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The development of sarcoidosis has been associated with the participation of intracellular microorganisms, such as mycobacteria,[18] propionibacterium,[19] or chlamydia.[20] Another reported potential disease-causing agent is mould.[21, 22] Ter?elj et?al. demonstrated increased cytokine production from lymphocytes isolated from patients with sarcoidosis after CAL-101 in vitro glucan exposition in vitro.[21] Fungal exposure was detected in homes of patients with sarcoidosis.[22] The immune response to fungi is accompanied by increased expression of TREM-1 receptor.[6] Elevated levels of soluble forms of TREM-1 in sarcoidosis were shown in our previous study.[23] TREM-2 expression is increased on the activated macrophages, and this receptor may be involved in cell fusion and granuloma formation,[15] typical feature of sarcoidosis. BAL procedure is an invasive examination, and there is an ethical problem to enrol healthy individuals as the control cohort. The disadvantage of our control group (patients with other ILD) is that it represents a heterogeneous group of different clinical diagnoses. Nevertheless, the comparison of TREM-1 and TREM-2 expressions on BALF myeloid cell surfaces in PS and other ILD may be interesting in differential diagnosis. We found approximately two times higher total see more number of TREM-1 positive cells, percentage of TREM-1 positive cells and TREM-1 MFI in PS than in control group. The total number of TREM-2 positive cells and the percentage of TREM-2 positive cells were approximately three times higher, and the MFI of TREM-2 positive cells four times higher, in PS than in control group. All these differences were statistically Sitaxentan significant (P?