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R Manetti

Publications and source records attributed to R Manetti.

84 records · Page 5Linked to original sources
PubMedDate not supplied

An update on human Th1 and Th2 cells.

The existence of functionally polarized human T cell responses based on their profile of cytokine secretion in both the CD4+ T helper (Th) and the CD8+ T cytotoxic cell subset has been established. Human Th1 and Th2 cells not only produce a different set of cytokines but also exhibit distinct functional properties and preferential expression of some activation markers, such as LAG-3 and CD30, respectively. Several factors are involved in the Th cell differentiation into the polarized Th1 or Th2 pathway. They include the cytokine profile of 'natural immunity' evoked by different offending agents, the nature of the peptide ligand, as well as the activity of some costimulatory molecules and microenvironmentally secreted hormones, in the context of different host genetic backgrounds. Polarized Th1-type and Th2-type responses play different roles in protection, Th1 being effective in the defense against intracellular pathogens and Th2 against intestinal nematodes. Moreover, they are responsible for different types of immunopathological reactions. Th1 responses predominate in organ-specific autoimmune disorders, acute allograft rejection, unexplained recurrent abortions, and in some chronic inflammatory disorders of unknown etiology. In contrast, Th2 responses predominate in Omenn's syndrome, transplantation tolerance, chronic graft versus host disease, systemic sclerosis; moreover allergen-reactive Th2 cells are involved in the triggering of atopic disorders.

Autoimmune Diseases↗
PubMedDate not supplied

Th1 and th2 responses, HIV-1 coreceptors, and HIV-1 infection.

The Th1/Th2 model provides an interesting paradigm for understanding several pathophysiological processes and possibly for developing new immunotherapeutical strategies. In HIV-1 infection the interaction between the type of HIV-1 strain and the pathway of the ongoing T-cell effector response, despite its complexity, may represent one of the crucial mechanisms in determining the outcome of virus infection. While the possibility of an HIV-1-driven Th1 to Th2 switch of the immune response is still debated, evidence is accumulating to suggest that cytokines produced during an immune response can contribute to promote a selective pressure toward the evolution of HIV-1 viral strains with different tropism. This article summarizes the results of our recent studies in which the expression of CCR5 and CXCR4 HIV-1 co-receptors, as well as the activity of R5- or X4- tropic strains of HIV-1 in different in vitro models of Th1/Th2 polarization was analyzed.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

CD8+ T lymphocytes producing Th2-type cytokines (Tc2) in HIV-infected individuals.

Unusual high proportions of CD8+ T-cell clones able to produce IL-4, but no IFN-gamma (Tc2 cells), were generated from both skin biopsies and peripheral blood of HIV-infected individuals in advanced phase of infection. Tc2 cells showed unusual phenotypic and functional features, such as CD30 expression, B-cell helper activity for IgE synthesis and reduced cytolytic potential. Cloning CD8+ T-cell from HIV-infected individuals in autologous feeder cells resulted in a marked increase of CD8+ T-cell clones showing a Tc2 profile. The addition in bulk culture before cloning of both IL-12 and a neutralizing anti-IL-4 antibody dramatically reversed the cytokine profile of CD8+ T-cell clones of HIV-infected individuals to the classic Tc1 pathway. Finally, cloning CD8+ T-cells from healthy HIV-seronegative donors in the presence of feeder cells from HIV-infected individuals resulted in the development of enhanced proportions of CD8+ T-cell clones able to produce IL-4. These data suggest that CD8+ T-cells from HIV-infected individuals can develop into Tc2 cells likely because of either the defective production of IL-12 by HIV-infected macrophages and/or other microenvironmental conditions favoring early IL-4 production. The Tc2 shift during HIV infection may play some role in the reduced defence against viral infections, including HIV itself, in patients with AIDS.

CD8-Positive T-Lymphocytes↗