About this Research Topic
Sarcoidosis is recognized as a prototypical Th1-type granulomatous inflammation that occurs when three factors converge: potential causative antigens such as Cutibacterium acnes (formerly Propionibacterium acnes) and Mycobacterium; host susceptibility factors, including dysregulated immune responses; and environmental triggers that provoke the onset of the disease.
Historically, diagnostic and therapeutic approaches in clinical practice have not always been based on the etiology of the disease. Typically, treatments have often involved moderate to high doses of systemic steroids without identifying the causative antigen. However, current diagnostic practices in Japan, based on the C. acnes etiology, now enable the identification of C. acnes in granulomas through immunostaining with a PAB antibody directed against the species-specific cell membrane-bound lipoteichoic acid of C. acnes, facilitating the diagnosis of so-called C. acnes-associated sarcoidosis.
Regarding treatment, the SARCORT trial demonstrated that a daily dose of 20 mg of prednisolone is as effective as 40 mg, suggesting that high-dose steroids are unnecessary for preventing relapses. It is crucial to adjust the dose according to individual disease activity and susceptibility. In refractory sarcoidosis patients, long-term administration of steroids at the minimum effective dose for each individual and each organ lesion can suppress relapses, serving as a treatment goal that takes into account the nature of sarcoidosis. This nature involves a Th1-type hypersensitivity reaction to difficult-to-control antigens due to a breakdown of antigen-specific immunoregulatory mechanisms, similar to organ-specific autoimmune diseases.
We aim to implement diagnosis and treatment of sarcoidosis based on its etiology and invite contributions to accumulate evidence supporting this approach. Topics of interest include:
Diagnosis Based on Etiology:
1. Tests for identifying antigens.
2. Clinical markers that can track spontaneous remission and the onset or reactivation of the disease.
Treatment Based on Etiology:
1. Discussion on steroid dosage (tailored to the individual and specific organ lesions), maintenance doses, and duration of administration.
2. Use of antimicrobial agents.
3. Discussion on other therapeutic drugs such as immunomodulators, chloroquine, and anti-fibrotic agents.
Historically, diagnostic and therapeutic approaches in clinical practice have not always been based on the etiology of the disease. Typically, treatments have often involved moderate to high doses of systemic steroids without identifying the causative antigen. However, current diagnostic practices in Japan, based on the C. acnes etiology, now enable the identification of C. acnes in granulomas through immunostaining with a PAB antibody directed against the species-specific cell membrane-bound lipoteichoic acid of C. acnes, facilitating the diagnosis of so-called C. acnes-associated sarcoidosis.
Regarding treatment, the SARCORT trial demonstrated that a daily dose of 20 mg of prednisolone is as effective as 40 mg, suggesting that high-dose steroids are unnecessary for preventing relapses. It is crucial to adjust the dose according to individual disease activity and susceptibility. In refractory sarcoidosis patients, long-term administration of steroids at the minimum effective dose for each individual and each organ lesion can suppress relapses, serving as a treatment goal that takes into account the nature of sarcoidosis. This nature involves a Th1-type hypersensitivity reaction to difficult-to-control antigens due to a breakdown of antigen-specific immunoregulatory mechanisms, similar to organ-specific autoimmune diseases.
We aim to implement diagnosis and treatment of sarcoidosis based on its etiology and invite contributions to accumulate evidence supporting this approach. Topics of interest include:
Diagnosis Based on Etiology:
1. Tests for identifying antigens.
2. Clinical markers that can track spontaneous remission and the onset or reactivation of the disease.
Treatment Based on Etiology:
1. Discussion on steroid dosage (tailored to the individual and specific organ lesions), maintenance doses, and duration of administration.
2. Use of antimicrobial agents.
3. Discussion on other therapeutic drugs such as immunomodulators, chloroquine, and anti-fibrotic agents.
Keywords: Intracellular bacteria, Allergic endogenous infection, Autoinflammatory disease, Immune tolerance, Th1/Th17
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