Publication Date:
2007-11-17
Description:
CD4+ T helper 1 (TH1) cells are important mediators of inflammation and are regulated by numerous pathways, including the negative immune receptor Tim-3. We found that Tim-3 is constitutively expressed on cells of the innate immune system in both mice and humans, and that it can synergize with Toll-like receptors. Moreover, an antibody agonist of Tim-3 acted as an adjuvant during induced immune responses, and Tim-3 ligation induced distinct signaling events in T cells and dendritic cells; the latter finding could explain the apparent divergent functions of Tim-3 in these cell types. Thus, by virtue of differential expression on innate versus adaptive immune cells, Tim-3 can either promote or terminate TH1 immunity and may be able to influence a range of inflammatory conditions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, Ana C -- Anderson, David E -- Bregoli, Lisa -- Hastings, William D -- Kassam, Nasim -- Lei, Charles -- Chandwaskar, Rucha -- Karman, Jozsef -- Su, Ee W -- Hirashima, Mitsuomi -- Bruce, Jeffrey N -- Kane, Lawrence P -- Kuchroo, Vijay K -- Hafler, David A -- R01 AI067544/AI/NIAID NIH HHS/ -- R01 AI067544-01A2/AI/NIAID NIH HHS/ -- R56 AI067544/AI/NIAID NIH HHS/ -- R56 AI067544-01A1/AI/NIAID NIH HHS/ -- R56 AI067544-02/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 16;318(5853):1141-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Immunology, Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18006747" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
Antigens, CD11b/immunology
;
Astrocytes/immunology
;
Central Nervous System Neoplasms/immunology
;
Dendritic Cells/immunology
;
Encephalomyelitis, Autoimmune, Experimental/immunology
;
Galectins/immunology
;
Glioblastoma/immunology
;
Humans
;
Immunity, Innate
;
Inflammation Mediators/*immunology
;
Lipopolysaccharides/immunology
;
Macrophages/immunology
;
Membrane Proteins/biosynthesis/*immunology
;
Mice
;
Microglia/immunology
;
Multiple Sclerosis/immunology
;
Rats
;
Receptors, Immunologic/biosynthesis/*immunology
;
Receptors, Virus/biosynthesis/*immunology
;
Signal Transduction
;
T-Lymphocytes/immunology
;
Th1 Cells/*immunology
;
Toll-Like Receptors
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
