Acne vulgaris is a multifactorial disease of as yet incompletely elucidated etiology and pathogenesis. The following have been identified as the most significant factors: follicular hyperkeratosis, increased sebum secretion, Propionibacterium (P.) acnes, and inflammation. Increased sebum production and follicular hyperkeratosis result in the development of microcomedones, and changes in follicular milieu in intensive growth of P. acnes. P. acnes secretes several proinflammatory products, which play an important role in the development of inflammation. These include lipases, proteases, hyaluronidases, and chemotactic factors. Immune response to P. acnes includes humoral and cell-mediated immunity as well as complement activation. Recent results indicate that keratinocytes and sebocytes, as major components of pilosebaceous unit, may act as immune cells and may be activated by P. acnes via toll-like receptors (TLRs) and CD14, and through CD1 molecules may recognize altered lipid content in sebum, followed by the production of inflammatory cytokines.