Increase of tuberculous infection in the organs of B cell-deficient mice

Vordermeier, H. M.; Venkataprasad, N.; Harris, David P.; Iványi, Juraj

doi:10.1046/j.1365-2249.1996.d01-845.x

Cited by 137 publications

(114 citation statements)

References 20 publications

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“…Despite this controversy, studies by our group and others have found that B cells can influence tuberculosis (TB) 3 susceptibility and pathologic progression in murine models (3)(4)(5). Moreover, the efficacy of specific mAbs (6 -8) and arabinomannan conjugate vaccines (9) against M. tuberculosis infection indicate that B cell biology may be augmented to enhance protection during TB.…”

mentioning

confidence: 99%

Fcγ Receptors Regulate Immune Activation and Susceptibility during Mycobacterium tuberculosis Infection

Maglione

Casadevall

et al. 2008

The Journal of Immunology

132

152

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The critical role of cellular immunity during tuberculosis (TB) has been extensively studied, but the impact of Abs upon this infection remains poorly defined. Previously, we demonstrated that B cells are required for optimal protection in Mycobacterium tuberculosis-infected mice. FcγR modulate immunity by engaging Igs produced by B cells. We report that C57BL/6 mice deficient in inhibitory FcγRIIB (RIIB−/−) manifested enhanced mycobacterial containment and diminished immunopathology compared with wild-type controls. These findings corresponded with enhanced pulmonary Th1 responses, evidenced by increased IFN-γ-producing CD4+ T cells, and elevated expression of MHC class II and costimulatory molecules B7-1 and B7-2 in the lungs. Upon M. tuberculosis infection and immune complex engagement, RIIB−/− macrophages produced more of the p40 component of the Th1-promoting cytokine IL-12. These data strongly suggest that FcγRIIB engagement can dampen the TB Th1 response by attenuating IL-12p40 production or activation of APCs. Conversely, C57BL/6 mice lacking the γ-chain shared by activating FcγR had enhanced susceptibility and exacerbated immunopathology upon M. tuberculosis challenge, associated with increased production of the immunosuppressive cytokine IL-10. Thus, engagement of distinct FcγR can divergently affect cytokine production and susceptibility during M. tuberculosis infection.

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confidence: 99%

Fcγ Receptors Regulate Immune Activation and Susceptibility during Mycobacterium tuberculosis Infection

Maglione

Casadevall

et al. 2008

The Journal of Immunology

132

152

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“…[21][22][23][24] Several studies have demonstrated that the spectrum of specificities of antimycobacterial antibodies was much narrower in B6 and B10 inbred mice as compared to several other inbred strains. 25,26 These differences were observed after infection with live MTB and BCG as well as after immunization with antigenic preparations of mycobacteria.…”

Section: Resultsmentioning

confidence: 99%

Genetic architecture of tuberculosis resistance in a mouse model of infection

Yan

Kirby

et al. 2006

Genes Immun

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Tuberculosis remains a significant public health problem: one-third of the human population is infected with virulent Mycobacterium tuberculosis (MTB) and 10% of those are at risk of developing tuberculosis during their lifetime. In both humans and experimental animal models, genetic variation among infected individuals contributes to the outcome of infection. However, in immunocompetent individuals (the majority of patients), genetic determinants of susceptibility to tuberculosis remain largely unknown. Mouse models of MTB infection, allowing control of exposure and other potential environmental contributors, have proven extremely useful for examining this genetic component. In a cross of C3HeB/FeJ (susceptible) by C57BL/6J (resistant) inbred mouse strains, we have previously identified one major genetic locus, sst1, the susceptible allele of which did not confer an overt immunodeficiency, but rather specifically affected progression of lung tuberculosis. Having generated and tested the sst1 congenic strains, we have observed that this locus only partially explained the difference in susceptibility of the parental strains to MTB. We now present further studies controlling for the effect of the sst1, identify four additional tuberculosis susceptibility loci and characterize their effects by testing an independent cross, knockout or congenic mice.

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“…Organs from M. tuberculosis infected IgG -mice had three to eight fold elevated counts of viable bacilli compared with those from normal mice. This result suggested that B cells play a role in the containment of murine tuberculous infection [68]. In another study, B cell gene disrupted mice (B cell KO) and controls were infected by aerosol with M. tuberculosis to allow the latter group to generate an antibody response in the upper respiratory tract.…”

Section: Studies Performed In Transgenic Micementioning

confidence: 99%