Down‐Regulation of Interleukin‐10 Expression and Production Is Associated with Spontaneous Proliferation by Lymphocytes from Human T Lymphotropic Virus Type II‐Infected Persons
Autor: | Donna R. Sasso, Charlene S. Dezzutti, Renu B. Lal, Donna L. Rudolph |
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Rok vydání: | 1998 |
Předmět: |
Interleukin 2
genetic structures medicine.medical_treatment Down-Regulation Lymphocyte proliferation Biology Peripheral blood mononuclear cell Interferon-gamma Antigens CD medicine Humans Immunology and Allergy Lymphocytes RNA Messenger Cells Cultured CD86 Membrane Glycoproteins Interleukin equipment and supplies eye diseases Interleukin-10 Interleukin 10 Infectious Diseases Cytokine HTLV-II Infections Immunology B7-1 Antigen Leukocytes Mononuclear Interleukin-2 B7-2 Antigen Interleukin-4 sense organs Interleukin-5 Cell Division CD80 medicine.drug |
Zdroj: | The Journal of Infectious Diseases. 177:1489-1496 |
ISSN: | 1537-6613 0022-1899 |
DOI: | 10.1086/515311 |
Popis: | Cytokines from peripheral blood mononuclear cells (PBMC) from human T lymphotropic virus (HTLV)-II-infected persons were studied to delineate the mechanism(s) of spontaneous lymphocyte proliferation (SLP). Culturing HTLV-II-infected PBMC that spontaneously proliferate (SLP+) resulted in greater mRNA expression and production of interferon-gamma, interleukin (IL)-4, and IL-5, with a concomitant decrease in IL-10, than was seen with nonproliferating (SLP ) and normal PBMC. While IL-2 mRNA expression was higher, production was lower in SLP+ PBMC than in SLP and normal PBMC, implying that the proliferating cells are utilizing IL-2. Neutralization of IL-2 resulted in partial inhibition, suggesting that other cytokines also affect SLP. Addition of recombinant IL-10 inhibited the proliferation of SLP+ PBMC. Further, blocking costimulatory signals with monoclonal antibodies against CD80/CD86 resulted in increased IL-10 production with concomitant inhibition of SLP. The mechanism(s) underlying HTLV-II-associated SLP in vitro involve increased utilization of IL-2 and down-regulation of IL-10. |
Databáze: | OpenAIRE |
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