CXCL10 (IFN-γ-Inducible Protein-10) Control of Encephalitogenic CD4+ T Cell Accumulation in the Central Nervous System During Experimental Autoimmune Encephalomyelitis

Fife, Brian T.; Kennedy, Kevin J.; Paniagua, Mary C.; Lukacs, Nicholas W.; Kunkel, Steven L.; Luster, Andrew D.; Karpus, William J.

doi:10.4049/jimmunol.166.12.7617

Cited by 243 publications

(210 citation statements)

References 44 publications

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“…Obviously more work is warranted evident by the inconsistent results in the current study using CXCL10−/− mice and the previous study incorporating neutralizing antibody to CXCL10 [12]. However, the discrepancy between these two studies is not unique since experimental models of multiple sclerosis show inconsistent results using anti-CXCL10 antibody versus CXCL10−/− mice [40,41].…”

Section: Cd4 + T Cell Infiltration Into the Cornea Is Reduced In Cxclmentioning

confidence: 59%

CD4+ T cell migration into the cornea is reduced in CXCL9 deficient but not CXCL10 deficient mice following herpes simplex virus type 1 infection

Wuest

Farber

Luster

et al. 2006

Cellular Immunology

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The role of CXCL9 and CXCL10 in the ocular immune response to herpes simplex virus type 1 (HSV-1) infection was investigated using mice deficient in either CXCL9 or CXCL10. CXCL10 but not CXCL9 deficient mice showed an increase in sensitivity to ocular virus infection as measured by an elevation in virus titer recovered in the tear film and corneal tissue. The increase in virus was associated with an increase in the expression of the chemokine CCL2 but no significant change in the infiltration of CD4 + T cells or NK cells into the corneal stroma. In contrast, a significant reduction in CD4 + T cell infiltration into the cornea was found in CXCL9 deficient mice following HSV-1 infection consistent with the absence of CXCL9 expression and reduction in expression of other chemokines including CCL3, CCL5, CXCL1, and CXCL10. Collectively, the results suggest a nonredundant role for CXCL9 and CXCL10 in response to ocular HSV-1 infection in terms of controlling virus replication and recruitment of CD4 + T cells into the cornea.

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Section: Cd4 + T Cell Infiltration Into the Cornea Is Reduced In Cxclmentioning

confidence: 59%

CD4+ T cell migration into the cornea is reduced in CXCL9 deficient but not CXCL10 deficient mice following herpes simplex virus type 1 infection

Wuest

Farber

Luster

et al. 2006

Cellular Immunology

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“…IP-10 is part of the CXC family of chemokines, attracting activated T-helper 1 (Th1) and natural killer (NK) cells expressing the CXCR3 receptor [13,14]. IP-10 plays a role in lymphocyte recruitment in autoimmune thyroid disorders [15] and demyelinating neuropathies [16,17]. Moreover, high serum levels of IP-10 are seen in Type 1 diabetic patients [18].…”

mentioning

confidence: 99%

IL-1β and IFN-γ induce the expression of diverse chemokines and IL-15 in human and rat pancreatic islet cells, and in islets from pre-diabetic NOD mice

