Abstract
IL-4 signaling is required for optimal Th1 responses during Leishmania major infection
The Journal of immunology (1950), Vol.200(1_Supplement), pp.52-52.4
05/01/2018
DOI: 10.4049/jimmunol.200.Supp.52.4
Abstract
Abstract Leishmania spp. is a global health problem that affects more than 2 million people every year with 300 million people at risk worldwide. It is well established that a dominant Th1 response (IFN-gamma, a hallmark Th1 cytokine) provides resistance, while a dominant Th2 response (IL-4, a hallmark Th2 cytokine) confers susceptibility during Leishmania spp. infections. Given the important role of IL-4 during Leishmania major infections, we used IL-4 neutralizing antibody to study and investigate the cellular and molecular events regulated by IL-4 signaling. As previously published, neutralization of IL-4 in Leishmania major-infected BALB/c mice (a Leishmania susceptible strain) provided protection when compared to control Leishmania major-infected BALB/c mice. Interestingly, despite the protection, IFN-gamma production by T cells was dramatically reduced. This demonstrates two important and previously unknown points-1) the protection against Leishmania major does not depend on the amount of IFN-gamma, but rather on the amount of IL-4, and 2) IL-4 is required for optimal production of IFN-gamma by T cells. In conclusion, our studies break the pre-existing dogma of resistance/susceptibility to Leishmania spp. infections and open new research grounds to investigate the unsuspecting role of IL-4 in controlling Th1 responses. A complete understanding of these cellular and molecular crosstalk will hopefully uncover a much-needed novel therapeutic target to treat Leishmania major infections.
Details
- Title: Subtitle
- IL-4 signaling is required for optimal Th1 responses during Leishmania major infection
- Creators
- Prajwal Gurung - Roy J. and Lucille A. Carver College of MedicineBarun Poudel - Roy J. and Lucille A. Carver College of Medicine
- Resource Type
- Abstract
- Publication Details
- The Journal of immunology (1950), Vol.200(1_Supplement), pp.52-52.4
- DOI
- 10.4049/jimmunol.200.Supp.52.4
- ISSN
- 0022-1767
- eISSN
- 1550-6606
- Language
- English
- Date published
- 05/01/2018
- Academic Unit
- Internal Medicine; Stead Family Department of Pediatrics; Infectious Diseases
- Record Identifier
- 9984362354002771
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