ gene usage associates with specific isotype subclasses and differential CSR timing. CSR and somatic hypermutation are temporally decoupled, with antigen-specific clones remaining hypomutated up to 10 weeks post-immunization. These findings complement textbook models of CSR and inform strategies for vaccines requiring switching to key isotypes such as IgG1 or IgA2. - Source: PubMed
Publication date: 2026/06/04
Montamat-Garcia GuillemNg Joseph C FStewart Alexander TSinclair EmmaMensah Benedicta BGiam Yan HuiBlair PaulKateregga DianaGander AmirKipling DavidGuo DongjunServius LuteciaPiper Christopher J MBaig ZaraFraternali FrancaMauri ClaudiaDunn-Walters Deborah K - Aberrant O-linked glycosylation of the IgA hinge segment resulting in galactose-deficient IgA1 (Gd-IgA1) is frequently observed in patients with IgA nephropathy (IgAN), and it is hypothesized to be pathogenic. Here, we genetically disrupted the expression of galactosyltransferase 1 (C1galt1) to elevate Gd-IgA1 levels in mice and examine its role in glomerular deposition. - Source: PubMed
Publication date: 2026/03/27
Wu JingyiXie TongZhang ZhaoLiu XingziZhou XujieZhang YongTian WenminGale Daniel PZhu ShuBarratt JonathanJin JingZhang YuemiaoZhang HongLv Jicheng - Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease with complex immune dysregulation. While previous studies have reported tertiary lymphoid structures (TLS) and IgA-producing B cells in HS skin lesions, the pathogenic role of IgA autoantibodies remains insufficiently characterized. Here, we demonstrate that lesional skin from patients with HS exhibits elevated expression of IGHA1, IGHA2, and J chain, as confirmed by qPCR, immunofluorescence, and Western blot analyses. Single-cell RNA sequencing identified local plasma cells and B cells as the primary source of IgA. Autoantigen profiling revealed a diverse repertoire of IgA autoantibodies targeting nuclear, cytoplasmic, and membrane antigens, with levels correlating with disease severity and other clinical manifestations. We identified IgA autoantibodies binding to CD68⁺ macrophages, which induced secretion of TNF, IL-6, and IL-1β and upregulated inflammasome and profibrotic pathways. Anti-neutrophil extracellular trap (NET) IgA was elevated in HS and promoted NET formation, establishing a pathogenic feedback loop. NET-IgA immune complexes induced macrophages to secrete CCL18, driving collagen production by fibroblasts and promoting a type I interferon (IFN) gene signature. IgA immune complexes presented by myeloid dendritic cells activated CD4⁺ T cells, triggering IFN-γ production and further amplifying local inflammation. Notably, supernatants from macrophages exposed to IgA were able to polarize naïve CD4⁺ T cells toward a Th17 phenotype, linking innate immune activation to the expansion of pathogenic adaptive immune responses. Direct exposure of fibroblasts to NET-IgA complexes triggered expression of adhesion molecules, chemokines, and regulators of adaptive immunity. Together, these findings uncover a role for IgA autoantibodies in HS, implicating them as central drivers of chronic inflammation, fibrosis, and immune crosstalk across neutrophils, macrophages, fibroblasts, and T cells. - Source: PubMed
Publication date: 2026/03/24
Carmona-Rivera CarmeloO'Neil Liam JPatino-Martinez EduardoAmbler William GMallela TejaHanata NorioZadu Arsema KJiang KanOkoye Ginette AByrd Angel SSayed Christopher JKaplan Mariana J - Breast cancer (BC) demonstrates a high worldwide prevalence and remains among the primary contributors to cancer mortality in females. Venous thromboembolism (VTE), a common oncological complication, strongly correlates with poorer survival in BC patients. However, the predictive value of VTE-related genes (VTERGs) in BC prognosis and their impact on clinical outcomes remain underexplored, lacking systematic investigation. - Source: PubMed
Publication date: 2026/01/21
Liu ZhuoyunGuo ShuangXu XianqunTang PengXue HanLong Xinghua