About: Nickel (Ni) allergy has been reported in contact dermatitis Type IV (Ni-specific T cells mediated) and asthmatic Type I (IgE-mediated) hypersensitivities. Associations between the two hypersensitivities have been found in some patients, but the underlying mechanisms remain enigmatic. Using Her2-specific IgEs as models, we found additional binding to Ni-NTA without observable changes in binding to Her2 and that glutamine, together with the canonical Ni2+-binding histidine, could form Ni2+ binding signatures. This mechanism may underlie Type I hypersensitivity in the selection of anti-Ni2+ IgEs. This mechanism may also underlie Type IV hypersensitivity and the interaction of immunoglobulin proteins with other heavy metal ions. Our findings shed light to how Ni hypersensitivities can occur and how they can be avoided in therapeutics design, or even incorporated for biotechnological purification purposes.

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About: Nickel (Ni) allergy has been reported in contact dermatitis Type IV (Ni-specific T cells mediated) and asthmatic Type I (IgE-mediated) hypersensitivities. Associations between the two hypersensitivities have been found in some patients, but the underlying mechanisms remain enigmatic. Using Her2-specific IgEs as models, we found additional binding to Ni-NTA without observable changes in binding to Her2 and that glutamine, together with the canonical Ni2+-binding histidine, could form Ni2+ binding signatures. This mechanism may underlie Type I hypersensitivity in the selection of anti-Ni2+ IgEs. This mechanism may also underlie Type IV hypersensitivity and the interaction of immunoglobulin proteins with other heavy metal ions. Our findings shed light to how Ni hypersensitivities can occur and how they can be avoided in therapeutics design, or even incorporated for biotechnological purification purposes. Goto Sponge NotDistinct Permalink

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value	Nickel (Ni) allergy has been reported in contact dermatitis Type IV (Ni-specific T cells mediated) and asthmatic Type I (IgE-mediated) hypersensitivities. Associations between the two hypersensitivities have been found in some patients, but the underlying mechanisms remain enigmatic. Using Her2-specific IgEs as models, we found additional binding to Ni-NTA without observable changes in binding to Her2 and that glutamine, together with the canonical Ni2+-binding histidine, could form Ni2+ binding signatures. This mechanism may underlie Type I hypersensitivity in the selection of anti-Ni2+ IgEs. This mechanism may also underlie Type IV hypersensitivity and the interaction of immunoglobulin proteins with other heavy metal ions. Our findings shed light to how Ni hypersensitivities can occur and how they can be avoided in therapeutics design, or even incorporated for biotechnological purification purposes.
subject	Nickel Hypersensitivity Biology and pharmacology of chemical elements Chemical elements Computer-aided design software »more»
part of	Molecular insight into Nickel(II) binding by Her2-specific IgE: a possible mechanistic insight into the pathogenesis of Type I nickel hypersensitivity
is abstract of	Molecular insight into Nickel(II) binding by Her2-specific IgE: a possible mechanistic insight into the pathogenesis of Type I nickel hypersensitivity
is hasSource of	covid:ann/target/ffc71e5226e82b69fb6dd8028275cb67c0787375 covid:ann/target/e683faaee2a753f1e0321abd3455c78a4b804e54 covid:ann/target/8581971d4bb39a737d6223889821d334ac5ccf16 covid:ann/target/26075c910ec02d4b237a9fc1f61c1056b8bdcb9e covid:ann/target/c013dea61b87db1dd6d680cbacca3a7bd329da1d »more»

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