CIITA Lentiviral Activation Particles (h): sc-401762-LAC

Human CIITA (class II, major histocompatibility complex, transactivator) is a non–DNA-binding transcriptional coactivator that serves as the master regulator of MHC class II gene expression and antigen presentation. CIITA integrates IFN-γ/JAK–STAT signaling with transcriptional programs controlling HLA-DP/DQ/DR, invariant chain (CD74), and accessory antigen-processing components, shaping adaptive immune activation in professional antigen-presenting cells. By coordinating chromatin remodeling and enhanceosome assembly at MHC II promoters, CIITA influences immune surveillance, inflammatory responses, and tolerance. Dysregulated CIITA activity or expression is linked to impaired antigen presentation and altered tumor–immune interactions, making it relevant for studies of autoimmunity, infection biology, and cancer immunology.

CIITA 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 CIITA upregulation across a broader range of human cell types.

CIITA 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 CIITA transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous CIITA expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native CIITA 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.