Recombinant Human LAG3 /CD223 Protein
- Known as:
- Recombinant Human LAG3 /CD223 Protein
- Catalog number:
- la-801
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Proxinobio
- Gene target:
- Recombinant Human LAG3 /CD223 Protein
Related genes to: Recombinant Human LAG3 /CD223 Protein
- Gene:
- LAG3 NIH gene
- Name:
- lymphocyte activating 3
- Previous symbol:
- -
- Synonyms:
- CD223
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1991-06-03
- Date modifiied:
- 2016-10-05
Related products to: Recombinant Human LAG3 /CD223 Protein
Related articles to: Recombinant Human LAG3 /CD223 Protein
- Rasmussen encephalitis (RE) is a rare neuroinflammatory disease characterized by intractable seizures and progressive brain atrophy that is usually confined to one cerebral hemisphere. Disease management involves anti-seizure medications and immunotherapy, although surgical resection remains the only effective treatment option to achieve seizure freedom. The presence of clonally expanded resident memory T cells in brain tissue removed to control seizures suggests the involvement of an autoimmune response in the etiology of the disease. Blocks of fresh brain tissue were obtained from three RE surgery cases (ages 5, 8, and 26 years at the time of surgery) and immune cells were isolated. Single cell RNA sequencing was used to define the types of immune cells present in the affected brain tissue and potential crosstalk between them, along with multiplex immunofluorescence immunostaining of sections from the same specimens. We matched T cell receptor sequences to T cell phenotypes and used ViralTrack software to search for evidence of activation of latent viruses in the immune cells. The immune cells isolated from the three RE cases comprised primarily activated microglia and resident memory CD8 T cells with fewer CD4 T cells, NK cells and monocyte-derived macrophages and dendritic cells. The majority of CD8 T cells expressed killer cell lectin-like receptors, and a virus responsive gene signature that included XCL1, TNFRSF9 and CRTAM, but also the exhaustion markers LAG-3 and TIM-3. Microglia expressed transcripts found in disease-associated microglia and transcripts associated with NLRP3 inflammasomes. We found no evidence for active latent viruses; however, we found endogenous HERV-K retrovirus sequences that were transcribed from multiple provirus insertion sites. - Source: PubMed
Publication date: 2026/05/13
Quinones-Valdez GiovanniChang Julia WMagaki Shino DVinters Harry VSalamon NorikoWang Anthony CFallah AriaOwens Geoffrey C - LAG-3 is an emerging immune checkpoint whose extracellular D1 domain engages MHC class II through a broad protein-protein interface traditionally considered difficult to modulate with small molecules. To evaluate the ligandability of this region, we combined triplicate 100-ns molecular dynamics (MD) simulations, structure-based virtual screening, and biophysical and biochemical assays. MD sampling of the isolated D1 domain revealed a recurrent, transient cavity adjacent to the MHCII-binding surface. A representative pocket-open conformation was used to screen a ∼10,240-compound diversity library, yielding a single validated hit, N05. N05 bound the D1 domain with micromolar affinity measured by microscale thermophoresis (Kd = 59.2 μM, TRIC/MST channel) and by spectral-shift detection (Kd = 56.1 μM), and it partially inhibited the LAG-3/MHCII interaction (EC = 42.9 μM; maximal inhibition ∼76%). Triplicate 30-ns MD simulations of the LAG-3-N05 complex showed stable ligand engagement within the MD-identified cavity and consistent stabilizing interactions with residues forming the pocket. These results demonstrate that the LAG-3 D1 domain possesses an accessible, dynamically formed binding site capable of accommodating small molecules, providing a structural and biophysical foundation for future exploration of LAG-3 ligandability. - Source: PubMed
Publication date: 2026/05/08
