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Biomedical subjects

P Comoli

Publications and source records attributed to P Comoli.

42 records · Page 3Linked to original sources
PubMed1993

HLA-unrestricted killing of HSV-1-infected mononuclear cells. Involvement of either gamma/delta+ or alpha/beta+ human cytotoxic T lymphocytes.

The characterization of HSV-specific human CTL, obtained in short term cultures by stimulating PBMC of healthy HSV-immune donors with autologous, PHA-activated, HSV-1-infected mononuclear cells, is described. CTL induced by using this technique are able to mediate a strong lytic activity against both HSV-1- and HSV-2-infected targets, whereas they do not kill autologous EBV-lymphoblastoid cell lines unless they are superinfected with HSV-1. TCR-gamma/delta+ cells are mainly responsible for HSV-specific cytotoxic activity in some donors, whereas TCR-alpha/beta+ CTL are primarily involved in other subjects. The large majority of HSV-specific CTL bearing either TCR-gamma/delta or TCR-alpha/beta also express CD8 and/or CD56 molecules. Virus-specific CTL, here described, require the expression of HLA class I Ag on the surface of target cells to mediate lytic activity. Nevertheless, the response is apparently HLA-unrestricted in that HSV-1-induced CTL are also able to lyse target cells mismatched for A, B, C, DR, and DQ loci. Our data suggest that both TCR-gamma/delta+ and TCR-alpha/beta+ CTL may play a role in the immune response to HSV in humans.

Antigens, CD↗
PubMed1992

Herpes simplex virus-1-specific human cytotoxic T lymphocytes are induced in vitro by autologous virus-infected mononuclear cells.

A new technique for in vitro activation of cytotoxic T lymphocytes (CTLs) specific for herpes simplex virus type 1 (HSV-1) is described. Autologous phytohemagglutinin (PHA)-activated, HSV-1-infected peripheral blood mononuclear cells (PBMC) were used, after fixation with 1% paraformaldehyde, to activate virus-specific CTLs in short-term cultures. The same unfixed PBMC were used as target cells in the cytotoxicity assay. By using this technique high levels of HSV-1-specific cytotoxic activity (50.06 +/- 16.76% at 30:1 effector:target ratio) were repeatedly obtained in 24 experiments using PBMC from 16 HSV-1 antibody-positive healthy donors, while no cytotoxic activity was observed using PBMC from 3 HSV-1 antibody-negative donors. HSV-1-induced CTLs were shown to be virus-specific as they did not lyse autologous, PHA-activated PBMC infected with influenza A virus or autologous Epstein-Barr virus (EBV) lymphoblastoid cell line (LCL), while they were able to lyse both HSV-1-infected, autologous PHA-activated PBMC and EBV-LCL. HSV-1-specific cytotoxicity was mediated by T lymphocytes, since depletion of CD3-positive cells from the effector population completely removed the killing of HSV-1-infected target cells. CD8-positive CTLs were primarily involved in the killing of HSV-1-infected targets since depletion of CD8-positive cells caused a strong reduction of virus-specific cytotoxic activity while elimination of CD4-positive lymphocytes increased killing capacity. Finally, this technique has proven to be highly reproducible, easy to perform, and thus suitable for clinical investigations.

Cell Line↗
PubMedDate not supplied

[Polyomavirus BK-associated nephropathy after kidney transplantation].

Polyomavirus BK (BKV) infection has been lately recognized as a major cause of renal allograft dysfunction. BKV-related interstitial nephropathy (PVAN) may affect 1-10% of renal allograft recipients, occurring more frequently in the first 6 months after transplantation. Progression to irreversible allograft failure has been observed in up to 45% of all cases; thanks to increased PVAN awareness and improved diagnostic techniques, the rate of graft loss has lowered, more consistently in centres with active screening and intervention programs. PVAN pathogenesis is characterized by multiple synergizing factors, among which immunodepression plays a key role. PVAN diagnosis requires the evaluation of a renal biopsy showing polyomavirus cytopathic changes and confirming BKV through an ancillary technique such as immunohistochemistry. Given the focal nature of the disease, early diagnosis may be difficult to obtain. Thus, quantification of BKV-DNA in plasma has been suggested as surrogate marker for PVAN. To date, given the lack of controlled trials, there is no consensus on a 'standard' management of PVAN. However, evidence based on reported observations suggests that a step-wise reduction of immunosuppression, preceded by pulsed steroids in case of coexistent acute rejection, may improve outcomes. Additional options may be represented by drugs with antiviral activity, such as cidofovir, leflunomide or quinolones. Application of a preventive treatment based on viremia monitoring has been recently proposed.

Adrenal Cortex Hormones↗