Table 2.

Central features and questions in the pathobiology of sarcoidosis

Pathobiologic features of sarcoidosis
• Highly polarized Th1 immunity at sites of disease
• Oligoclonal T-cell expansions consistent with T-cell antigen-driven inflammation
• Regulatory T-cell functional deficiency
• Genetic susceptibility predominantly involving HLA genes within the MHC locus
• Microbial triggers implicated in the etiology of a subset of sarcoidosis
• Innate immune pathway dysregulation
Pathobiologic questions in sarcoidosis
• Role of specific microorganisms in sarcoidosis etiology and pathogenesis (e.g., mycobacteria, propionibacteria, others)
• Role of active infection in sarcoidosis
• Role of serum amyloid A aggregation in promoting chronic disease
• Role of Th17 immunity in clinical phenotype
• Role of Th1, Th17, and Th2 immune transition in fibrotic sarcoidosis

Definition of abbreviations: HLA = human leukocyte antigen; MHC = major histocompatibility complex; Th = T helper cell.