TY - JOUR
T1 - Differential activation of dendritic cells by Mycobacterium tuberculosis Beijing genotype
AU - Reyes-Martínez, Juana Elizabeth
AU - Nieto-Patlán, Erik
AU - Nieto-Patlán, Alejandro
AU - Gonzaga-Bernachi, Job
AU - Santos-Mendoza, Teresa
AU - Serafín-López, Jeanet
AU - Chávez-Blanco, Alma
AU - Sandoval-Montes, Claudia
AU - Flores-Romo, Leopoldo
AU - Estrada-Parra, Sergio
AU - Estrada-García, Iris
AU - Chacón-Salinas, Rommel
N1 - Funding Information:
This work was supported by SIP, IPN and Conacyt (157100 CB-2010-01).
PY - 2014
Y1 - 2014
N2 - Mycobacterium tuberculosis (Mtb) inhibits dendritric cells (DC) function in order to delay T cell response. Furthermore, there is increasing evidence that genetic diversity of Mtb strains can affect their interaction with the immune system. Beijing genotype has attracted attention because of its high prevalence and multi-drug resistance. Although it is known that this genotype is hypervirulent and differentially activates macrophages when compared to other genotypes, little is known about its interaction with DC. In order to address this issue, murine bone marrow derived DC (BMDC) were stimulated with soluble extracts (SE) from BCG, H37Rv, Canetti and Beijing genotypes. We observed that unlike other mycobacteria strains, SE-Beijing was unable to induce maturation of DC as assessed by cell surface MHC-II expression. DC stimulated with SE-Beijing failed to produce IL-12 and TNF-α, but did secrete IL-10. Interestingly, SE-Beijing induced CCR7 and PDL-1 on BMDC, but did not induce the expression of CD86. When BMDC stimulated with SE-Beijing were used to activate CD4+ cells they were unable to induce a Th1 response when compared with less virulent genotypes. These results indicate that Beijing is able to modulate DC activation and function, which may be related to the pathogenesis induced by this genotype.
AB - Mycobacterium tuberculosis (Mtb) inhibits dendritric cells (DC) function in order to delay T cell response. Furthermore, there is increasing evidence that genetic diversity of Mtb strains can affect their interaction with the immune system. Beijing genotype has attracted attention because of its high prevalence and multi-drug resistance. Although it is known that this genotype is hypervirulent and differentially activates macrophages when compared to other genotypes, little is known about its interaction with DC. In order to address this issue, murine bone marrow derived DC (BMDC) were stimulated with soluble extracts (SE) from BCG, H37Rv, Canetti and Beijing genotypes. We observed that unlike other mycobacteria strains, SE-Beijing was unable to induce maturation of DC as assessed by cell surface MHC-II expression. DC stimulated with SE-Beijing failed to produce IL-12 and TNF-α, but did secrete IL-10. Interestingly, SE-Beijing induced CCR7 and PDL-1 on BMDC, but did not induce the expression of CD86. When BMDC stimulated with SE-Beijing were used to activate CD4+ cells they were unable to induce a Th1 response when compared with less virulent genotypes. These results indicate that Beijing is able to modulate DC activation and function, which may be related to the pathogenesis induced by this genotype.
KW - Beijing genotype
KW - Cytokine production
KW - Dendritic cells
KW - Mycobacterium tuberculosis
UR - http://www.scopus.com/inward/record.url?scp=84901593879&partnerID=8YFLogxK
U2 - 10.3109/08820139.2014.880120
DO - 10.3109/08820139.2014.880120
M3 - Artículo
C2 - 24654560
SN - 0882-0139
VL - 43
SP - 436
EP - 446
JO - Immunological Investigations
JF - Immunological Investigations
IS - 5
ER -