Human Polyclonal PRF1 Ab
- Known as:
- Human Polyclonal PRF1 Antibody
- Catalog number:
- a0093
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal PRF1
Related genes to: Human Polyclonal PRF1 Ab
- Gene:
- PRF1 NIH gene
- Name:
- perforin 1
- Previous symbol:
- -
- Synonyms:
- PFP, P1, HPLH2
- Chromosome:
- 10q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-02-23
- Date modifiied:
- 2019-04-23
Related products to: Human Polyclonal PRF1 Ab
Related articles to: Human Polyclonal PRF1 Ab
- Histologic assessment of endomyocardial biopsy (EMB) remains the standard for diagnosing acute cardiac allograft rejection, yet molecular profiling may provide complementary quantitative insights. - Source: PubMed
Publication date: 2026/05/25
Zhou WenjunHuang LangjingTang Wenwen - Inflammatory bowel disease (IBD), encompassing ulcerative colitis (UC) and Crohn's disease (CD), is marked by chronic intestinal inflammation and dysregulated immunity. Although UC and CD affect different areas of the gastrointestinal tract, both diseases share aberrant CD4+ memory T cell responses, with HLA-DRB1 as a major genetic risk factor. HLA-DRB1 encodes MHC class II molecules that influence the CD4+ T cell receptor (TCR) repertoire, yet how these genotypes shape TCR specificity in IBD remains unclear. Here, we genotyped HLA-DRB1 and profiled 3.13 million TCRb sequences from circulating memory CD4+ T cells in 33 IBD patients (20 UC, 13 CD) and 14 healthy controls. Using the GLIPH2 algorithm, we distilled 468,441 candidates based on CDR3 amino acid motifs into 440 high-confidence TCR specificity groups significantly enriched among individuals sharing HLA-DRB1 alleles. Notably, five specificity groups were IBD-enriched and shared between UC and CD, suggesting common antigen targets in both diseases. We also observed increased frequencies of clonally expanded cytotoxic GZMB+PRF1+ memory CD4+ T cells and KIRs+CD8+ T cells in a subset of risk-allele carriers with IBD. These findings elucidate distinct, HLA-linked TCR specificity groups in IBD and provide mechanistic insights that may advance antigen discovery and personalized medicine. - Source: PubMed
Publication date: 2026/06/09
Chan Joshua EMohsin AzamKrijgsman JensLindelauf CiskaMu QinghuiCavalla BriannaJi XuhuaiStreett Sarah Evan Unen VincentDavis Mark M - Adoptive cellular immunotherapy (ACT) such as CAR‑T therapy holds promise for cancer treatment. However, genetically engineered T cells often undergo terminal differentiation during ex vivo expansion, which limits their persistence and antitumor efficacy . Early‑differentiated T‑cell subsets exhibit better survival and proliferative capacity after infusion. In our previous work, we isolated four T‑cell subsets at different differentiation stages: naïve T cells (T), stem cell‑like memory T cells (TSCM), central memory T cells (T), and effector memory T cells (T), and obtained their miRNA expression profiles via high‑throughput sequencing. In the present study, we found that hsa‑miR‑142‑5p is highly expressed in TSCM cells and gradually decreases during T‑cell differentiation. - Source: PubMed
Publication date: 2026/05/18
Wang HongqiongXia ShengfangChen JiaZhong HuishanZeng XianpeiLu ZitaoZhang WenfengWu Fenglin - Natural killer (NK) cells contribute to the innate immune system and are pivotal for the defence against opportunistic pathogens, including fungi. (AF), a filamentous mold, can cause invasive pulmonary aspergillosis in immunocompromised patients, e.g. in patients after allogeneic stem cell transplantation (alloSCT). In this pilot study, we challenged NK cell samples from alloSCT recipients collected 90, 120, and 180 days after transplantation and from healthy individuals with AF and characterize the proteome response differences. We identified 2259 differentially abundant proteins between the NK cell proteomes of alloSCT recipients and healthy individuals. Among these, 1118 proteins were differentially abundant at all time points and 1931 proteins specifically at day 180 post-alloSCT. Following stimulation of NK cells with AF, we found a profoundly different early proteome (day 90, =1652 proteins), while at day 180, only 77 proteins remained significantly differentially abundant. We identified, among others, a major differentially abundant protein cluster related to IL27RA (including OAS, STAT1, and MX). Furthermore, for selected markers [granzyme A (GZMA), Neural Cell Adhesion Molecule 1 (NCAM1/CD56), perforin-1 (PRF1)], we confirmed our proteome data by flow cytometry in NK cells from an independent second patient and healthy individual cohort. In conclusion, we demonstrate the advantage of combining comprehensive proteomic profiling with targeted flow cytometry to investigate NK cell responses to AF. Our data analysis connects STAT1 with IL27RA as well as granzyme, IFNg, and NCAM1 activity, which may be exploited towards future therapeutics warranting confirmation in larger study cohorts. - Source: PubMed
Publication date: 2026/05/15
Springer JanDrobny MatthiasHeilig LindaKraus SabrinaKniemeyer OlafKrüger ThomasOlischer ChristianBussemer LydiaPanagiotou GianniBrakhage Axel AEinsele HermannSchäuble SaschaLöffler Jürgen - Chagas disease, caused by , is the major cause of infectious cardiopathology worldwide. Although cytotoxic CD4 T-cells (CD4 CTLs) have recently been recognized as crucial effectors in infections and inflammation, the mechanisms that control their differentiation and impact on pathological outcomes remain largely undefined. Here, we demonstrate that the ectonucleotidase CD73, which generates adenosine from extracellular AMP, acts as a key immunoregulator of CD4 CTL response during infection. Using murine models, we found that infection induced a robust expansion of CD4 T-cells expressing granzyme B, perforin, and IFN-γ. CD73 deficiency improved parasite control and amplified the frequency and cytotoxic program of CD4 T-cells during the acute phase. However, the absence of CD73 also led to sustained cardiac inflammation, extensive fibrosis, and impaired contractility during chronic infection. In patients with asymptomatic chronic Chagas disease, circulating CD4 T-cells exhibited elevated granzyme B expression, predominantly within the CD73 subset. Consistently, cardiac tissue from patients with chronic terminal Chagas cardiomyopathy showed transcriptomic enrichment of granzyme B (), perforin (), and IFN-γ (), with CD4 T-cells as the major contributors. Together, these findings identify CD73 ectoenzyme as a critical immunometabolic checkpoint that modulates CD4 CTL responses, revealing a dual role for this pathway in controlling infection and limiting tissue damage. - Source: PubMed
Publication date: 2026/05/12
Bergero GastónMazzocco Yanina LCejas Gallardo Zoé MRivarola WalterDel Rosso SebastianAoki Maria P