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Latent Tuberculosis Patients Have an Increased Frequency of IFN-γ-Producing CD5+ B Cells, Which Respond Efficiently to Mycobacterial Proteins.

Authors :
Flores-Gonzalez, Julio
Ramón-Luing, Lucero A.
Romero-Tendilla, Jesus
Urbán-Solano, Alexia
Cruz-Lagunas, Alfredo
Chavez-Galan, Leslie
Source :
Pathogens; Jun2023, Vol. 12 Issue 6, p818, 17p
Publication Year :
2023

Abstract

Tuberculosis (TB) remains a public health problem worldwide and is one of the deadliest infectious diseases, only after the current COVID-19 pandemic. Despite significant advances in the TB field, there needs to be more immune response comprehension; for instance, the role played by humoral immunity is still controversial. This study aimed to identify the frequency and function of B1 and immature/transitional B cells in patients with active and latent TB (ATB and LTB, respectively). Here we show that LTB patients have an increased frequency of CD5+ B cells and decreased CD10+ B cells. Furthermore, LTB patients stimulated with mycobacteria's antigens increase the frequency of IFN-γ-producing B cells, whereas cells from ATB do not respond. Moreover, under the mycobacterial protein stimulus, LTB promotes a pro-inflammatory environment characterized by a high level of IFN-γ but also can produce IL-10. Regarding the ATB group, they cannot produce IFN-γ, and mycobacterial lipids and proteins stimulate only the IL-10 production. Finally, our data showed that in ATB, but not in LTB, B cell subsets correlate with clinical and laboratory parameters, suggesting that these CD5+ and CD10+ B cell subpopulations have the potential to be biomarkers to differentiate between LTB and ATB. In conclusion, LTB has increased CD5+ B cells, and these cells can maintain a rich microenvironment of IFN-γ, IL-10, and IL-4. In contrast, ATB only maintains an anti-inflammatory environment when stimulated with mycobacterial proteins or lipids. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
20760817
Volume :
12
Issue :
6
Database :
Complementary Index
Journal :
Pathogens
Publication Type :
Academic Journal
Accession number :
164703124
Full Text :
https://doi.org/10.3390/pathogens12060818