Background Accessory function (AF) is one way antigen presenting cells generate sufficient secondary signals for optimal T-cell proliferation and IL-2 production. In general, alveolar macrophages (AM) are inferior accessory cells in comparison to monocytes whereas in sarcoidosis AF of AM is increased. Methods We compared the accessory index (AI) of AM and peripheral blood monocytes (PBM) of 41 patients with inactive sarcoidosis (SAR I, n = 12); active sarcoidosis with new or progressing symptoms (SAR II, n = 19), active sarcoidosis with spontaneous remission (SAR III, n = 10), tuberculosis (TB, n = 12), hypersensitivity pneumonitis (HP, n = 12), Wegener's disease (WD, n = 2), undefined alveolitis (UA, n = 8) and chronic obstructive pulmonary disease (COPD, n = 6) by employing the histoincompatibility-insensitive Jurkat cells as indicator cells. Results Compared with the controls (1.08 ± 0.3) AMs of all groups but SAR I (AI: 0.96 ± 0.42) exhibited significantly increased AIs (SAR II: 3.6 ± 3.9; SAR III: 3.2 ± 2.4; TB: 2.8 ± 2.2; HP: 3 ± 2; UA: 2.7 ± 2.3; COPD: 3.1 ± 2.2; p < 0.05 for all comparisons). Only in HP, AI of PBM was significantly increased compared with controls (3 ± 1.5, 1.3 ± 0.5, respectively; p < 0.001). Alveolar macrophages from patients with sarcoidosis, TB, and HP express the costimulatory molecule CD80 on their surface and anti-CD80 antibodies inhibited the IL-2 release of Jurkat cells in this system to 59 ± 27%. Conclusions Our data demonstrate that AM from patients with various diseases have the capability to act as competent accessory cells and that the reported accessory function of these cells is at least in part mediated by the expression of CD80.
Zissel et al. (1997) studied this question.