Pathogenicity of Type I Interferons in Mycobacterium tuberculosis .
Akaash MundraAram YegiazaryanHaig KarsianDijla AlsaighVictor BonavidaMitchell FrameNicole MayAreg GargaloyanArbi AbnousianVishwanath VenketaramanPublished in: International journal of molecular sciences (2023)
Tuberculosis (TB) is a leading cause of mortality due to infectious disease and rates have increased during the emergence of COVID-19, but many of the factors determining disease severity and progression remain unclear. Type I Interferons (IFNs) have diverse effector functions that regulate innate and adaptive immunity during infection with microorganisms. There is well-documented literature on type I IFNs providing host defense against viruses; however, in this review, we explore the growing body of work that indicates high levels of type I IFNs can have detrimental effects to a host fighting TB infection. We report findings that increased type I IFNs can affect alveolar macrophage and myeloid function, promote pathological neutrophil extracellular trap responses, inhibit production of protective prostaglandin 2, and promote cytosolic cyclic GMP synthase inflammation pathways, and discuss many other relevant findings.
Keyphrases
- mycobacterium tuberculosis
- infectious diseases
- pulmonary tuberculosis
- immune response
- dendritic cells
- coronavirus disease
- sars cov
- systematic review
- oxidative stress
- biofilm formation
- adipose tissue
- acute myeloid leukemia
- cardiovascular events
- escherichia coli
- emergency department
- regulatory t cells
- cardiovascular disease
- hiv aids
- type iii
- genetic diversity
- drug induced