Centenarians carry genetic and platelet-based mechanisms that suppress age-related inflammation through CD47 expression, which dampens monocyte activation. The LAV-BPIFB4 variant drives this protective effect, and recombinant administration of the protein replicates these benefits in non-carriers, establishing a translatable therapeutic target for inflammaging and cardiovascular disease.
Key Points
- LAV-BPIFB4 increases CD47 on platelets to suppress monocyte inflammation
- Centenarians show elevated CD47+ reticulated platelets as immune signature
- Recombinant LAV-BPIFB4 protein replicates genetic protective effects in vivo
Longevity Analysis
This research identifies a specific immune-modulation pathway that distinguishes centenarians from the general population. Rather than a broad anti-inflammatory state, long-lived individuals possess a selective mechanism that suppresses specific inflammatory signals—particularly monocyte IL-6 release—while preserving immune competence. The capacity to dampen chronic inflammation without compromising defense mechanisms represents a fundamental hallmark of healthy aging. The fact that recombinant protein can induce this phenotype in non-genetic carriers suggests the mechanism is not fixed by genetics alone but can be influenced through external administration, opening a pathway to intervene in the inflammatory cascade that drives age-related disease.
Original published by Wiley Aging Cell, by Elena Ciaglia, Roberta Maria Esposito, Valentina Lopardo, Francesco Montella, Cristina Basile, Roberta Longo, Anna Maciag, Giuseppe Rescigno, Antonio Damato, Francesco Del Plato, Alfonso Finizio, Carmine Vecchione, Albino Carrizzo, Annibale Alessandro Puca .