In situ expression of interleukin-10 and interleukin-12 in active human cutaneous leishmaniasis

• Published in: FEMS immunology and medical microbiology 1996-09, Vol.15 (2-3), p.101-107
• Main Authors: Melby, Peter C., Andrade-Narvaez, Fernando, Darnell, Barbara J., Valencia-Pacheco, Guillermo
• Format: Article
• Language: English
• Subjects: Adolescent; Adult; Blotting, Southern; Cell activation; Cellular immunity; Child; Cutaneous leishmaniasis; Cytokine; Cytokines; Female; Gene Expression; Healing; Humans; Immune response; Immune response (cell-mediated); Interferon; Interferon-gamma - biosynthesis; Interferon-gamma - genetics; Interleukin 10; Interleukin 12; Interleukin-10 - biosynthesis; Interleukin-10 - genetics; Interleukin-12 - biosynthesis; Interleukin-12 - genetics; Leishmania; Leishmaniasis, Cutaneous - immunology; Lesions; Lymphocytes T; Macrophages; Male; Middle Aged; mRNA; Parasitic diseases; Polymerase Chain Reaction; RNA, Messenger - genetics; RNA, Messenger - metabolism; Vector-borne diseases; γ-Interferon
• ISSN: 0928-8244; 1574-695X; 2049-632X
• DOI: 10.1111/j.1574-695X.1996.tb00059.x

Abstract Th1-type cellular immune responses (interferon-γ) play a critical role in protection against Leishmania spp. infection, whereas Th2-type cytokines (interleukin (IL)-4, IL-10) have a counter-protective effect. IL-12, a potent inducer of Th1-type cellular immune responses, may play a pivotal role in the development of a protective response. We found that IL-10 and IL-12 mRNAs were expressed in most lesions of individuals with active cutaneous leishmaniasis. The quantity of IL-12 mRNA was highly variable but correlated strongly with the level of interferon-γ expression. IL-12 expression also paralleled the expression of IL-10, a potent in vitro suppressor of IL-12 and interferon-γ production. The more chronic, non-healing lesions generally had higher levels of IL-12 mRNA indicating that the expression of this cytokine alone was not sufficient to induce healing. Although the in situ production of IL-10 did not appear to block IL-12 expression, IL-10 may still promote disease by direct suppression of macrophage activation.