ABSTRACT
Sarcoidosis is a chronic granulomatous disorder characterized by an accumula-
tion of lymphocytes and macrophages in the alveoli. Ultimately, long-lasting,
nontreated disease results in a distortion of the microarchitecture of the lower
respiratory tract. Our present understanding of its pathogenesis is that several
sequential immunological events are involved resulting eventually in granuloma
formation: (i) exposure to one or several still elusive antigen(s), (ii) acquiring
T-cell-immunity against the antigen(s) mediated by antigen processing and
presentation by macrophages, (iii) generation of specific T-effector cells,
(iv) activation of macrophages, and (v) induction of granuloma formation. These
events, however, are dependent on a susceptible genetic background described
by a variety of functional polymorphisms (1,2).
