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Non‐tuberculous mycobacteria immunopathogenesis: Closer than they appear. a prime of innate immunity trade‐off and NTM ways into virulence
Author(s) -
CruzAguilar Marisa,
CastilloRodal Antonia I.,
ArredondoHernández René,
LópezVidal Yolanda
Publication year - 2021
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/sji.13035
Subject(s) - immunology , immune system , biology , immunity , innate immune system , disease , single nucleotide polymorphism , snp , medicine , genotype , genetics , gene , pathology
The growing incidence of non‐tuberculous mycobacteria (NTM) and changes in epidemiological factors have indicated that immune dysregulation may be associated with the emergence of NTM. Minireview entails to acknowledge complex interaction and new ways NTM are evolving around diverse immune status. Methods In order to perform this review, we selected peer reviewed, NLM database articles under the terms NTM, mycobacterium complex ‘AND’ ‐Host‐ immune response, immunity regulation, Disease, Single Nucleotide Polymorphism (SNP´s), and ‐pathogen‐ followed by a snow ball rolling basis search on immune components and NTM related with diseases distribution. Results The universal exposure and diversity of NTM are well‐documented; however, hospitals seldom establish vigilant control of water quality or immunodeficiencies for patients with NTM infections. Depending on the chemical structures and immune mechanisms presented by various NTM varieties, they can trigger different effects in dendritic and natural killer cells, which release interleukin (IL)‐17, tumour necrosis factor‐α (TNF‐α), interferon‐γ (IFN‐γ) and rIL‐1B. The T helper (Th)2‐acquired immune response is responsible for autoimmune responses in patients with NTM infections, and, quite disturbingly, immunocompetent patients have been reported to suffer from NTM infections. Conclusion New technologies and a comprehensive view has taught us; to acknowledge metabolic/immune determinants and trade‐offs along transit through mutualism‐parasite continuous.