Table of Contents Author Guidelines Submit a Manuscript
Developmental Immunology
Volume 6 (1998), Issue 1-2, Pages 3-11

Langerhans Cell Migration in Murine Cutaneous Leishmaniasis: Regulation by Tumor Necrosis Factor α Interleukin-1β , and Macrophage Inflammatory Protein-1α

1Research Center for Infectious Diseases, University of Würzburg, Würzburg D-97070, Germany
2Research Center for Infectious Diseases, University of Würzburg, Röntgenring 11, Würzburg D-97070, Germany

Received 16 August 1996; Accepted 14 August 1997

Copyright © 1998 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


After intradermal infection of mice with the obligatory intracellular parasite Leishmania major, Langerhans cells (LC) are intimately involved in the induction of the primary T-cell immune response. LC can phagocytose Leishmania and transport ingested parasites from the infected skin to the regional lymph nodes. Since TNFα and IL-1β have been shown to induce LC migration after epicutaneous exposure to skin-sensitizing chemicals, we investigated the involvement of both cytokines in the migration of Leishmania-infected LC. In addition, the relevance of two chemokines of theβ subfamily, macrophage inflammatory protein 1α(MIP-1α) and macrophage chemoattractant protein 1 (MCP-1), was analyzed.In vivo depletion of TNFα significantly reduced the amount of infected LC and the parasite load in the draining lymph nodes. Administration of recombinant TNFα caused the reverse effect. In contrast, the depletion of IL1β enhanced the parasite-induced LC migration, whereas treatment with recombinant IL-1β, as well as recombinant MIP- c, reduced the rate of infected LC in the lymph nodes. MCP- did not influence LC migration. Our data demonstrate that TNFα and IL-1β are regulating the LCmediated transport of Leishmania and also provide evidence for the involvement of macrophage attractant chemokines in this process.