Structural basis of metal hypersensitivity

Wang, Yan; Dai, Shaodong

doi:10.1007/s12026-012-8351-1

Cited by 60 publications

(49 citation statements)

References 70 publications

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“…This assumption is based on the observation of lymphocyte subpopulations in the peri-implant tissues surrounding MoM implants and on the well-characterized ability of metal ions to activate adaptive immunity by acting as haptens with host proteins. 91 The best characterized example of this type IV hypersensitivity reaction is dermal allergy to nickel. 92 Despite the fact that a similar dermal allergy can develop against cobalt and chromium, the extent to which type IV hypersensitivity contributes to the reaction against implant-derived metals is still somewhat controversial.…”

Section: Metal Wear and The Role Of Adaptive Immune Systemmentioning

confidence: 99%

Innate Immune Reactions in Septic and Aseptic Osteolysis around Hip Implants

Pajarinen

Jämsen

Konttinen

et al. 2014

J Long Term Eff Med Implants

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According to the long-standing definition, septic and aseptic total joint replacement loosening are two distinct conditions with little in common. Septic joint replacement loosening is driven by bacterial infection whereas aseptic loosening is caused by biomaterial wear debris released from the bearing surfaces. However, recently it has been recognized that the mechanisms that drive macrophage activation in septic and aseptic total joint replacement loosening resemble each other. In particular, accumulating evidence indicates that in addition to mediating bacterial recognition and the subsequent inflammatory reaction, toll-like receptors (TLRs) and their ligands, pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPS), play a key role in wear debris-induced inflammation and macrophage activation. In addition, subclinical bacterial biofilms have been identified from some cases of seemingly aseptic implant loosening. Furthermore, metal ions released from some total joint replacements can activate TLR signaling similar to bacterial derived PAMPs. Likewise, metal ions can function as haptens activating the adaptive immune system similar to bacterial derived antigens. Thus, it appears that aseptic and septic joint replacement loosening share similar underlying pathomechanisms and that this strict dichotomy to sterile aseptic and bacterial-caused septic implant loosening is somewhat questionable. Indeed, rather than being two, well-defined clinical entities, peri-implant osteolysis is, in fact, a spectrum of conditions in which the specific clinical picture is determined by complex interactions of multiple local and systemic factors.

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Section: Metal Wear and The Role Of Adaptive Immune Systemmentioning

confidence: 99%

Innate Immune Reactions in Septic and Aseptic Osteolysis around Hip Implants

Pajarinen

Jämsen

Konttinen

et al. 2014

J Long Term Eff Med Implants

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“…This last class was created because the HLA-DR structure is similar to the HLA-DP2 structure [6], which provides the opportunity to compare the physical properties of peptides binding to HLA-DR and HLA-DP2. All peptides in each class were cut to a length of 10 amino acids.…”

Section: Methodsmentioning

confidence: 99%

Chronic Beryllium Disease: Revealing the Role of Beryllium Ion and Small Peptides Binding to HLA-DP2

Petukh

Stefl

et al. 2014

PLoS ONE

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Chronic Beryllium (Be) Disease (CBD) is a granulomatous disorder that predominantly affects the lung. The CBD is caused by Be exposure of individuals carrying the HLA-DP2 protein of the major histocompatibility complex class II (MHCII). While the involvement of Be in the development of CBD is obvious and the binding site and the sequence of Be and peptide binding were recently experimentally revealed [1], the interplay between induced conformational changes and the changes of the peptide binding affinity in presence of Be were not investigated. Here we carry out in silico modeling and predict the Be binding to be within the acidic pocket (Glu26, Glu68 and Glu69) present on the HLA-DP2 protein in accordance with the experimental work [1]. In addition, the modeling indicates that the Be ion binds to the HLA-DP2 before the corresponding peptide is able to bind to it. Further analysis of the MD generated trajectories reveals that in the presence of the Be ion in the binding pocket of HLA-DP2, all the different types of peptides induce very similar conformational changes, but their binding affinities are quite different. Since these conformational changes are distinctly different from the changes caused by peptides normally found in the cell in the absence of Be, it can be speculated that CBD can be caused by any peptide in presence of Be ion. However, the affinities of peptides for Be loaded HLA-DP2 were found to depend of their amino acid composition and the peptides carrying acidic group at positions 4 and 7 are among the strongest binders. Thus, it is proposed that CBD is caused by the exposure of Be of an individual carrying the HLA-DP2*0201 allele and that the binding of Be to HLA-DP2 protein alters the conformational and ionization properties of HLA-DP2 such that the binding of a peptide triggers a wrong signaling cascade.

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“…Allergic contact dermatitis to nickel is common, estimated to affect 10 % of the human population [108]. More significant allergic reactions, including reactive airway disease, have been reported [109,110].…”

Section: Clinical Presentation and Lifethreatening Complicationsmentioning

confidence: 99%

Antimony and Nickel

Sztajnkrycer¹

2016

Critical Care Toxicology

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Structural basis of metal hypersensitivity

Cited by 60 publications

References 70 publications

Innate Immune Reactions in Septic and Aseptic Osteolysis around Hip Implants

Innate Immune Reactions in Septic and Aseptic Osteolysis around Hip Implants

Chronic Beryllium Disease: Revealing the Role of Beryllium Ion and Small Peptides Binding to HLA-DP2

Antimony and Nickel

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