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The Long Pentraxin 3 (PTX3) Suppresses Immunity to Cutaneous Leishmaniasis by Regulating CD4+ T Helper Cell Response
- Source :
- Cell Reports, Vol 33, Iss 11, Pp 108513-(2020)
- Publication Year :
- 2020
- Publisher :
- Elsevier, 2020.
-
Abstract
- Summary The long pentraxin 3 (PTX3) plays a critical role in inflammation, tissue repair, and wound healing. Here, we show that PTX3 regulates disease pathogenesis in cutaneous leishmaniasis (CL). PTX3 expression increases in skin lesions in patients and mice during CL, with higher expression correlating with severe disease. PTX3-deficient (PTX3−/−) mice are highly resistant to L. major and L. braziliensis infections. This enhanced resistance is associated with increases in Th17 and IL-17A responses. The neutralization of IL-17A abolishes this enhanced resistance, while rPTX3 treatment results in decrease in Th17 and IL-17A responses and increases susceptibility. PTX3−/− CD4+ T cells display increased differentiation to Th17 and expression of Th17-specific transcription factors. The addition of rPTX3 suppresses the expression of Th17 transcription factors, Th17 differentiation, and IL-17A production by CD4+ T cells from PTX3−/− mice. Collectively, our results show that PTX3 contributes to the pathogenesis of CL by negatively regulating Th17 and IL-17A responses.
- Subjects :
- 0301 basic medicine
Inflammation
General Biochemistry, Genetics and Molecular Biology
Pathogenesis
resistance
03 medical and health sciences
cutaneous leishmaniasis
0302 clinical medicine
Cutaneous leishmaniasis
Immunity
medicine
pentraxin 3
Transcription factor
lcsh:QH301-705.5
PTX3
Chemistry
immunopathogenesis
T helper cell
medicine.disease
regulation of immunity
3. Good health
030104 developmental biology
medicine.anatomical_structure
lcsh:Biology (General)
Immunology
medicine.symptom
Wound healing
030217 neurology & neurosurgery
Subjects
Details
- Language :
- English
- ISSN :
- 22111247
- Volume :
- 33
- Issue :
- 11
- Database :
- OpenAIRE
- Journal :
- Cell Reports
- Accession number :
- edsair.doi.dedup.....ff4a9428031a8d660b38a6f0f53fbc18