Beyond Single Checkpoints — Systems-Level Immuno-Oncology Biomarker Profiling
The clinical success of checkpoint inhibitors proved that the immune system can be redirected against cancer. But the next generation of Immuno-Oncologyresearch demands moving beyond PD-L1 IHC as a single biomarker. Tumors evade immunity through multiple redundant checkpoint pathways simultaneously (PD-L1 + LAG3 + TIM-3 + TIGIT). T-cell exhaustion is a graded process — progressively losing IL-2 production, then TNF-α, then IFN-γ, then Granzyme B — that cannot be captured by any single marker. And the tumor stroma actively excludes T cells through MMP-mediated matrix remodeling, adhesion molecule modulation, and chemokine silencing — processes invisible to checkpoint-only assays. The 111/131-Plex panels address this complexity by measuring the full network in a single assay.
Analyte Categories in the Immuno-Oncology Panels
- Soluble immune checkpoints (15+): PD-1 (2 epitopes), PD-L1/B7-H1 (2 epitopes), PD-L2, CTLA-4, LAG3, HAVCR2/TIM-3, TIGIT, OX40/TNFRSF4, GITR/TNFRSF18, CD28, ICOS, CD27, HVEM/TNFRSF14, CD40L (soluble), ICOS-L/B7-H2, GITRL/TNFSF18 — covering inhibitory checkpoints, co-stimulatory receptors, and their ligands.
- B-cell lineage & CAR-T targets: BAFF, BAFF-R/TNFRSF13C, BCMA/TNFRSF17, APRIL/TNFSF13, CD20 — B-cell biology, CAR-T target antigen monitoring (BCMA), and tertiary lymphoid structure research.
- Cytokines & chemokines (60+): Full Th1/Th2/Th17/Treg cytokine panel plus chemokines directing immune cell trafficking (IP-10, MCP-1/2/4, MIP-1α/1β, MIG, I-TAC, RANTES) — capturing the cytokine milieu in which checkpoint blockade operates.
- Cytotoxic effector molecules (131-Plex): Granzyme A, Granzyme B, Perforin — the three pore-forming and serine protease effectors of cytotoxic T lymphocytes and NK cells. Direct molecular readout of immune-mediated tumor cell killing.
- Tumor-stroma interface (131-Plex): MMP-1, MMP-2, MMP-7, MMP-9 (Total), ProMMP-9, Galectin-9/GAL9, Nectin-4, E-Selectin, P-Selectin, Pentraxin 3, S100A12, RAGE/AGER — matrix remodeling enzymes, adhesion molecules, and damage-associated inflammatory mediators that shape TME architecture and immune access.
- Additional immune regulators (131-Plex): LIGHT/TNFSF14, APRIL/TNFSF13, CD27, TLR1, gp130/sIL-6Rβ, CD276/B7-H3 — extending the immune signaling network coverage.
