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Despite Increased CD4 Foxp3 Cells within the Infection Site, BALB/c IL-4 Receptor-Deficient Mice Reveal
 

Summary: Despite Increased CD4 Foxp3 Cells within the Infection Site,
BALB/c IL-4 Receptor-Deficient Mice Reveal
CD4 Foxp3-Negative T Cells as a Source of IL-10
in Leishmania major Susceptibility1
Hisashi Nagase,2
* Kathryn M. Jones,* Charles F. Anderson,
and Nancy Noben-Trauth3
*
BALB/c IL-4R /
mice, despite the absence of IL-4/IL-13 signaling and potent Th2 responses, remain highly susceptible to
Leishmania major substain LV39 due exclusively to residual levels of IL-10. To address the contribution of CD4 CD25 T
regulatory (Treg) cells to IL-10-mediated susceptibility, we depleted CD4 CD25 cells in vivo and reconstituted IL-4R RAG2
recipients with purified CD4 CD25 T cells. Although anti-CD25 mAb treatment significantly decreased parasite numbers in
IL-4R /
mice, treatment with anti-IL-10R mAb virtually eliminated L. major parasites in both footpad and dermal infection
sites. In addition, IL-4R RAG2 mice reconstituted with CD4 cells depleted of CD25 Treg cells remained highly susceptible
to infection. Analysis of L. major-infected BALB/c and IL-4R /
inflammatory sites revealed that the majority of IL-10 was
secreted by the CD4 Foxp3 population, with a fraction of IL-10 coming from CD4 Foxp3 Treg cells. All T cell IFN-
production was also derived from the CD4 Foxp3 population. Nevertheless, the IL-4R /

  

Source: Arnold, Jonathan - Nanoscale Science and Engineering Center & Department of Genetics, University of Georgia

 

Collections: Biotechnology