TCRbeta enhancer activation in early and late lymphoid progenitors.

An earlier report from our laboratory indicates that the activation of the T cell receptor (TCR) beta enhancer (Ebeta) is not always an indicator of T lineage potential in bone marrow-resident pre-lymphocytes. In order to more precisely investigate the consequences of Ebeta activation in lymphopoiesis, a genetic reporter animal, in which the expression of green fluorescent protein (GFP) is controlled by Ebeta, was used to examine two well-defined lymphopotent populations. Adoptive transfer experiments suggest that primitive lymphoid precursor populations (specifically, hematopoietic stem cells) consist of two discrete-populations discernible by Ebeta-GFP activation, although the two populations display no overt differences in lineage potential.

Inhibitory receptor gp49B regulates eosinophil infiltration during allergic inflammation.

gp49B, an Ig-like receptor, negatively regulates the activity of mast cells and neutrophils through cytoplasmic immunoreceptor tyrosine-based inhibition motifs. To characterize the role of gp49B further in vivo, gp49B-deficient mice were tested in two allergic models. Responses to ragweed (RW) challenge in the lung and conjunctiva were assessed in models of allergic inflammation and during an infection with parasitic larvae of the nematode Ascaris suum.

Ascaris suum-derived products suppress mucosal allergic inflammation in an interleukin-10-independent manner via interference with dendritic cell function.

We have previously demonstrated that protection from allergic inflammation by Ascaris suum infection was characterized by a global increase in interleukin-10 (IL-10) and the development of protective CD4(+)/CD25(+) T cells (L. Schopf, S. Luccioli, V.

Differential modulation of allergic eye disease by chronic and acute ascaris infection.

Purpose: To assess alterations in allergic ocular responses to nonparasite antigens in an experimental system in which mice were skewed toward a Th2 cytokine profile by helminth infection.

Methods: Mice were inoculated with Ascaris suum (A. suum) eggs concurrent with ragweed (RW) sensitization (RW/acute) or by repeated inoculation before RW sensitization (RW/chronic).

Regulation of chronic colitis in athymic nu/nu (nude) mice.

The objective of this study was to assess the roles of NK cells, B cells and/or intraepithelial lymphocytes (IEL) in suppressing the development of colitis in nude mice reconstituted with CD4(+)CD45RB(high) T cells. BALB/c nude mice were lethally irradiated and reconstituted with bone marrow from different immunodeficient mice to generate athymic chimeras devoid of one or more lymphocyte populations. Transfer of CD4(+)C45RB(high) T cells into chimeric recipients devoid of B cells, T cells and IEL produced severe colitis within 6-8 weeks, whereas transfer of these same T cells into B cell- and T cell-deficient or T cell-deficient chimeras produced little to no gut inflammation.

TCRbeta enhancer activation occurs in some but not all cells with T cell lineage developmental potential.

Previous studies have shown that murine bone marrow contains a fraction of CD3(-)/B220(-)/Thy1(lo) cells that have pre T cell activity following adoptive transfer and produce sterile transcripts of the T cell receptor beta chain gene. The relationship between progenitors and TCRbeta transcription has not been examined. Transgenic mice were generated that express green fluorescent protein under the control of the TCRbeta enhancer (Ebeta).