Immunopathology of tuberculosis: roles of macrophages and monocytes

Fenton, Matthew J.; Vermeulen, Mary W.

doi:10.1128/iai.64.3.683-690.1996

Cited by 257 publications

(97 citation statements)

References 95 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Dendritic cells present in the lung migrate in order to prime T lymphocytes in the lymph nodes. It is believed that M. tuberculosis resides within the phagosome of the DC and exploits the migration thereby circulating within the host undetected (Fenton and Vermeulen, 1996;Henderson et al, 1997;Banchereau and Steinman, 1998). The discovery of new DC-SIGN binding ligands: DnaK, Cpn60.1, GAPDH and lprG, may help further research into designing inhibitors to prevent interactions between DC-SIGN and M. tuberculosis with the aim of blocking uptake and intracellular survival of mycobacterial cells.…”

Section: Resultsmentioning

confidence: 99%

Identification of four novel DC-SIGN ligands on Mycobacterium bovis BCG

Carroll

Sim

Bigi³

et al. 2010

Protein Cell

View full text Add to dashboard Cite

Dendritic-cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN; CD209) has an important role in mediating adherence of Mycobacteria species, including M. tuberculosis and M. bovis BCG to human dendritic cells and macrophages, in which these bacteria can survive intracellularly. DC-SIGN is a C-type lectin, and interactions with mycobacterial cells are believed to occur via mannosylated structures on the mycobacterial surface. Recent studies suggest more varied modes of binding to multiple mycobacterial ligands. Here we identify, by affinity chromatography and mass-spectrometry, four novel ligands of M. bovis BCG that bind to DC-SIGN. The novel ligands are chaperone protein DnaK, 60 kDa chaperonin-1 (Cpn60.1), glyceraldehyde-3 phosphate dehydrogenase (GAPDH) and lipoprotein lprG. Other published work strongly suggests that these are on the cell surface. Of these ligands, lprG appears to bind DC-SIGN via typical proteinglycan interactions, but DnaK and Cpn60.1 binding do not show evidence of carbohydrate-dependent interactions. LprG was also identified as a ligand for DC-SIGNR (L-SIGN; CD299) and the M. tuberculosis orthologue of lprG has been found previously to interact with human toll-like receptor 2. Collectively, these findings offer new targets for combating mycobacterial adhesion and within-host survival, and reinforce the role of DC-SIGN as an important host ligand in mycobacterial infection.

show abstract

Section: Resultsmentioning

confidence: 99%

Identification of four novel DC-SIGN ligands on Mycobacterium bovis BCG

Carroll

Sim

Bigi³

et al. 2010

Protein Cell

View full text Add to dashboard Cite

show abstract

“…Innate immune responses directed by macrophages predominate early in infection. Subsequent recruitment of dendritic cells leads to cell-mediated responses involving CD4 + and CD8 + T cells and eventual granuloma formation (for a review, see Fenton and Vermeulen, 1996;Flynn and Chan, 2001). The vast majority of immunocompetent individuals are able to contain, but not eliminate, the pathogen in pulmonary granulomas, leading to latent tuberculosis infection (Manabe and Bishai, 2000).…”

Section: Introductionmentioning

confidence: 99%

Mycobacterium tuberculosiscell envelope lipids and the host immune response

Karakousis

Bishai

Dorman

2004

Cellular Microbiology

130

106

View full text Add to dashboard Cite

“…Following the establishment of the adaptive response, T cells specific for mycobacterial antigens are generated and migrate to the affected site(s) of the lung. A number of cytokines and chemokines are produced locally resulting in an increased local inflammatory reaction and granuloma formation [17][18][19][20][21]. During this phase of the disease (2-4 weeks), T lymphocytes contribute to antimycobacterial defence by stimulating infected macrophages to kill intracellular mycobacteria [11,[21][22][23][24].…”

Section: Introductionmentioning

confidence: 99%

“…If macrophages fail to completely eradicate mycobacteria, even after activation by mycobacteria-specific T cells, a successful © 2004 Blackwell Publishing Ltd, Clinical and Experimental Immunology , 135 : [19][20][21][22][23][24][25][26][27][28] host strategy to control the disease largely relies on the ability to form well-developed lung granulomata and thus to contain mycobacterial spreading [27,28]. In cases when this goal is not achieved, infection progresses and affects additional areas of the lung.…”

Section: Introductionmentioning

confidence: 99%

Lung cell responses toM. tuberculosisin genetically susceptible and resistant mice following intratracheal challenge

Eruslanov

Majorov

Orlova

et al. 2003

Clinical and Experimental Immunology

View full text Add to dashboard Cite

SUMMARYOne approach to study the role of distinct cellular mechanisms in susceptibility/resistance to tuberculosis (TB) is to compare parameters of response to infection in the lungs of mouse strains exhibiting genetically determined differences in TB susceptibility/severity. Interstrain differences in antimycobacterial macrophage reactions, T cell responses & inflammation in the lungs of TB-susceptible I/St, TBresistant A/Sn and (I/St ¥ A/Sn)F1 mice were analysed following intratracheal inoculation of 10 3 CFUs of M. tuberculosis H37Rv. The antimycobacterial responses in the lungs of susceptible I/St mice were characterized by: (i) increased inflammatory infiltration by all major immune cell subsets; (ii) decreased type 1 cytokine production; (iii) impaired antimycobacterial activity of lung macrophages; (iv) unusually high proliferation of lung T lymphocytes. Differences in several parameters of anti-TB immunity between susceptible and resistant mice corresponded well to the polygenic pattern of TB control previously established in this mouse model. Importantly, lung macrophages isolated from noninfected mice were unable to respond to IFN-g by increasing their mycobactericidal function, but between weeks 3 and 5 of the infection this capacity developed in all mice. However, by this time point susceptible but not resistant mice demonstrated a pronounced decrease in IFN-g production by lung cells. This chain of events may explain the inability of I/St mice to control both early and chronic TB infection.

show abstract

Immunopathology of tuberculosis: roles of macrophages and monocytes

Cited by 257 publications

References 95 publications

Identification of four novel DC-SIGN ligands on Mycobacterium bovis BCG

Identification of four novel DC-SIGN ligands on Mycobacterium bovis BCG

Mycobacterium tuberculosiscell envelope lipids and the host immune response

Lung cell responses toM. tuberculosisin genetically susceptible and resistant mice following intratracheal challenge

Contact Info

Product

Resources

About