Qingre Liangxue Acupuncture for Psoriasis: A Cholinergic Neuroimmune Framework

Psoriasis is a chronic immune-mediated inflammatory disorder sustained by reciprocal interactions among keratinocytes, immune cells, vascular elements, and neural signals. This mechanism-oriented narrative review examines Qingre Liangxue (clearing heat and cooling blood) acupuncture through the cholinergic anti-inflammatory pathway (CAP) and the cutaneous non-neuronal cholinergic system. Qingre Liangxue acupuncture is treated here as a therapeutic principle implemented through a family of related, rather than universally fixed, acupoint prescriptions. We distinguish four evidence sources: direct human psoriasis evidence, psoriasis-like animal or cellular evidence, cross-disease CAP/acupuncture evidence, and theoretical mechanistic inference. Direct human evidence supports the presence and potential relevance of cutaneous cholinergic signaling but does not establish that acupuncture engages CAP in plaque psoriasis. Psoriasis-like models suggest that α7 nicotinic acetylcholine receptor signaling may restrain myeloid and keratinocyte inflammatory programs, whereas α9-associated signaling may contribute to keratinocyte turnover and epidermal homeostasis. Cross-disease studies show that site- and parameter-dependent acupuncture inputs can access autonomic anti-inflammatory circuits, but these findings cannot be assumed to translate directly to psoriasis. Psoriasis-related acupuncture studies report changes in lesion severity, Th17/Treg balance, neuropeptide signaling, and keratinocyte proliferation, although the evidence is predominantly preclinical or methodologically heterogeneous. Clinically, acupuncture is best considered an adjunctive and mechanistically exploratory intervention rather than an alternative to topical therapy, phototherapy, conventional systemic treatment, or biologics. Overall, CAP provides a testable neuroimmune framework linking upstream autonomic regulation to local immune-epidermal responses, with α7 and α9 receptors representing distinct candidate effector nodes. Confirmation requires standardized, sham-controlled studies that integrate clinical outcomes with autonomic, receptor, cytokine, and keratinocyte measurements.