Role of Interferons in Mycobacterium tuberculosis Infection.
Gaithrri ShanmuganathanDavit OrujyanWilliam NarinyanNicole PoladianSanya DhamaArpitha ParthasarathyAlexandra HaDaniel TranPrathosh VelpuriKevin H NguyenVishwanath VenketaramanPublished in: Clinics and practice (2022)
Considerable measures have been implemented in healthcare institutions to screen for and treat tuberculosis (TB) in developed countries; however, in low- and middle-income countries, many individuals still suffer from TB's deleterious effects. TB is caused by an infection from the Mycobacterium tuberculosis ( M. tb ) bacteria. Symptoms of TB may range from an asymptomatic latent-phase affecting the pulmonary tract to a devastating active and disseminated stage that can cause central nervous system demise, musculoskeletal impairments, and genitourinary compromise. Following M. tb infection, cytokines such as interferons (IFNs) are released as part of the host immune response. Three main classes of IFNs prevalent during the immune defense include: type I IFN (α and β), type II IFN (IFN-γ), and type III IFN (IFN-λ). The current literature reports that type I IFN plays a role in diminishing the host defense against M. tb by attenuating T-cell activation. In opposition, T-cell activation drives type II IFN release, which is the primary cytokine mediating protection from M. tb by stimulating macrophages and their oxidative defense mechanisms. Type III IFN has a subsidiary part in improving the Th1 response for host cell protection against M. tb . Based on the current evidence available, our group aims to summarize the role that each IFN serves in TB within this literature review.
Keyphrases
- mycobacterium tuberculosis
- immune response
- dendritic cells
- pulmonary tuberculosis
- type iii
- healthcare
- systematic review
- emergency department
- stem cells
- pulmonary hypertension
- physical activity
- high throughput
- bone marrow
- mesenchymal stem cells
- cerebrospinal fluid
- electronic health record
- adverse drug
- antiretroviral therapy