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Increased expressio...
Increased expression of leukocyte Ig-like receptor-1 and activating role of UL18 in the response to cytomegalovirus infection
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Wagner, C. S. (author)
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- Riise, Gerdt C., 1956 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för invärtesmedicin,Institute of Medicine, Department of Internal Medicine
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- Bergström, Tomas, 1950 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för infektionssjukdomar,Institute of Biomedicine, Department of Infectious Medicine
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- Kärre, K. (author)
- Karolinska Institutet
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- Carbone, E. (author)
- Karolinska Institutet
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- Berg, L. (author)
- Karolinska Institutet
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(creator_code:org_t)
- The American Association of Immunologists, 2007
- 2007
- English.
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In: J Immunol. - : The American Association of Immunologists. - 0022-1767 .- 1550-6606. ; 178:6, s. 3536-43
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Abstract
Subject headings
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- NK and T cells are important for combating CMV infection. Some NK and T cells express leukocyte Ig-like receptor-1 (LIR-1), an inhibitory receptor recognizing MHC class I and the CMV-encoded homolog UL18. We previously demonstrated an early increase in LIR-1-expressing blood lymphocytes in lung-transplanted patients later developing CMV disease. We now show that NK and T cells account for the observed LIR-1 augmentation. Coincubation of PBMC from CMV-seropositive donors with virus-infected lung fibroblasts led to a T cell-dependent secretion of IFN-gamma, produced mainly by LIR-1(+) T cells and by NK cells. Cytokine production during coculture with fibroblasts infected with virus containing the UL18 gene was augmented compared with the UL18 deletion virus, suggesting a stimulatory role for UL18. However, purified UL18Fc proteins inhibited IFN-gamma production of LIR-1(+) T cells. We propose that cytokine production in the transplant induces NK and T cells to express LIR-1, which may predispose to CMV disease by MHC/LIR-1-mediated suppression. Although the UL18/LIR-1 interaction could inhibit T cell responses, this unlikely plays a role in response to infected cells. Instead, our data point to an activating role for viral UL18 during infection, where indirect intracellular effects cannot be excluded.
Subject headings
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Lungmedicin och allergi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Respiratory Medicine and Allergy (hsv//eng)
Keyword
- Adult
- Aged
- Bystander Effect/immunology
- Capsid Proteins/biosynthesis/*immunology
- Cells
- Cultured
- Coculture Techniques
- Cytomegalovirus/immunology
- Cytomegalovirus Infections/etiology/*immunology/metabolism
- Female
- Fibroblasts/immunology/metabolism/virology
- Histocompatibility Antigens Class I/immunology/metabolism
- Humans
- *Immune Tolerance
- Immunity
- Cellular
- Killer Cells
- Natural/immunology/metabolism
- Lung Transplantation/*immunology
- Male
- Middle Aged
- Receptors
- Immunologic/biosynthesis/*immunology
- T-Lymphocytes/*immunology/metabolism
Publication and Content Type
- ref (subject category)
- art (subject category)
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