By reverse phase PCR and Northern blotting, RNA of the 14 kDa galactose-binding protein (galectin-1) could be identified in primary cultures of human tubular epithelial cells. To assess protein synthesis and the possible function of galectin-1 on TEC, the cellular proteins were biosyntheticically labeled with [34S]-methionine and absorbed to immobilized laminin. Multiple radiolabeled proteins were eluted, a strong band in the area of 14 kDa was seen, coinciding with the galectin-1 band as identified by Western blotting. Surface expression of galectin-1 was seen by cytofluorometry with two different polyclonal antibodies to galectin-1. These data are in line with the finding that tubular epithelial cells adhere to laminin, partly in a Ca(2+)-independent manner.
Mice were infected with 200 untreated or vaccinated with 500 ultraviolet-attenuated cercariae of either Schistosoma japonicum or S. mansoni. For three weeks, cell numbers in axillary and mediastinal lymphnodes were counted and cell populations typed by cytofluorometry. In the axillary lymphnodes, numbers of B-cells and CD3+CD4+ T-cells but not CD3+CD8+ T-cells increased. Following vaccination with either species, parasite migration was apparently delayed in the skin and interrupted at the lungs, the lymphnodes gained weight, and cell numbers of axillary lymph nodes increased more than after infection. In mediastinal lymphnodes, only immunization with S. japonicum but not S. mansoni cercariae led to an increase of CD3+CD4+ T-cells. Following infection, both schistosome species induced higher CD3+CD4+, but not CD3+CD8+ T-cells in mediastinal nodes, and the peak was earlier with S. japonicum (about seven days after infection) than with S. mansoni (about 10 days). In analogy to T-cell observations by others using a gamma-attenuated cercarial vaccine in S. mansoni, the present results suggest that CD3+CD4+ cells also play a role in the ultraviolet-attenuated vaccine against S. japonicum.
In various inflammatory kidney diseases, tubular epithelial cells (TEC) express major histocompatibility complex class II antigens. To assess whether they might have the capacity to directly activate T cells, human TEC in culture were treated with gamma interferon to induce class II expression. TEC were then cocultivated with staphylococcus enterotoxin and cloned T cells or highly purified peripheral T cells. After 1–2 days, release of interleukin 2 and of gamma interferon was seen; after 3–5 days T cell proliferation occurred. The proliferation could be inhibited by antibodies to class II antigens or by antibodies to ICAM-1; the latter is also expressed on TEC in inflammatory processes and on TEC in culture as well. In conclusion, human TEC might function as accessory cells for T cell activation and might support T cell dependent immune response.
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