CXCL10 Is Required to Maintain T-Cell Populations and to Control Parasite Replication during Chronic Ocular Toxoplasmosis

Abstract

The maintenance of the T-cell response and the control of T. gondii in the eye during chronic infection is dependent on CXCL10.

Identification of a Novel Neurotrophic Factor from Primary Retinal Müller Cells Using Stable Isotope Labeling by Amino Acids in Cell Culture (SILAC)

“…Experiments on mixed rat hippocampal neuronal and glial cell cultures showed chronically expressed CXCL10 to be protective in certain neuroinflammatory conditions (56). During chronic ocular toxoplasmosis, CXCL10 is required to maintain T-cell populations and to control parasite replication (57). In the retina, CXCL10 has recently been discussed as playing a role in diabetic retinopathy (58).…”

Immunological and Immunogenetic Parameters on the Diversity of Ocular Toxoplasmosis: Evidence to Support Morphological Criteria to Classify Retinal/Retinochoroidal Scar Lesions in Epidemiologic Surveys

“…Curiously, for the CXCL 10 chemokine, which is inducible in response to IFN-, the highest frequency of high producers was observed among patients with type C scar lesions (53%), and the lowest frequency of high producers was observed among patients with type B scar lesions (21%), which is comparable to the frequency of high production observed in patients without ocular lesions (SL) (23%); 38% of patients with type A scar lesions were high producers of CXCL10. These data suggest that CXCL10 in humans can have the same role regarding T. gondii infection that it plays in mice: to control the numbers of CD3+, CD4+, and CD8+ T cells and the amount of IFN- mRNA expression in the retina and, in consequence, the replication of parasites in the eye during the chronic phase of T. gondii infection [26]. In addition, it is evident that patients who present type C scar lesions secrete high levels of IL-13, a cytokine that can control the levels of pro-inflammatory cytokines without affecting IFN- secretion within the eye, as shown in experimental models.…”

“…The third chemokine, CXCL 10 (interferon gamma-induced protein 10-IP-10), is secreted in response to IFN- stimulation. Recently, it was demonstrated in a murine model that treatment of chronically infected mice with anti-CXCL10 antibodies led to decreases in the numbers of CD3+, CD4+, and CD8+ T cells and the amount of IFN- mRNA expression in the retina and an increase in replicating parasites and ocular pathology, which provides evidence that the maintenance of the T-cell response and the control of T. gondii in the eye during chronic infection is dependent on CXCL10 [26]. Cytokines and chemokine measurements were carried out using supernatants collected from PBMC cultures stimulated with T. gondii antigens.…”

Suitable in vitro culture of Eimeria bovis meront II stages in bovine colonic epithelial cells and parasite-induced upregulation of CXCL10 and GM-CSF gene transcription

“…In case of coccidia, CXCL10 was found to be upregulated in T. gondii-and Neospora caninum-infected bovine endothelial cells (Taubert et al 2006a). Especially in case of T. gondii, several reports indicate CXCL10 as a crucial factor of (Khan et al 2000) and chronic ocular toxoplasmosis (Norose et al 2011). In addition, CXCL10 was found upregulated in C. parvum-infected gut epithelial cells (Wang et al 2007).…”

“…CXCL10 is a IFNγ-responsive proinflammatory chemokine (for review, see Liu et al 2011) which acts primarily on T cells via binding to the CXCR3 receptor (Lo et al 2010) but also exhibits chemoattractant properties on NK cells, monocytes, and neutrophils (Cyster 2005). CXCL10 plays a pivotal role in several protozoan infections (Vasquez et al 2008;Jain et al 2008;Campanella et al 2008;Amin et al 2010;Norose et al 2011) and is even used as a biomarker for the severity of human African trypanosomosis (Amin et al 2010). In case of coccidia, CXCL10 was found to be upregulated in T. gondii-and Neospora caninum-infected bovine endothelial cells (Taubert et al 2006a).…”