HLA-B∗1502–bound peptides: Implications for the pathogenesis of carbamazepine-induced Stevens-Johnson syndrome

Yang, Chih-Wen Ou; Chung, Wen‐Hung; Juo, Chiun-Gung; Lin, Ya‐Ping; Fang, Wu-Hsiang; Lu, I-Ling; Chen, Shui‐Tein; Chen, Yuan-Tsong

doi:10.1016/j.jaci.2007.06.017

Cited by 119 publications

(96 citation statements)

References 45 publications

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“…The bacterial membrane fraction (4 g) was incubated with 20 l of hRNase 7-conjugated gel in 10 mM sodium phosphate, pH 7.4. Specific proteins were pulled down by hRNase 7-conjugated gel, verified by competition assay with excess amounts of free hRNase 7, excised from SDS-PAGE gel, and subjected to in-gel trypsin digestion and liquid chromatography-tandem mass spectrometry as described previously (19).…”

Section: Methodsmentioning

confidence: 99%

Outer Membrane Protein I of Pseudomonas aeruginosa Is a Target of Cationic Antimicrobial Peptide/Protein

Lin

Chang

et al. 2010

Journal of Biological Chemistry

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Cationic antimicrobial peptides/proteins (AMPs) are important components of the host innate defense mechanisms against invading microorganisms. Here we demonstrate that OprI (outer membrane protein I) of Pseudomonas aeruginosa is responsible for its susceptibility to human ribonuclease 7 (hRNase 7) and ␣-helical cationic AMPs, instead of surface lipopolysaccharide, which is the initial binding site of cationic AMPs. The antimicrobial activities of hRNase 7 and ␣-helical cationic AMPs against P. aeruginosa were inhibited by the addition of exogenous OprI or anti-OprI antibody. On modification and internalization of OprI by hRNase 7 into cytosol, the bacterial membrane became permeable to metabolites. The lipoprotein was predicted to consist of an extended loop at the N terminus for hRNase 7/lipopolysaccharide binding, a trimeric ␣-helix, and a lysine residue at the C terminus for cell wall anchoring. Our findings highlight a novel mechanism of antimicrobial activity and document a previously unexplored target of ␣-helical cationic AMPs, which may be used for screening drugs to treat antibiotic-resistant bacterial infection.

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Section: Methodsmentioning

confidence: 99%

Outer Membrane Protein I of Pseudomonas aeruginosa Is a Target of Cationic Antimicrobial Peptide/Protein

Lin

Chang

et al. 2010

Journal of Biological Chemistry

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“…14 At present, several HLA haplotypes are associated with a high risk for some CADR, particularly HLA-B*57:01 for abacavir hypersensitivity syndrome, 15,16 and HLA-B*15:02 for carbamazepine-induced SJS/TEN in Han Chinese. [17][18][19] As there are few studies from Europe, the objective of our work was to evaluate whether this HLA allele also has a higher association with allopurinol-induced sCADR in our population and to calculate the relative risk of HLA-B*58:01 carriers in developing sCADR from allopurinol.…”

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confidence: 99%

HLA-B58:01*is a risk factor for allopurinol-induced DRESS and Stevens-Johnson syndrome/toxic epidermal necrolysis in a Portuguese population

et al. 2013

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“…Abacavir and carbamazepine are thought to cause TEN through the altered peptide model 15,16 . A direct interaction between carbamazepine and HLA-B* 1502 may induce TEN 17,18 . Genetic susceptibility may be explained by the possibility that specific drug-related HLA alleles increases the likelihood of TEN happening 19 21 .…”

Section: Drug Antigen Presentationmentioning

confidence: 99%

A Review of the Pathogenesis of Toxic Epidermal Necrolysis

Kinoshita

Saeki

2016

J Nippon Med Sch

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Toxic epidermal necrolysis (TEN) is a rare skin condition, most often drug-induced, known for its skin detachment and high mortality. In general, acute TEN is considered a T-cell mediated, type IV hypersensitivity disorder. It mostly results from a cumulative effect of risks from the drug structure, drug metabolism, HLA alleles and T cell clonotypes. However, the precise mechanism of TEN is still unknown.Apoptosis or necroptosis causes keratinocytes to lose their shape and adhesion, and necrosis predominates within a few days. Total epidermal necrosis separates the epidermis from the dermis. TEN is regarded as an immune reaction with predominantly CD8+ T lymphocytes, monocytes/macrophages, and natural killer cells. Impaired regulatory T-cells, T-helper 17 cells, cytotoxic granules such as perforingranzyme and granulysin, tumor necrosis factor α, annexin, microRNA-18a-5p, and drug metabolites are all thought to be involved. From what is known, it can be assumed their mechanism is complex, and there is still much to be investigated. New findings will contribute to the identification of effective active methods of intervention. (J Nippon Med Sch 2016; 83: 216 222)

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HLA-B∗1502–bound peptides: Implications for the pathogenesis of carbamazepine-induced Stevens-Johnson syndrome

Cited by 119 publications

References 45 publications

Outer Membrane Protein I of Pseudomonas aeruginosa Is a Target of Cationic Antimicrobial Peptide/Protein

Outer Membrane Protein I of Pseudomonas aeruginosa Is a Target of Cationic Antimicrobial Peptide/Protein

HLA-B58:01*is a risk factor for allopurinol-induced DRESS and Stevens-Johnson syndrome/toxic epidermal necrolysis in a Portuguese population

A Review of the Pathogenesis of Toxic Epidermal Necrolysis

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HLA-B∗1502–bound peptides: Implications for the pathogenesis of carbamazepine-induced Stevens-Johnson syndrome

Cited by 119 publications

References 45 publications

Outer Membrane Protein I of Pseudomonas aeruginosa Is a Target of Cationic Antimicrobial Peptide/Protein

Outer Membrane Protein I of Pseudomonas aeruginosa Is a Target of Cationic Antimicrobial Peptide/Protein

HLA-B*58:01is a risk factor for allopurinol-induced DRESS and Stevens-Johnson syndrome/toxic epidermal necrolysis in a Portuguese population

A Review of the Pathogenesis of Toxic Epidermal Necrolysis

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HLA-B58:01*is a risk factor for allopurinol-induced DRESS and Stevens-Johnson syndrome/toxic epidermal necrolysis in a Portuguese population