Producing IFN (producing + ifn)

Distribution by Scientific Domains

Kinds of Producing IFN

  • cell producing ifn


  • Selected Abstracts


    Stimulation via Toll-like receptor 9 reduces Cryptococcus neoformans -induced pulmonary inflammation in an IL-12-dependent manner

    EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 1 2005
    Lorna Edwards
    Abstract Cytosine-phosphate-guanosine-containing oligodeoxynucleotides (CpG ODN) are important vaccine adjuvants that promote Th1-type immune responses. Cryptococcus neoformans is a serious human pathogen that replicates in the lung but may disseminate systemically leading to meningitis, particularly in immunocompromised individuals. Immunization of susceptible C57BL/6 mice with CpG ODN deviates the immune response from a Th2- toward a Th1-type response following infection with C. neoformans. CpG also induces IL-12, TNF, MCP-1 and macrophage nitric oxide production. CD4+ and CD8+ T,cells producing IFN-, increase in frequency, while those producing IL-5 decrease. More importantly, pulmonary eosinophilia is significantly reduced, an effect that depends on IL-12 and CD8+ T,cells but not NK cells. CpG treatment also reduces the burden of C. neoformans in the lung, an effect that is IL-12-, NK cell- and T,cell-independent and probably reflects a direct effect of CpG on pathogen opsonization or an enhancement of macrophage antimicrobial activity. An equivalent beneficial effect is also observed when CpG ODN treatment is delivered during established cryptococcal disease. This is the first study documenting that promotion of lung TLR9 signaling using synthetic agonists enhances host defense. Activation of innate immunity has clear therapeutic potential and may even be beneficial in patients with acquired immune deficiency. [source]


    Local Applications of GM-CSF Induce the Recruitment of Immune Cells in Cervical Low-Grade Squamous Intraepithelial Lesions

    AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 2 2010
    Pascale Hubert
    Citation Hubert P, Doyen J, Capelle X, Arafa M, Renoux V, Bisig B, Seidel L, Evrard B, Bousarghin L, Gerday C, Boniver J, Foidart J-M, Delvenne P, Jacobs N. Local applications of GM-CSF induce the recruitment of immune cells in cervical low-grade squamous intraepithelial lesions. Am J Reprod Immunol 2010; 64: 126,136 Problem, Quantitative alterations of antigen-presenting cells (APC) in (pre)neoplastic lesions of the uterine cervix associated with human papillomavirus (HPV) infection suggest a diminished capacity to capture viral antigens and to induce a protective immune response. Method of study, To test whether a cervical application of GM-CSF could restore an immune response against HPV in women with cervical low-grade squamous intraepithelial lesions (LSIL), we performed two clinical trials with 11 healthy women and 15 patients with LSIL. Results, GM-CSF applications were well tolerated in all enrolled women, and no difference in toxicity between the treated and placebo groups was observed during the follow-up (until 30 months). Interestingly, in the GM-CSF treated group, a significant increase of APC and cytotoxic T-lymphocyte infiltration was observed in the cervical biopsies with no change in regulatory T cell numbers. All the HPV16+ patients exhibited an immune response against HPV16 after GM-CSF applications, as shown by NK and/or T cells producing IFN-, whereas no cellular immune response was observed before the treatment. Moreover, the anti-virus-like particles antibody titers also increased after the treatment. Conclusion, These encouraging results obtained from a limited number of subjects justify further study on the therapeutic effect of APC in cervical (pre)neoplastic lesions. [source]


    Role of TNF, in Early Chemokine Production and Leukocyte Infiltration into Heart Allografts

    AMERICAN JOURNAL OF TRANSPLANTATION, Issue 1 2010
    D. Ishii
    The acute phase cytokines IL-1,, IL-6 and TNF, are produced early during inflammatory processes, including ischemia-reperfusion. The appearance and role of these cytokines in the early inflammation following reperfusion of grafts remain poorly defined. This study investigated the role of TNF, in the induction of early leukocyte infiltration into vascularized heart allografts. TNF, and IL-6 mRNA levels reached an initial peak 3 h posttransplant and a second peak at 9,12 h with equivalent levels in iso- and allografts. A single dose of anti-TNF, mAb given at reperfusion decreased neutrophil and macrophage chemoattractant levels and early neutrophil, macrophage and memory CD8 T-cell infiltration into allografts. Anti-TNF, mAb also extended graft survival from 8.6 ± 0.6 days to 14.1 ± 0.8 days. When assessed on day 7 posttransplant, the number of donor-reactive CD8 T cells producing IFN-, in the spleen was reduced almost 70% in recipients treated with anti-TNF, mAb. Whereas anti-CD154 mAb prolonged survival to day 21, administration of anti-TNF, and anti-CD154 mAb delayed rejection to day 32 and resulted in long-term (>80 days) survival of 40% of the heart allografts. These data implicate TNF, as an important mediator of early inflammatory events in allografts that undermine graft survival. [source]


    CCR5 Is Required for Regulation of Alloreactive T-Cell Responses to Single Class II MHC-Mismatched Murine Cardiac Grafts

    AMERICAN JOURNAL OF TRANSPLANTATION, Issue 10 2009
    T. Nozaki
    The effector CD4 T-cell response in wild-type C57BL/6 recipients of single class II MHC-disparate B6.H-2bm12 cardiac allografts is restricted by CD4+CD25+ regulatory T cells (Tregs) resulting in long-term allograft survival. To investigate the role chemokine receptors might play in Treg function, this study tested the requirement for CCR5 on Tregs to suppress the alloimmune response in C57BL/6 recipients of B6.H-2bm12 cardiac allografts. In contrast to the long-term survival of B6.H-2bm12 allografts in wild-type recipients (>100 days), the allografts were acutely rejected within 25 days in CCR5,/, recipients with intense infiltration of CD4 T cells. Numbers and duration of donor-reactive CD4 T cells producing IFN-, and IL-4 were markedly increased in spleens of B6.CCR5,/, versus wild-type recipients. Wild-type and B6.CCR5,/, mice had equivalent numbers of splenic FoxP3+ Tregs before and following transplantation, and these Tregs were equivalently suppressive in vitro. However, diminished numbers of FoxP3+ Tregs infiltrated B6.H-2bm12 allografts in B6.CCR5,/, recipients. Adoptive transfer of wild-type, but not CCR5-deficient, CD4+CD25+ Tregs to CCR5,/, recipients restored long-term survival of B6.H-2bm12 cardiac grafts. Collectively, these results indicate that CCR5 expression is required for the regulatory functions of Tregs that restrict alloreactive CD4 T-cell responses to single class II MHC-mismatched cardiac allografts. [source]