et al. 2003

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Aims/hypothesis. Cytokines and chemokines are important mediators of immune responses due to their ability to recruit and activate leukocytes. Using microarray analysis we observed that rat beta cells exposed to IL-1β and IFN-γ have increased mRNA levels of chemokines and IL-15. The aim of this study was to characterize the expression of IP-10, MIP-3α, fractalkine and IL-15 in rat beta cells, human pancreatic islets, and in islets isolated from NOD mice, both during the pre-diabetic period and following islet transplantation. Methods. FACS-purified rat beta cells and human islets were cultured with IL-1β, IFN-γ and/or TNF-α. Islets were isolated from NOD or BALB/c mice at different ages. For syngeneic islet transplantation, 2-or 3-week-old NOD islets were grafted under the kidney capsule of spontaneously diabetic NOD recipients. Chemokine and IL-15 mRNA expression and protein release were evaluated, respectively, by RT-PCR and ELISA.Results. Human islets and rat beta cells express IP-10, MIP-3α, fractalkine and IL-15 mRNAs upon exposure to cytokines. The expression of IL-15, IP-10 and fractalkine is regulated by IFN-γ, while the expression of MIP-3α is IL-1β-dependent. Moreover, cytokines induced IL-15, IP-10, Mig, I-TAC and MIP-3α protein accumulation in culture medium from human islets. In vivo, there was an age-related increase in IL-15, IP-10 and MIP-3α expression in islets isolated from NOD mice. Following syngeneic islet transplantation, increased expression of IL-1β, IFN-γ, fractalkine, IP-10, MCP-1 and MIP-3α mRNAs were observed in the grafts. Conclusion/interpretation. Cytokine-exposed islets or beta cells express chemokines and IL-15. This could contribute to the recruitment and activation of mononuclear cells and development of insulitis in early Type 1 diabetes and during graft destruction. [Diabetologia (2003) 46:255-266] Keywords Type 1 diabetes mellitus, chemokines, IL-15, NOD mice, beta cells, interferon-γ, interleukin-1β, pancreatic islets, islet transplantation, insulitis.

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“…The ligand for CXCR3 is CXCL10, also termed IFN-γ-inducible protein-10 (IP-10). Increasing evidence suggests a role of this chemokine in immunoinflammatory diseases, including multiple sclerosis, autoimmune hepatitis and thyroiditis [4,5,6,7].…”

mentioning

confidence: 99%

Serum concentrations of the interferon-γ-inducible chemokine IP-10/CXCL10 are augmented in both newly diagnosed Type I diabetes mellitus patients and subjects at risk of developing the disease

et al. 2002

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Aims/hypothesis. Chemokines are chemotactic cytokines controlling the recruitment of leukocytes from the blood by regulating integrin adhesiveness. It has been shown that the migration of CD4+Th1 and CD4+Th2 cells is governed by specific chemokines.Increasing evidence suggests that the CD4+Th1 cheomoattractant chemokine CXCL10, also termed Interferon (IFN)-γ -inducible protein (IP)-10 is pathogenetically involved in several immunoinflammatory and autoimmune diseases. Methods. IFN-γ and IP-10 were quantified by solidphase ELISA in sera of patients with either newly diagnosed or long-term Type I (insulin-dependent) diabetes mellitus, and in sera of their healthy first degree relatives. The latter were subdivided into "low" and "high" risk prediabetic subjects depending on whether they were negative or positive for the anti-beta-cell autoantibodies ICA and GAD. Results. Compared with healthy control subjects (18%, 9/50), those with a low risk of disease (21%, 5/24) and the group of patients with long-term Type I diabetes (24%, 12/50), IP-10 was found more frequently and at increased concentrations in both newly diagnosed Type I diabetic patients (84%, 42/50) and in those with a high risk of disease (73%, 16/22); in the latter, the IP-10 concentrations correlated with those of IFN-γ. Conclusion/interpretation. Circulating IP-10 concentrations is increased in patients with Type I diabetes, but only during the early and subclinical stage of the disease. [Diabetologia (2002[Diabetologia ( ) 45:1107[Diabetologia ( -1110

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CXCL10 (IFN-γ-Inducible Protein-10) Control of Encephalitogenic CD4+ T Cell Accumulation in the Central Nervous System During Experimental Autoimmune Encephalomyelitis

Cited by 243 publications

References 44 publications

CD4+ T cell migration into the cornea is reduced in CXCL9 deficient but not CXCL10 deficient mice following herpes simplex virus type 1 infection

CD4+ T cell migration into the cornea is reduced in CXCL9 deficient but not CXCL10 deficient mice following herpes simplex virus type 1 infection

IL-1β and IFN-γ induce the expression of diverse chemokines and IL-15 in human and rat pancreatic islet cells, and in islets from pre-diabetic NOD mice

Serum concentrations of the interferon-γ-inducible chemokine IP-10/CXCL10 are augmented in both newly diagnosed Type I diabetes mellitus patients and subjects at risk of developing the disease

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