Cutting edge: T cell Ig mucin-3 reduces inflammatory heart disease by increasing CTLA-4 during innate immunity

Sylvia Frisancho-Kiss, Jennifer F. Nyland, Sarah E. Davis, Masheka A. Barrett, Shannon J.L. Gatewood, Dolores B. Njoku, Daniela Cihakova, Ellen K. Silbergeld, Noel R. Rose, De Lisa Fairweather

Research output: Contribution to journalArticle

100 Scopus citations

Abstract

Autoimmune diseases can be reduced or even prevented if proinflammatory immune responses are appropriately down-regulated. Receptors (such as CTLA-4), cytokines (such as TGF-β), and specialized cells (such as CD4+ CD25+ T regulatory cells) work together to keep immune responses in check. T cell Ig mucin (Tim) family proteins are key regulators of inflammation, providing an inhibitory signal that dampens proinflammatory responses and thereby reducing autoimmune and allergic responses. We show in this study that reducing Tim-3 signaling during the innate immune response to viral infection in BALB/c mice reduces CD80 costimulatory molecule expression on mast cells and macrophages and reduces innate CTLA-4 levels in CD4+ T cells, resulting in decreased T regulatory cell populations and increased inflammatory heart disease. These results indicate that regulation of inflammation in the heart begins during innate immunity and that Tim-3 signaling on cells of the innate immune system critically influences regulation of the adaptive immune response.

Original languageEnglish (US)
Pages (from-to)6411-6415
Number of pages5
JournalJournal of Immunology
Volume176
Issue number11
DOIs
StatePublished - Jun 1 2006

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ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Frisancho-Kiss, S., Nyland, J. F., Davis, S. E., Barrett, M. A., Gatewood, S. J. L., Njoku, D. B., Cihakova, D., Silbergeld, E. K., Rose, N. R., & Fairweather, D. L. (2006). Cutting edge: T cell Ig mucin-3 reduces inflammatory heart disease by increasing CTLA-4 during innate immunity. Journal of Immunology, 176(11), 6411-6415. https://doi.org/10.4049/jimmunol.176.11.6411