CD4 Cells In Mice Research Articles

Antigen-Clustered Nanovaccine Achieves Long-Term Tumor Remission by Promoting B/CD 4 T Cell Crosstalk.

Current cancer vaccines using T cell epitopes activate antitumor T cell immunity through dendritic cell/macrophage-mediated antigen presentation, but they lack the ability to promote B/CD4 T cell crosstalk, limiting their anticancer efficacy. We developed antigen-clustered nanovaccine (ACNVax) to achieve long-term tumor remission by promoting B/CD4 T cell crosstalk. The topographic features of ACNVax were achieved using an iron nanoparticle core attached with an optimal number of gold nanoparticles, where the clusters of HER2 B/CD4 T cell epitopes were conjugated on the gold surface with an optimal intercluster distance of 5-10 nm. ACNVax effectively trafficked to lymph nodes and cross-linked with BCR, which are essential for stimulating B cell antigen presentation-mediated B/CD4 T cell crosstalk in vitro and in vivo. ACNVax, combined with anti-PD-1, achieved long-term tumor remission (>200 days) with 80% complete response in mice with HER2+ breast cancer. ACNVax not only remodeled the tumor immune microenvironment but also induced a long-term immune memory, as evidenced by complete rejection of tumor rechallenge and a high level of antigen-specific memory B, CD4, and CD8 cells in mice (>200 days). This study provides a cancer vaccine design strategy, using B/CD4 T cell epitopes in an antigen clustered topography, to achieve long-term durable anticancer efficacy through promoting B/CD4 T cell crosstalk.

IL-15 plays a major role in the persistence of Tax-specific CD8 cells in HAM/TSP patients.

IL-15 is a critical cytokine for the maintenance of memory-phenotype CD8 cells in mice. Here, we investigated the role of IL-15 in the neurological disease termed human T cell lymphotropic virus I-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The high number of viral-specific CD8 cells in these patients is associated with inflammatory responses in the central nervous system. Because IL-15 is overexpressed in these patients, we asked whether IL-15 contributes to the persistence of human T cell lymphotropic virus I viral-specific CD8 cells. Using ex vivo cultures of HAM/TSP peripheral blood mononuclear cells, we demonstrated that in the majority of patients examined here blocking IL-15 action resulted in a decrease in the number of viral-specific CD8 cells. This decrease was caused by both inhibition of proliferation and induction of apoptosis in these cells. The data indicate that IL-15 plays a major role in the maintenance of viral-specific CD8 cells in HAM/TSP.

A factor isolated from Taenia solium metacestodes stimulates T lymphocytes to proliferate and produce gamma interferon.

A metacestode factor (MF) isolated from live metacestodes of Taenia solium suppresses humoral and cellular responses, and inhibits the inflammatory reaction around metacestodes implanted subcutaneously in mice. When this MF is digested with RNase (dMF), it loses the suppressive capacity, but acquires T-cell stimulant ability. By filtering MF through a Bio-gel P6 column, two components were separated. The first (F1) was suppressive. while the second (F2) stimulated T cells to proliferate. In these experiments, F2 or dMF was used with mouse spleen cells in stimulation assays in vitro. Spleen cells from mice treated with F2 or dMF were also stimulated with concanavalin A (Con-A) ex vivo. Flow cytometry analyses were performed to estimate cell proliferation, intracellular cytokine production. and restoration of CD4 cells. Spleen lymphocytes from mice previously treated with F2 or dMF and then stimulated with Con-A ex vivo exhibited a significant increase in cell proliferation and gamma interferon production by CD4+ (P<0.05) and CD8+ cells. These effects were concentration-dependent and inversely correlated with the amount of dMF or F2. Similar results were observed in normal mouse spleen T cells incubated with F2 or dMF and Con-A in vitro. Finally, dMF induced a significant restoration of CD4-cells in mice depleted of these cells.

Review of Possible Biomedical Applications of Carbonallay

This review indicates a possible biological concept for an application of carbon-based materials based on a recent established physiological knowledge. A key point of this review is to open a new avenue to povide a new material into our life by integtating a poject-oriented task work together with several different kinds of scientific fields. In order to disclose the above concept, severalexperimental evidences have been demonstrated. Firstly, immunological reactions of activated carbon fibers (ACFs) have been detected by measuring CD4 and CD8 cells in mice that have been implanted ACFs subcutaneously for 6 months. Histological examinations have been done. An important parameter of surface area and/or pore-size has been demonstrated. Second, ability of IgE-induced histamine release from rat mast cells was also investigated in vitro to confirm whether ACFs has a potency of inducers of acute allergic reactions. Thirdly, fundtions of cells growing and/proliferation were influenced under coexisting enviroment with ACFs in vitro. It was found by using newly planned and sythesized materials (our ID: HDI) that an optimal survival parameter of a cell survival was dependent on the pore-size of materials. In addiction, bioimplantable materials have been reviewed and application fields of carbon-based materials have been discussed. As an overall, this review has shown that scientific field of this carbonalloy (carbon-based materials) has a great potency to lead into a new scientific frontier toward many biomedical applications.

Asthma and respiratory syncytial virus infection in infancy: is there a link?

Asthma and respiratory syncytial virus infection in infancy: is there a link?

In vivo immunomodulation by monoclonal anti-CD4 antibody. II. Effect on T cell response to myelin basic protein and experimental allergic encephalomyelitis.

In vivo administration of anti-CD4 mAb (GK1.5) has been shown to be effective in preventing acute and relapsing experimental allergic encephalomyelitis (EAE). In the present report we have studied the depletion of CD4+ cells by a single dose of GK1.5 on the immune response to myelin basic protein and in the development of EAE. Our studies show that depletion of CD4 cells in mice that had received encephalitogenic CD4+ T cells altered the kinetics of acute and relapsing EAE, but did not prevent disease altogether. The in vitro T cell proliferative response to myelin basic protein in lymph node cells was maintained in the presence of significant depletion of CD4+ cells. These studies indicate that the population of Ag-reactive cells to be large and relatively refractory to antibody therapy. The implication of these results to therapy of human autoimmune disease is discussed.