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See detailTesting the 'toxin hypothesis of allergy': mast cells, IgE, and innate and acquired immune responses to venoms.
Tsai, Mindy; Starkl, Philipp; Marichal, Thomas ULg et al

in Current opinion in immunology (2015), 36

Work in mice indicates that innate functions of mast cells, particularly degradation of venom toxins by mast cell-derived proteases, can enhance resistance to certain arthropod or reptile venoms. Recent ... [more ▼]

Work in mice indicates that innate functions of mast cells, particularly degradation of venom toxins by mast cell-derived proteases, can enhance resistance to certain arthropod or reptile venoms. Recent reports indicate that acquired Th2 immune responses associated with the production of IgE antibodies, induced by Russell's viper venom or honeybee venom, or by a component of honeybee venom, bee venom phospholipase 2 (bvPLA2), can increase the resistance of mice to challenge with potentially lethal doses of either of the venoms or bvPLA2. These findings support the conclusion that, in contrast to the detrimental effects associated with allergic type 2 (Th2) immune responses, mast cells and IgE-dependent immune responses to venoms can contribute to innate and adaptive resistance to venom-induced pathology and mortality. [less ▲]

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See detailTolerance to the Foeto-Placental 'Graft': Ten Ways to Support a Child for Nine Months
Thellin, Olivier ULg; Coumans, Bernard ULg; Zorzi, Willy ULg et al

in Current Opinion in Immunology (2000), 12(6), 731-7

Tolerance to the foetal 'allograft' has been extensively studied in the past few years, providing interesting new insights. In addition to a potential role for HLA-G, which has been widely discussed ... [more ▼]

Tolerance to the foetal 'allograft' has been extensively studied in the past few years, providing interesting new insights. In addition to a potential role for HLA-G, which has been widely discussed, there are hypotheses suggesting roles for several other molecules or cells: leukemia inhibitory factor and its receptor; indoleamine 2. 3-dioxygenase; the Th1/Th2 balance; suppressor macrophages; hormones such as progesterone or the placental growth hormone; CD95 and its ligand; and, as recently proposed, annexin II. Tolerance of the foetal allograft is probably the consequence of a wide panel of mechanisms that may or may not be pregnancy-specific, that are of major or secondary importance and that may be interconnected. [less ▲]

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