Transgenic T cell-specific expression of CXCR3 enhances splenic and hepatic T cell accumulation but does not affect the outcome of visceral leishmaniasis.
The outcome of visceral leishmaniasis, caused by parasite Leishmania donovani, depends on the recruitment of leishmanicidal Th1 cells. Chemokine receptor CXCR3, preferentially expressed by Th1 cells, is critical for migration of these T cells during infection. During chronic VL, there is a decrease in the presence of CXCR3-expressing CD4+T cells in the spleen, which is associated with high parasitic burden in this organ. We therefore examined whether T cell-specific expression of CXCR3 in mice (CXCR3Tg) would promote resistance to VL. L. donovani infected CXCR3Tgmice showed increased accumulation of T cells in the spleens compared to WT littermates (CXCR3+/+). However, CXCR3+T cells from CXCR3Tgmice showed low CD69 expression and these mice developed fewer granulomas. Additionally, both groups of mice showed similar cytokine profiles and parasitic burdens during the course of infection. In summary, although T cell-specific expression of CXCR3 promoted the accumulation of CXCR3-expressing T cells during L. donovani infection, this did not enhance resistance to VL.
Department of Pathology, Wexner Medical Center, The Ohio State University, Columbus, OH, USA.
Sanjay
S
Varikuti
Department of Microbiology, The Ohio State University, Columbus, OH, USA.
Gayathri
G
Natarajan
College of Public Health, The Ohio State University, Columbus, OH, USA.
Steve
S
Oghumu
Department of Pathology, Wexner Medical Center, The Ohio State University, Columbus, OH, USA.
Rachel H
RH
Sperling
Department of Pathology, Wexner Medical Center, The Ohio State University, Columbus, OH, USA.
Ellen
E
Moretti
Department of Pathology, Wexner Medical Center, The Ohio State University, Columbus, OH, USA.
James
J
Stock
College of Veterinary Medicine, The Ohio State University Medical Center, Columbus, USA.
Tracey L
TL
Papenfuss
Department of Pathology, Wexner Medical Center, The Ohio State University, Columbus, OH, USA; Department of Microbiology, The Ohio State University, Columbus, OH, USA. Electronic address: abhay.satoskar@osumc.edu.
Abhay R
AR
Satoskar
D000818:Animals; D015703:Antigens, CD / Q000378:metabolism; D000945:Antigens, Differentiation, T-Lymphocyte / Q000378:metabolism; D002465:Cell Movement / Q000235:genetics; D002478:Cells, Cultured; D037181:Lectins, C-Type / Q000378:metabolism; D007893:Leishmania donovani / Q000276:immunology*; D007898:Leishmaniasis, Visceral / Q000276:immunology*; D008099:Liver / Q000469:parasitology / Q000502:physiology*; D008213:Lymphocyte Activation; D051379:Mice; D008807:Mice, Inbred BALB C; D018345:Mice, Knockout; D009928:Organ Specificity; D054367:Receptors, CXCR3 / Q000235:genetics / Q000378:metabolism*; D013154:Spleen / Q000469:parasitology / Q000502:physiology*; D018417:Th1 Cells / Q000276:immunology* / Q000469:parasitology; D058408:Th1-Th2 Balance; D019076:Transgenes / Q000235:genetics; D000099192:CD69 Antigens
D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D037181:Lectins, C-Type; D054367:Receptors, CXCR3; D000099192:CD69 Antigens; C515188:Cxcr3 protein, mouse
CXCR3; Chemokine receptor; Cytokines; Granuloma; Leishmania donovani; T cells; Transgenic; Visceral leishmanisis