Stimulation of B-cell lymphopoiesis by interleukin-7 leads to aggravation of murine leishmaniasis.

The effect of recombinant interleukin-7 (IL-7) on the clinical course of murine leishmaniasis and the development of the accompanying immune response was investigated. Previously, IL-7 has been shown to possess stimulatory capacity for different cell types of the immune and haematopoietic system critically involved in the defence against Leishmania major (L. major), such as macrophages which are activated for the elimination of the parasite by IL-7. In contrast to these in vitro data, the present study indicates that treatment of genetically susceptible BALB/c mice with IL-7 at the onset of the infection leads to enhanced lesion development and a significantly accelerated death of the animals. This was correlated with a 40-fold increased parasite burden in spleens and lymph nodes. While the specific antibody response against L. major was not altered and lymphocytes of IL-7-treated mice produced comparable amounts of the T-helper type-2 (Th2) cytokines IL-4 and IL-10, less interferon-gamma (IFN-gamma) was measurable after antigenic stimulation of lymph node and spleen cells in vitro. One of the major changes appearing by the first week after infection in IL-7-treated mice was the increase of the total cell number in spleen and lymph nodes draining the local infection. Analysis of the cellular composition revealed that the enhanced cellularity was predominantly due to a rise in the B-cell compartment. Since antigen presentation by B cells has been implicated in the development of Th2 cells, the disease-aggravating activity of IL-7 is thought to be primarily due to augmentation of B lymphopoiesis.