Abstract | Using this model we find that hybrid spreading is critical to seed and establish infection, and that cell-to-cell spread and increased CD4+ T cell activation are important for HIV-1 progression. |
Introduction | The course of HIV-1 infection is typified by three phases; acute infection characterized by a rapid viraemia peak (3—6 weeks post-infection) followed by a rapid fall in virus levels, a stable chronic phase of variable length characterized by low level viraemia and slowly declining CD4+ T cell numbers, and a final stage (Acquired Immune Deficiency Syndrome, AIDS) characterized by multiple opportunistic infections and a rapid fall in CD4+ T cell count. |
Introduction | However the interplay of cell-to-cell spread and increased CD4+ T cell activation, that are likely to have profound influences on the progression of the disease have been hitherto little studied. |
Introduction | In this paper, unless otherwise stated, “T cells” refers to CD4+ T cells . |
Results | The production rate of new quiescent T cells from sources, such as thymus, within the human body is represented by b. Quiescent T cells are activated and become susceptible at a variable activation rate a(NM/N), where a is the activation coefficient and NM is the density of T cells at which proliferation stops. |
Abstract | We illustrate our methods potential to find intervention targets for cancer treatment and cell differentiation by applying it to a leukemia signaling network and to the network controlling the differentiation of helper T cells . |
Blocking stable motifs may obstruct specific attractors | Intervention targets for each control strategy in the helper T cell network. |
Blocking stable motifs may obstruct specific attractors | More specifically, we use our network control framework to predict network control interventions on previously developed logical dynamic models for a leukemia signaling network and for the network controlling the differentiation of helper T cells . |
Blocking stable motifs may obstruct specific attractors | T cell large granular lymphocyte leukemia network. |
Abstract | Hence paracrine signaling will generally extend beyond the synapse but can be limited to cellular microenvi-ronments through uptake by target cells or strong competitors, such as regulatory T cells . |
Introduction | [9] have found that interleukin(IL)-4 is seen by most T cells in the lymph node upon parasite infection, including nonspecific ‘by-stander’ cells. |
Introduction | In this case, many T cells throughout the lymph node could be IL-4 producers. |
Introduction | However, it has been demonstrated that cyto-kine concentrations are not always well mixed, and locally higher cytokine concentrations can occur also in eX vivo T cell cultures [12]. |
The immunological synapse controls type and strength of cytokine signals | However, T cells release IL-2 and other cytokines in a polarized fashion into the immunological synapse [10,21—23]. |