García-Vázquez NelsonGabr Moustafa T - CD20 × CD3 bispecific antibodies (BsAbs) have emerged as a meaningful therapeutic option for relapsed or refractory diffuse large B-cell lymphoma (DLBCL), redirecting endogenous T cells against malignant B cells independently of major histocompatibility complex-mediated antigen presentation, and have received regulatory approval after at least two prior lines of therapy. However, a substantial proportion of patients experience primary resistance or early relapse, underscoring the need to characterize the underlying biological mechanisms, which are the focus of this review. Several tumor-intrinsic determinants of resistance have been identified, including CD20 loss driven by mutations, alternative splicing, and gene deletion, as well as genomic reprogramming involving , , and alterations. T-cell dysfunction represents another critical resistance domain, encompassing inadequate intratumoral cytotoxic CD8+ T-cell infiltration, expansion of immunosuppressive regulatory and follicular helper T cells, progressive exhaustion with upregulation of PD-1, LAG-3, TIM-3, and TIGIT, and impaired T-cell fitness from prior treatment exposure. Microenvironmental barriers, including checkpoint ligand upregulation, PD-L1-enriched extracellular vesicles, spatial exclusion of effector cells from immune-cold germinal center-like niches, hypoxia, and metabolic competition, further reinforce immune escape. Emerging strategies to overcome resistance include epigenetic priming, checkpoint inhibitor combinations, 4-1BB costimulatory approaches, and next-generation multispecific antibody designs. - Source: PubMed
Publication date: 2026/04/27
Maher NawarAl Deeban BasharDiop Ndeye MarieAssaf JoelleMoia RiccardoMouhssine SamirGaidano Gianluca - Alzheimer's Disease (AD) remains the leading cause of dementia globally, yet the exact etiology is not well defined and effective treatments remain unavailable. Here, we report that deletion of the immune checkpoint receptor lymphocyte activation gene 3 (Lag3) in a familial AD mouse model, 5xFAD, can rescue molecular, cellular and behavioral phenotypes of neurodegeneration. Specifically, we demonstrate that amyloidosis and microgliosis in the 5xFAD mice are significantly reduced by Lag3 deletion. Moreover, we show that Lag3 deletion attenuates deficits in neurodegeneration-related behavioral phenotypes in the 5xFAD mice. Transcriptional profiling reveals that Lag3 deletion suppresses aberrant overexpression of disease associated microglia (DAM) genes in 5xFAD microglia, effectively restoring homeostatic transcriptional programs. Finally, we observe reduced CD8 T cell infiltration in the brain of 5xFAD animals after Lag3 deletion which likely mediates molecular, cellular and behavioral effects resulting from microglia DAM gene activation. Our results highlight a previously unrecognized role for Lag3 in AD as a critical regulator of microglia function and suggest Lag3 might be a viable target for novel AD therapeutic interventions. - Source: PubMed
Publication date: 2026/05/11
Perl Andrew TWu JuanDong John DBrooks Ashley MYoblinski Andrew RVierling Tia TLi Jian-LiangRuby Dana RRadzicki DanielDudek Serena MCushman Jesse DGjoneska Elizabeta - This narrative review examines recent progress in immunotherapy for breast cancer (BC), focusing on immune checkpoint inhibitors (ICIs) alone and in combination with other modalities. Landmark trials such as KEYNOTE-522 and IMpassion130 have established the efficacy of pembrolizumab and atezolizumab in triple-negative breast cancer (TNBC). However, BC remains a leading cause of cancer-related fatalities, underscoring the need for novel approaches. We synthesize combination strategies into three mechanistic categories: (I) those that remodel the immunosuppressive tumor microenvironment (chemotherapy, PARP inhibitors, oncolytic viruses); (II) those that enhance effector cell persistence (CAR-T, CAR-NK, cytokine support); and (III) those that modulate immune checkpoint axes beyond PD-1/CTLA-4 (LAG-3, TIM-3, TIGIT). Combining ICIs with CAR-T cells, CAR-NK cells, oncolytic viruses, and exosomes has been shown to improve antitumor immune responses. This review provides a translational framework for biomarker-driven patient stratification and critically evaluates the clinical maturity of emerging platforms. Further research and clinical trials are needed to expand applicability across BC subtypes and improve patient outcomes. - Source: PubMed
Publication date: 2026/05/05
Abbaspour MaryamEsmaeil NafisehAkbari VajiheGhoreishi MohammadRafiepoor Haniyeh