Serum soluble interleukin-2 receptor level is more sensitive than angiotensin-converting enzyme or lysozyme for diagnosis of sarcoidosis and may be a marker of multiple organ involvement.
In addition, these data implicate an elevated expression of interleukin-2, -10 and -12 and interferon-gamma in active compared to nonactive sarcoidosis.
Although the cause of sarcoid is unknown, these observations are consistent with the concept that sarcoid is associated with local stimuli at the site of disease eliciting the Leu-3+ T cell IL 2 gene activation that plays such a critical role in the pathogenesis of this disease.
Furthermore, the CCL1 levels in the BALF were correlated with the total cell count (ρ = 0.539, p < 0.001), lymphocyte fraction (R = 0.406, P < 0.05), lymphocyte count (R = 0.686, P < 0.001), TNF-α level, (R = 0.748, P < 0.001), and IL-2 level (R = 0.757, P < 0.001) in the BALF of sarcoidosis patients.
Cytokines released by T lymphocytes activated in the course of sarcoidosis, e.g., interleukin-2 (IL-2) and interferon-gamma (IFN-gamma), indicate the presence of Th1 cells leading to the question of Th1/Th0/Th2 balance in sarcoidosis.
However these results support the contention that M. tuberculosis may play a pathogenetic role at least in the part of sarcoidosis patients with elevated interleukin-2 receptor values.
In this regard, sarcoidosis represents a "model" human disorder to test in vivo the known in vitro action of corticosteroids on suppressing the activated IL 2 gene.