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Literature summary for 3.3.2.6 extracted from

  • Narendran, G.; Kavitha, D.; Karunaianantham, R.; Gil-Santana, L.; Almeida-Junior, J.L.; Reddy, S.D.; Kumar, M.M.; Hemalatha, H.; Jayanthi, N.N.; Ravichandran, N.; Krishnaraja, R.; Prabhakar, A.; Manoharan, T.; Nithyananthan, L.; Arjunan, G.; Natrajan, M.; Swaminathan, S.; Andrade, B.B.
    Role of LTA4H polymorphism in tuberculosis-associated immune reconstitution inflammatory syndrome occurrence and clinical severity in patients infected with HIV (2016), PLoS ONE, 11, e0163298 .
    View publication on PubMedView publication on EuropePMC

Organism

Organism UniProt Comment Textmining
Homo sapiens P09960
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Synonyms

Synonyms Comment Organism
leukotriene A4 hydrolase
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Homo sapiens
LTA4H
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Homo sapiens

General Information

General Information Comment Organism
malfunction leukotriene A4 hydrolase (LTA4H) regulates the balance between the anti-inflammatory lipoxins and pro-inflammatory leukotriene B4, with direct implications in tuberculosis-driven inflammation. In humans, a single nucleotide polymorphism in the LTA4H promoter which regulates its transcriptional activity (rs17525495) is identified and described to impact clinical severity of tuberculosis presentation and response to corticosteroid therapy. A higher incidence of severe tuberculosis-associated immune reconstitution inflammatorysyndrome among patients with mutant LTA4H genotypes is observed compared to the wild type, despite similar incidence of tuberculosis-associated immune reconstitution inflammatory syndrome and similar immune restoration in both groups. Steroids are effective in alleviating IRIS in all the genotypes Homo sapiens
physiological function leukotriene A4 hydrolase (LTA4H) regulates the balance between the anti-inflammatory lipoxins and pro-inflammatory leukotriene B4, with direct implications in tuberculosis-driven inflammation. In humans, a single nucleotide polymorphism in the LTA4H promoter which regulates its transcriptional activity (rs17525495) is identified and described to impact clinical severity of tuberculosis presentation and response to corticosteroid therapy. A higher incidence of severe tuberculosis-associated immune reconstitution inflammatorysyndrome among patients with mutant LTA4H genotypes is observed compared to the wild type, despite similar incidence of tuberculosis-associated immune reconstitution inflammatory syndrome and similar immune restoration in both groups. Steroids are effective in alleviating IRIS in all the genotypes Homo sapiens