The ITIH2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T lymphocyte line. This pool carries a targeted disruption of the ITIH2 gene, abrogating inter-alpha-trypsin inhibitor heavy chain H2 protein expression. The polyclonal format yields a genetically heterogeneous loss-of-function model free of clonal selection bias. Gene disruption has been confirmed at the protein level by Western blotting, and the mixed population allows robust experimentation in a well-characterized T cell background.
Jurkat cells are a widely used human T lymphocyte line established from an acute T cell leukemia. They serve as a model for T cell receptor signaling, apoptosis, and activation due to their robust in vitro growth and expression of key markers such as CD3, CD4, and the T cell receptor complex, along with kinases Lck and ZAP70. Their responsiveness to PMA and ionomycin enables controlled activation studies. The ITIH2 knockout Jurkat polyclonal cells leverage this well-characterized platform, providing a relevant context to study matrix-dependent T cell regulation.
The ITIH2 gene product, inter-alpha-trypsin inhibitor heavy chain H2, is a secreted glycoprotein essential for hyaluronan-based extracellular matrix integrity. ITIH2 is covalently linked to hyaluronan via the enzymatic activity of TSG-6, forming stable pericellular complexes. This process is regulated by cytokines IL-6, TNF-alpha, and TGF-beta, which transcriptionally modulate ITIH2 expression. Downstream, the hyaluronan matrix scaffolds receptor engagement, notably CD44, and triggers NF-kB signaling. ITIH2 also interacts with bikunin and influences matrix metalloproteinase activity, positioning it at the nexus of matrix architecture and inflammatory signaling.
In Jurkat T lymphocytes, ITIH2 knockout disrupts the capacity to assemble a hyaluronan-rich pericellular coat, impairing cell adhesion and migration. Loss of functional ITIH2 prevents TSG-6-mediated transfer of heavy chains to hyaluronan, destabilizing the extracellular matrix. This deficiency likely alters CD44 downstream signaling and reduces NF-kB pathway activation, modulating T cell functions such as cytokine release and tissue infiltration. Thus, this polyclonal knockout model is a valuable tool to dissect how matrix stabilization by ITIH2 influences T cell biology, relevant to inflammatory diseases and cancer.
Typical applications include extracellular matrix biology, inflammation research, and T cell adhesion and migration studies. The cells are compatible with Western blotting to confirm ITIH2 loss, hyaluronan binding assays to assess matrix formation, and flow cytometry for CD44 expression. Migration and invasion assays using Transwell systems evaluate chemotactic responses, while cytokine ELISA measures altered secretion of IL-2 or IFN-gamma. These tools enable dissection of the ITIH2?Chyaluronan?CCD44?CNF-kB axis in immune function. For further details, contact Ascent Research.
