Therapeutic implications of photobiomodulation application on immune cells
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Photobiomodulation (PBM), the application of red/near-infrared light (600-1,000 nm) on cells, modulates cellular bioenergetics and immune signaling without thermal injury. This review presents mechanistic, preclinical, and clinical studies to clarify how wavelength, irradiance, and dose shape immune outcomes and outlines the therapeutic implications. Mechanistically, PBM accelerates mitochondrial electron transport and adenosine triphosphate production, tunes reactive oxygen species biphasically, and engages the nuclear factor kappalight- chain-enhancer of activated B cells, mitogen-activated protein kinase, and nuclear factor erythroid 2-related factor 2 pathways to reprogram inflammatory gene expression. Across lineages, PBM promotes macrophage polarization toward reparative phenotypes, limits neutrophil recruitment and degranulation, supports dendritic cell maturation and antigen presentation, and recalibrates T cell responses by expanding regulatory T cells and shifting T helper type 1 (Th1)/Th2/Th17 balance toward homeostasis. These effects translate into benefits in wound repair, arthritis, neuroinflammation, and select autoimmune conditions, and suggest combinability with vaccines, biologics, and cancer immunotherapies. Despite a favorable safety profile, heterogeneity in irradiance, fluence, duty cycle, and schedules hinders comparison and adoption. This review highlights the need for better reporting standards and condition-specific dosing windows anchored to target cell type, depth, and redox state. This can enable biomarker-guided trials that integrate immune phenotyping with clinical and safety endpoints.
Abstract
Photobiomodulation (PBM), the application of red/near-infrared light (600-1,000 nm) on cells, modulates cellular bioenergetics and immune signaling without thermal injury. This review presents mechanistic, preclinical, and clinical studies to clarify how wavelength, irradiance, and dose shape immune outcomes and outlines the therapeutic implications. Mechanistically, PBM accelerates mitochondrial electron transport and adenosine triphosphate production, tunes reactive oxygen species biphasically, and engages the nuclear factor kappalight- chain-enhancer of activated B cells, mitogen-activated protein kinase, and nuclear factor erythroid 2-related factor 2 pathways to reprogram inflammatory gene expression. Across lineages, PBM promotes macrophage polarization toward reparative phenotypes, limits neutrophil recruitment and degranulation, supports dendritic cell maturation and antigen presentation, and recalibrates T cell responses by expanding regulatory T cells and shifting T helper type 1 (Th1)/Th2/Th17 balance toward homeostasis. These effects translate into benefits in wound repair, arthritis, neuroinflammation, and select autoimmune conditions, and suggest combinability with vaccines, biologics, and cancer immunotherapies. Despite a favorable safety profile, heterogeneity in irradiance, fluence, duty cycle, and schedules hinders comparison and adoption. This review highlights the need for better reporting standards and condition-specific dosing windows anchored to target cell type, depth, and redox state. This can enable biomarker-guided trials that integrate immune phenotyping with clinical and safety endpoints.