Diffuse cutaneous leishmaniasis (DCL) is characterized by disseminated lesions and the absence of a specific cellular immune response. Here, the immunochemotherapy outcome of a patient with DCL from Amazonian Brazil infected with Leishmania (Leishmania) amazonensis is presented. After several unsuccessful chemotherapy treatment regimens and many relapses, a monthly immunotherapy scheme of L. amazonensis PH8 plus L. (Viannia) braziliensis M2903 monovalent vaccines associated with Bacillus Calmette-Guerin (BCG) was established, one round of which also included an M2903 vaccine associated with intermittent antimonial treatment. Temporary healing of all lesions was achieved, although Leishmania skin tests were negative and interferon gamma was not detected in mononuclear cell cultures stimulated with Leishmania antigens. The frequencies of CD16 (+)CD56(+) NK cells (approximately 2x) and CD14 (+)CD16(+) proinflammatory monocytes (approximately 8x) increased in peripheral blood, and CD56 (+) lymphocytes were found infiltrating the lesions. An association between the increase of the frequency of innate immune system cells and the healing of lesions is shown, suggesting that this protocol of immunotherapy reduced the parasite load and activated NK cells and monocytes.
Herein, we intended to perform flow‐cytometric analyses of peripheral blood NK‐cell subsets in patients with active tuberculosis (TB) and those putative resistant subjects displaying positive tuberculin skin test (TST+) and compared with TST− healthy controls. Our findings demonstrated distinct phenotypic features in TST+ as compared with TB. While lower values of NK‐cells with increased frequency of CD3−CD16+ CD56− and CD3−CD16−CD56+ subsets besides lower frequency of CD3−CD16+ CD56+ NK‐cells was observed in TST+, unaltered levels of NK‐cells with increased levels of CD3−CD16+ CD56− NK‐cells with lower frequency of CD3−CD16+ CD56+ NK‐cells was found in TB. Additional analysis highlighted a shift towards increased levels of CD3−CD16−/+CD56bright NK‐cells as the hallmark of TST+, whereas unaltered frequency was observed in TB. Increased levels of CD3+CD56+ cells were observed in both TST+ and TB. Further focusing on the monocyte/NK‐cell network, we have reported that enhanced frequency of CD14+ CD16+ monocytes particularly observed in TST+. Outstanding were the distinct correlation profiles observed between CD3−CD16−CD56+ NK‐cells and CD3+ CD56+ cells CD14+ CD16+ monocytes for TST+ and TB. These data suggested that high levels of CD3−CD16−CD56+ NK‐cells aside CD14+ CD16+ monocytes as well as non‐concurrent increment of CD3+ CD56+ cells, may be involved in protective mechanisms in putative tuberculosis‐resistant individuals. On the other hand, the basal levels of macrophage‐like monocytes despite its positive correlation with increased levels of CD3+ CD56+ cells may count for the lack of the protective immunity in patients with active tuberculosis. Further studies focusing on the cytokine profiling of peripheral blood innate immunity cells before and after chemotherapic treatment are currently under evaluation.
Tuberculosis (TB) is a lung disease caused by Mycobacterium tuberculosis. The interaction between the bacillus and the host may lead to a protective cellular immune response. In the present study, we propose the "in vitro" evaluation of this cellular immune response in patients with tuberculosis before and after chemotherapic treatment. Eleven patients with TB and 9 asymptomatic subjects with tuberculin skin test negative (TST؊) (purified protein derivative (PPD) ≤10 mm) were evaluated. The peripheral lymphocytes of the subjects were analyzed utilizing the following surface markers: CD3؉ and HLA-DR
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.