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Conversely, experimental studies have shown that overexpression of mtCK enhances cellular resilience to oxidative stress, maintains mitochondrial integrity, and improves functional recovery following ischemic injury [22]

Specifically, examining how LILRB2 signaling influences subcellular communication between myeloid and lymphoid cells could shed light on potential synergies between LILRB2 blockade and CAR-based therapies

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