The number of Fas+ cells was similar in the two ATL lesions but differed from healthy mucosa (Tables S1 and S2; Figure 3c). FasL+ cells presented a heterogeneous distribution in all groups studied, forming clusters close to vessels and glands. No difference was observed between ATL lesions. However, a significant difference in Caspase inhibitor the distribution/mm2 between lesion and healthy tissue was detected (Table S2; Figure 3d). In all samples, CLA+ cells were heterogeneously distributed in the lamina propria, with a higher concentration in the reticular portion and close to vessels and glands. The number of CLA+ cells in C–N was about half of that observed in ATL lesions. Differences were also observed between

ATL–O and C–O. However, there was no difference between ATL lesions (Tables S1 and S2; Figure 3e). Expression of NOS2 was observed in all groups but varied from small cell clusters (discrete) to diffuse distribution throughout all or most of the tissue (intense) (Figure 1e). Despite the wide variation LY2157299 in vitro in the intensity of NOS2 expression, large positive areas were observed in 41·7% of the cases of ATL–N but only in 14·3% of ATL–O (Figure 3f). Low expression

of NOS2, with discrete expression and distribution, was observed in clinically healthy tissues. Because of this heterogeneous distribution, a significant difference was only observed between ATL–N and C–N (Figure 3f). Correlation analysis between the detection of parasites and intensity of NOS2 expression in lesions showed an inverse correlation between the two parameters (P = 0·043). Endothelial cells expressing E-selectin (CD62E) were observed in all samples. In some fields, activated vessels were found close to nonactivated vessels. Low expression of E-selectin was observed in most control mucosa samples. No difference in the distribution of activated vessels was observed between ATL–O and C–O or between ATL–N and ATL–O. However, there was a significant difference between ATL–N and C–N (Figure 3g). In this study, we characterized the in situ inflammatory

response of oral and nasal ATL lesions to analyse the inflammatory profile in mucosal ATL. Our results showed that both oral and nasal ATL lesions selleck compound presented a marked inflammatory infiltrate mainly consisting of T cells, macrophages and, at a lower proportion, B lymphocytes and neutrophils. The predominance of T lymphocytes and macrophages has been demonstrated in ATL mucosal and cutaneous lesions (6,8–17) as well as in other infectious and noninfectious diseases, such as paracoccidioidomycosis (18), periodontitis, sinusitis, infectious rhinitis (19–22), lupus erythematosus and lichen planus (23,24). This predominance might result from the inflammatory process, which mainly stimulates cellular immune responses. In addition, a larger number of CD4+ T cells compared to CD8+ T cells was observed in ATL lesions.