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Monocyte cytokine and costimulatory molecule expression in patients infected with Leishmania mexicana
Author(s) -
CARRADA G.,
CAÑEDA C.,
SALAIZA N.,
DELGADO J.,
RUIZ A.,
SANCHEZ B.,
GUTIÉRREZKOBEH L.,
AGUIRRE M.,
BECKER I.
Publication year - 2007
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/j.1365-3024.2006.00924.x
Subject(s) - leishmania mexicana , immunology , lipophosphoglycan , proinflammatory cytokine , cutaneous leishmaniasis , leishmania , biology , tumor necrosis factor alpha , cytokine , monocyte , immune system , antigen , interleukin 6 , interleukin , leishmaniasis , inflammation , visceral leishmaniasis , parasite hosting , leishmania donovani , world wide web , computer science
SUMMARY Leishmania mexicana causes localized and diffuse cutaneous leishmaniasis. Patients with localized cutaneous leishmaniasis (LCL) develop a benign disease, whereas patients with diffuse cutaneous leishmaniasis (DCL) suffer from a progressive disease associated with anergy of the cellular response towards Leishmania antigens. We evaluated the production of the interleukins (IL) IL‐12, IL‐15, IL‐18 and tumour necrosis factor‐α (TNF‐α) and the expression of the costimulatory molecules CD40, B7‐1 and B7‐2 in monocytes from LCL and DCL patients, stimulated in vitro with Leishmania mexicana lipophosphoglycan (LPG) for 18 h. LCL monocytes significantly increased TNF‐α, IL‐15 and IL‐18 production, and this increase was associated with reduced amounts of IL‐12. DCL monocytes produced no IL‐15 or IL‐18 and showed a decreasing tendency of TNF‐α and IL‐12 production as the severity of the disease increased.No difference was observed in the expression of CD40 and B7‐1 between both groups of patients, yet B7‐2 expression was significantly augmented in DCL patients. It remains to be established if this elevated B7‐2 expression in DCL patients is cause or consequence of the Th2‐type immune response that characterizes these patients. These data suggest that the diminished ability of the monocytes from DCL patients to produce cell‐activating innate proinflammatory cytokines when stimulated with LPG is a possible cause for disease progression.