Pipeline / 01 · Platforms

Engineered Immune Cells Platform

CAR-like NK systems and γδ T cell therapies for adaptive, MHC-independent elimination of diseased cells.

T CELL SUBTYPE SELECTION Three lineages, selected by indication. αβ T cells CD8⁺ / CD4⁺ MHC-restricted recognition Tumor-specific, long-lived effectors. Dominant in mRNA vaccine approaches and conventional CAR-T programs. γδ T cells VΓ9VΔ2 MHC-independent recognition Trained-immunity response without prior priming. Bridges innate and adaptive arms. Mucosal homing via CD103⁺. NK cells CAR-LIKE NK Innate cytotoxicity Direct elimination of infected/transformed cells. No HLA matching required. Engineered for armored persistence.
T cell subtype selection across disease contexts — conventional αβ CD8+/CD4+ for tumor-specific contexts, Vγ9Vδ2 γδ T cells for MHC-independent recognition in infectious disease and mucosal sites.
Premise

The problem we are solving.

The immune system already knows how to eliminate infected and malignant cells. Our task is to give it the tools, the training, and the reach to do it reliably — across patients, across diseases, and across tissue barriers that conventional cell therapies cannot cross.

MACRO HRD engineers two complementary immune cell platforms: CAR-like NK systems for adaptive cytotoxic precision, and Vγ9Vδ2 γδ T cells for MHC-independent recognition and trained-immunity response. Together they address both the variable pathogen landscape of infectious disease and the antigen-heterogeneous reality of solid tumors.

Approach

How we tackle it.

Our γδ T cell programs leverage a distinctive biology: MHC-independent recognition means the same therapy works across HLA-diverse populations — critical for global infectious disease programs. Trained immunity means memory-like response without prior antigen exposure. Dual effector/APC phenotype means these cells both kill infected targets and prime adaptive responses.

NK systems follow a parallel path: pre-engineered with CAR-like recognition, armored for persistence, and edited to resist suppression by the tumor environment. Both platforms are produced to GMP standards, with identity, purity, and functional-potency confirmation before release.

FUNCTIONAL PAYLOAD DESIGN Engineered for persistence, potency, and TME resistance. ARMORING IL-15 · IL-21 · anti-TGF-β Cytokine support to maintain T cell function in suppressive tumor microenvironment. COSTIMULATION CD28 (rapid) · 4-1BB (persistence) Tunable signaling for effector kinetics — sharp killing or long-term memory. CHECKPOINT KO PD-1 · TIM-3 · LAG-3 CRISPR knockout or dominant-negative receptor expression for exhaustion resistance. HOMING CCR7 · CXCR3 · CD103 Constitutive expression for tissue-specific localization (CNS, mucosa, lymphoid sites).
Functional payload design for engineered T cells — armoring with IL-15/IL-21/anti-TGF-β, costimulation tuning (CD28 vs 4-1BB), and CRISPR-based checkpoint knockout (PD-1, TIM-3) for enhanced potency and persistence.
Vector engineering options for engineered T cell expression
Vector TypeEfficiencyUse CaseTrade-offs
LentiviralHighMost CAR-T trials; stable integrationManufacturing complexity
RetroviralHighFDA-approved CARs (e.g., Yescarta)Integration site bias
TransposonsModerateCost-effective, scalable non-viralLower transduction efficiency
mRNATransientSafety testing, transient payloadNot persistent
i.
Cell source selection
Leukapheresis, αβ depletion, and phenotype sorting for γδ subset enrichment.
ii.
Activation and expansion
GMP expansion with zoledronate and IL-2 for γδ; CAR transduction for NK systems.
iii.
Functional armoring
IL-15, IL-21, anti-TGF-β, and checkpoint knockout to resist tumor microenvironment suppression.
iv.
Release and deployment
Dual product QC confirms cell identity, purity, and peptide-loading before clinical release.
Capabilities

What makes this real.

01
MHC-independent γδ recognition
Vγ9Vδ2 cells recognize variable pathogen contexts without HLA restriction — a single therapy works across populations.
02
Trained-immunity memory
Memory-like response without prior antigen priming — relevant for pandemic preparedness and rapid-response deployment.
03
CAR-like NK platforms
Adaptive cytotoxic elimination engineered for tumor and viral reservoir contexts with armored persistence.
04
Bridging innate and adaptive arms
γδ T cells function as both effectors and antigen-presenting cells — priming downstream CD8+ and B cell responses.
SUBTYPE SELECTION BY INDICATION The right cell for the right disease. Glioblastoma SUBTYPE Vδ1⁺ or CD8⁺αβ with CXCR3 RATIONALE BBB penetration via CXCR3 + persistence in immunosuppressive TME HIV SUBTYPE CD8⁺αβ + PD-1 / CCR5 KO RATIONALE CCR5 KO for HIV resistance; PD-1 KO for exhaustion prevention TB SUBTYPE Vδ2⁺ γδ T cells RATIONALE Phosphoantigen recognition for Mtb without HLA restriction
Indication-specific T cell subtype selection. Vδ1+ or CD8+αβ with CXCR3 for glioblastoma; CD8+αβ with PD-1 or CCR5 knockout for HIV; Vδ2+ γδ T cells for TB phosphoantigen targeting.
Clinical & Research Network

Validated through partnership.

The γδ T-cell platform is anchored by a NASDAQ-listed, clinical-stage partner specializing in donor-derived, off-the-shelf γδ T-cell therapy, with an active first-in-human trial and established GMP manufacturing. This is a real clinical capability supplying the program — not a concept.

MACRO HRD integrates this cell source with its peptide, antibody, and decision-intelligence platforms, applying the same engineered immune cells across infectious-disease and oncology programs where each indication calls for a different effector lineage.

⸻ Continue the platform

“We do not invent new immune cells. We remind the ones you already have what they were made to do.”