By Frank J. Dixon

The fiftieth quantity in a monographic sequence on immunology. one of the issues lined listed here are avian T-cell ontogeny, adoptive move of human lymphoid cells to significantly immuno-deficient mice and histamine-releasing elements and cytokine-dependent activation of basophils and mast cells.

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Alternatively, one may argue that deletion of developing T cells by Vbse that work in concert with I-E are allowable, just as the absence of I-E is allowable, but that Vbse that delete developing T cells in association with I-A are not permissible just as I-A-negative mice have not been observed. The Vbse that associate with I-A may have too low an affinity for the Vp site on the TCR to cause frank deletion, as this effect would be too deleterious to the host. , 1989a,b, 1990). Thus, HLA-DQ is clearly competent to present bacterial toxic mitogens.

This virus is unrelated to Mtv and lacks the orfgene of the Mtv Vp SELECTIVE ELEMENTS 41 viruses. Nevertheless, it appears to encode a Vbse. Alternatively, it could be that the transformed B cell is expressing an Mtv sequence that is normally silent in the mouse strain from which it was derived, but that becomes active upon transformation, although this leaves the role of the gag protein open. This issue needs to be resolved. Nevertheless, it is wise to keep in mind the possibility that viruses other than the MMTV may encode Vbse.

Apparently, MMTV genomes have inserted into the germ line of mice over the past million years, moving to several different locations and varying in structure (Coffin, 1990). This gives rise to the surprising complexity of Vbse inheritance. 40 CHARLES A. JANEWAY, JR. D. Mtv TRANSCRIPTS ARE HIGHLY EXPRESSED IN ACTIVATEDB CELLS As noted earlier, B cells are the main stimulator type in responses to Vbse. Although MMTV and Mtv sequences were thought to be expressed predominantly in mammary gland, it is now known that Mtv is potently activated by B cell stimuli.

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