Biomedical subjects

Jan Leipe

Publications and source records attributed to Jan Leipe.

4 recordsLinked to original sources

PubMed2006

Palifermin as treatment in dose-intense conventional polychemotherapy induced mucositis.

Polychemotherapy or radiation frequently causes oral mucositis. Until now, only supportive options are available. Palifermin, a recombinant form of the human keratinocyte growth factor can avoid mucositis in patients treated with myeloablative polychemotherapy for allogeneic stem cell transplantation. Here, we present a patient treated with dose-intense conventional polychemotherapy suffering from severe mucositis leading to additional hospitalization. By using palifermin, the mucositis as well as further admissions were totally prevented. Furthermore, application in subsequent chemotherapy cycles demonstrated a safe and efficacious use. Hence, treatment with palifermin can prevent severe mucositis in a patient treated with dose-intense conventional polychemotherapy.

Dose-Response Relationship, Drug↗

PubMed2005

The role of the T cell in autoimmune inflammation.

T cells, in particular CD4+ T cells, have been implicated in mediating many aspects of autoimmune inflammation. However, current evidence suggests that the role played by CD4+ T cells in the development of rheumatoid inflammation exceeds that of activated proinflammatory T-helper (Th)1 effector cells that drive the chronic autoimmune response. Subsets of CD4+ T cells with regulatory capacity, such as CD25+ regulatory T (Treg) cells and Th2 cells, have been identified, and recent observations suggest that in rheumatoid arthritis the function of these regulatory T cells is severely impaired. Thus, in rheumatoid arthritis, defective regulatory mechanisms might allow the breakdown of peripheral tolerance, after which the detrimental Th1-driven immune response evolves and proceeds to chronic inflammation. Here, we review the functional abnormalities and the contribution of different T cell subsets to rheumatoid inflammation.

Abatacept↗

PubMed2005

Regulatory T cells in rheumatoid arthritis.

Apart from the deletion of autoreactive T cells in the thymus, various methods exist in the peripheral immune system to control specific human immune responses to self-antigens. One of these mechanisms involves regulatory T cells, of which CD4+CD25+ T cells are a major subset. Recent evidence suggests that CD4+CD25+ T cells have a role in controlling the development of autoimmune diseases in animals and in humans. The precise delineation of the function of CD4+CD25+ T cells in autoimmune inflammation is therefore of great importance for the understanding of the pathogenesis of autoimmune diseases. Moreover, the ability to control such regulatory mechanisms might provide novel therapeutic opportunities in autoimmune disorders such as rheumatoid arthritis. Here we review existing knowledge of CD4+CD25+ T cells and discuss their role in the pathogenesis of rheumatic diseases.

Arthritis, Rheumatoid↗

PubMed2004

GATA-3 in human T cell helper type 2 development.

The delineation of the in vivo role of GATA-3 in human T cell differentiation is a critical step in the understanding of molecular mechanisms directing human immune responses. We examined T cell differentiation and T cell-mediated effector functions in individuals lacking one functional GATA-3 allele. CD4 T cells from GATA-3+/- individuals expressed significantly reduced levels of GATA-3, associated with markedly decreased T helper cell (Th)2 frequencies in vivo and in vitro. Moreover, Th2 cell-mediated effector functions, as assessed by serum levels of Th2-dependent immunoglobulins (Igs; IgG4, IgE), were dramatically decreased, whereas the Th1-dependent IgG1 was elevated compared with GATA-3+/+ controls. Concordant with these data, silencing of GATA-3 in GATA-3+/+ CD4 T cells with small interfering RNA significantly reduced Th2 cell differentiation. Moreover, GATA-3 mRNA levels increased under Th2-inducing conditions and decreased under Th1-inducing conditions. Taken together, the data strongly suggest that GATA-3 is an important transcription factor in regulating human Th2 cell differentiation in vivo.

Adolescent↗