In the past Carol Cowing has collaborated on articles with Georg Widera and David Lo. One of their most recent publications is Short communicationStrain differences in tolerance induction to human γ-globulin subclasses: Dependence on macrophages☆. Which was published in journal Cellular Immunology.

More information about Carol Cowing research including statistics on their citations can be found on their Copernicus Academic profile page.

Carol Cowing's Articles: (4)

Short communicationStrain differences in tolerance induction to human γ-globulin subclasses: Dependence on macrophages☆

AbstractBALB/c and DBA/2 mice differ with respect to ease of tolerance induction with HGG, BALB/c mice being the resistant strain. When tested for susceptibility to tolerance induction with individual IgG subclasses, both strains were easily rendered unresponsive with IgG1 and IgG2 and less so with IgG4. A strain difference appeared with IgG3, where only BALB/c mice showed complete resistance to tolerance induction. Mixtures of the IgG subclasses Showed that IgG1 and IgG2 accounted for most of the tolerance to whole HGG seen in both strains, while addition of IgG3 to the mixture made DBA/2 completely tolerant but reversed the trend toward tolerance in the BALB/c mice. By rosette assay it was found that BALB/c macrophages had receptors for IgG3 (and to a lesser extent for IgG4). These results are consistent with the hypothesis that resistance to tolerance induction with HGG is dependent on the presence of a receptor on the macrophage for a minor IgG subclass.

ArticleTransgenic mice selectively lacking MHC class II (I-E) antigen expression on B cells: An in vivo approach to investigate la gene function

AbstractThe Ea MHC class II gene with 1.4 kb of 5′-flanking and 0.5 kb of 3′-flanking sequences was introduced into (H-2b × s)F2 mice, which do not express their endogenous Ea gene. The transgene was expressed in thymic tissue and in adherent spleen cells and was induced in peritoneal exudate cells by α-interferon. In contrast to the normal Ea gene, there was no expression in B lymphocytes. Since transgenic animals made with constructs containing 3.2 kb and 2 kb of 5′-flanking sequences show normal expression pattern of the Ea gene, it appears that deletion of 5′-flanking sequences between −1.4 kb and −2 kb inactivated or eliminated regulatory sequences required for expression of Ea specifically in B cells. The presence of pBR327 DNA linked to the −1.4 kb Ea transgene suppresses expression in peripheral adherent cells, yielding mice expressing Ea only in the thymus. These mice appear to be tolerant to I-E, as measured in mixed leukocyte response experiments.

Diabetes and tolerance in transgenic mice expressing class II MHC molecules in pancreatic beta cells

AbstractInsulin-dependent diabetes is caused by the loss of insulin-producing beta cells in pancreatic islets. It has been proposed that aberrant expression of Class II Major Histocompatibility Complex (MHC) molecules on beta cells stimulates an autoimmune attack against beta cell antigens. To test this hypothesis, we generated transgenic mice that express Class II MHC molecules (Eαd/Eβb, or I-Eb) on beta cells. Diabetes was found in 100% of transgenic progeny from three expressing transgenic mouse lines, but without evidence for lymphocytic infiltrates. Furthermore, T lymphocytes appeared to be tolerant to the transgene I-Eb molecule, despite the absence of expression of I-Eb in the thymus or any other lymphoid tissue. The results suggest that novel expression of Class II MHC molecules on nonlymphoid cells is by itself insufficient to initiate autoimmune responses against tissue-specific antigens.


Publisher SummaryThis chapter presents the cellular basis for establishing tolerance or immunity to bovine γ-globulin (BGG) in mice. In an experiment discussed in the chapter, the capacity of the reticuloendothelial systems of BALB/c and DBA/2 mice is compared to remove immunogenic material by studying biologic filtration in vivo. Large amounts of l25I-trace labeled BGG were given to groups of mice of either strain. Two days later they were bled out and the amount of residual BGG in the serum was estimated by scintillation counting. Various doses of this biologically-filtered BGG were given to normal BALB/c mice and their subsequent development of tolerance or immunity was assessed in the usual way. The cell responsible for resistance to tolerance induction in BALB/c mice is especially capable of filtering out an immunogenic fraction of ultracentrifuged BGG; this ability is undiminished by lethal irradiation, is abrogated by a macrophage-toxic substance, and resides in an adherent cell population.

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