CD223 Lentiviral Activation Particles (h): sc-406616-LAC

LAG3 (CD223) encodes an inhibitory immune checkpoint receptor expressed on activated T cells, regulatory T cells, NK cells, and subsets of exhausted lymphocytes. CD223 binds MHC class II and other ligands to attenuate TCR signaling, shaping immune synapse function, cytokine production, and effector differentiation, and it integrates with pathways that regulate activation thresholds and immune homeostasis. LAG3 is frequently upregulated in chronic antigen exposure contexts and is a hallmark of T cell dysfunction programs that co-occur with other checkpoint molecules. Altered LAG3 expression and signaling are therefore widely studied in tumor immunology, persistent viral infection models, and autoimmune inflammation as determinants of immune suppression versus immune activation states.

CD223 Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient LAG3 upregulation across a broader range of human cell types.

CD223 Lentiviral Activation Particles (h) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the LAG3 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous CD223 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native LAG3 genomic locus and regulatory architecture.

The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.