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2017 ; 26
(12
): 1239-1251
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Ultraviolet-A1 irradiation therapy for systemic lupus erythematosus
#MMPMID28480786
McGrath H Jr
Lupus
2017[Oct]; 26
(12
): 1239-1251
PMID28480786
show ga
Systemic lupus erythematosus (lupus, SLE) is a chronic autoimmune disease
characterized by the production of autoantibodies, which bind to antigens and are
deposited within tissues to fix complement, resulting in widespread systemic
inflammation. The studies presented herein are consistent with hyperpolarized,
adenosine triphosphate (ATP)-deficient mitochondria being central to the disease
process. These hyperpolarized mitochondria resist the depolarization required for
activation-induced apoptosis. The mitochondrial ATP deficits add to this
resistance to apoptosis and also reduce the macrophage energy that is needed to
clear apoptotic bodies. In both cases, necrosis, the alternative pathway of cell
death, results. Intracellular constituents spill into the blood and tissues,
eliciting inflammatory responses directed at their removal. What results is
"autoimmunity." Ultraviolet (UV)-A1 photons have the capacity to remediate this
aberrancy. Exogenous exposure to low-dose, full-body, UV-A1 radiation generates
singlet oxygen. Singlet oxygen has two major palliative actions in patients with
lupus and the UV-A1 photons themselves have several more. Singlet oxygen
depolarizes the hyperpolarized mitochondrion, triggering non-ATP-dependent
apoptosis that deters necrosis. Next, singlet oxygen activates the gene encoding
heme oxygenase (HO-1), a major governor of systemic homeostasis. HO-1 catalyzes
the degradation of the oxidant heme into biliverdin (converted to bilirubin), Fe,
and carbon monoxide (CO), the first three of these exerting powerful antioxidant
effects, and in conjunction with a fourth, CO, protecting against injury to the
coronary arteries, the central nervous system, and the lungs. The UV-A1 photons
themselves directly attenuate disease in lupus by reducing B cell activity,
preventing the suppression of cell-mediated immunity, slowing an epigenetic
progression toward SLE, and ameliorating discoid and subacute cutaneous lupus.
Finally, a combination of these mechanisms reduces levels of anticardiolipin
antibodies and protects during lupus pregnancy. Capping all of this is that UV-A1
irradiation is an essentially innocuous, highly manageable, and comfortable
therapeutic agency.
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