Beyond the antibody: B cells as a target for bacterial infection

García-Gil, Abraham; Lopez-Bailon, Luis; Ortiz-Navarrete, Vianney

doi:10.1002/jlb.mr0618-225r

Cited by 9 publications

(8 citation statements)

References 118 publications

(205 reference statements)

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“…Interestingly, human and animal B cells can be directly infected by Brucella ( Bratescu et al, 1981 ; Goenka et al, 2011 , 2012 ; Pesce Viglietti et al, 2016 ; García-Gil et al, 2019 ). Consequently, B cells may serve as a reservoir since Brucella cannot replicate in B cells ( Goenka et al, 2012 ; Pesce Viglietti et al, 2016 ), which in turn enables the development of immunosuppressive B cells ( Atluri et al, 2011 ; Goenka et al, 2011 , 2012 ; Spera et al, 2014 ).…”

Section: Brucella Immunologymentioning

confidence: 99%

Activation of mucosal immunity as a novel therapeutic strategy for combating brucellosis

et al. 2022

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Brucellosis is a disease of livestock that is commonly asymptomatic until an abortion occurs. Disease in humans results from contact of infected livestock or consumption of contaminated milk or meat. Brucella zoonosis is primarily caused by one of three species that infect livestock, Bacillus abortus in cattle, B. melitensis in goats and sheep, and B. suis in pigs. To aid in disease prophylaxis, livestock vaccines are available, but are only 70% effective; hence, improved vaccines are needed to mitigate disease, particularly in countries where disease remains pervasive. The absence of knowing which proteins confer complete protection limits development of subunit vaccines. Instead, efforts are focused on developing new and improved live, attenuated Brucella vaccines, since these mimic attributes of wild-type Brucella, and stimulate host immune, particularly T helper 1-type responses, required for protection. In considering their development, the new mutants must address Brucella’s defense mechanisms normally active to circumvent host immune detection. Vaccination approaches should also consider mode and route of delivery since disease transmission among livestock and humans is believed to occur via the naso-oropharyngeal tissues. By arming the host’s mucosal immune defenses with resident memory T cells (TRMs) and by expanding the sources of IFN-γ, brucellae dissemination from the site of infection to systemic tissues can be prevented. In this review, points of discussion focus on understanding the various immune mechanisms involved in disease progression and which immune players are important in fighting disease.

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Section: Brucella Immunologymentioning

confidence: 99%

Activation of mucosal immunity as a novel therapeutic strategy for combating brucellosis

et al. 2022

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“…B cell biology is not limited to antibody production; B cells exert also important functions as antigen-presenting and regulatory cells. It is well established that B cells are targets of intracellular bacteria, including Brucella , Salmonella , M. tuberculosis , and Francisella tularensis , among others [ 306 ]. In contrast to its effect on epithelial cells and macrophages, Salmonella inhibits pyroptosis in murine splenic B cells and abrogates IL-1β production by impairing NLRC4 transcription.…”

Section: Current Knowledge Of Immunosuppression and Chronicity Throug...mentioning

confidence: 99%

Immunosuppressive Mechanisms in Brucellosis in Light of Chronic Bacterial Diseases

2022

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Brucellosis is considered one of the major zoonoses worldwide, constituting a critical livestock and human health concern with a huge socio-economic burden. Brucella genus, its etiologic agent, is composed of intracellular bacteria that have evolved a prodigious ability to elude and shape host immunity to establish chronic infection. Brucella’s intracellular lifestyle and pathogen-associated molecular patterns, such as its specific lipopolysaccharide (LPS), are key factors for hiding and hampering recognition by the immune system. Here, we will review the current knowledge of evading and immunosuppressive mechanisms elicited by Brucella species to persist stealthily in their hosts, such as those triggered by their LPS and cyclic β-1,2-d-glucan or involved in neutrophil and monocyte avoidance, antigen presentation impairment, the modulation of T cell responses and immunometabolism. Attractive strategies exploited by other successful chronic pathogenic bacteria, including Mycobacteria, Salmonella, and Chlamydia, will be also discussed, with a special emphasis on the mechanisms operating in brucellosis, such as granuloma formation, pyroptosis, and manipulation of type I and III IFNs, B cells, innate lymphoid cells, and host lipids. A better understanding of these stratagems is essential to fighting bacterial chronic infections and designing innovative treatments and vaccines.

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“…1A and Data S1 ). LCLs are a powerful in vitro model, because they are karyotypically normal, and B cells are a natural site of Salmonella replication in vivo ( 6 ). Intracellular replication, or host cell permissivity, is a demonstrated proxy for Salmonella virulence in whole organisms ( 7 ).…”

Section: Main Textmentioning

confidence: 99%

Human variation impacting MCOLN2 restricts Salmonella Typhi replication by magnesium deprivation

Gibbs

Wang

Anderson

et al. 2022

Preprint

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Human genetic diversity can reveal critical factors in host-pathogen interactions. This is especially useful for human-restricted pathogens like Salmonella enterica serovar Typhi (S. Typhi), the cause of Typhoid fever. One key dynamic during infection is competition for nutrients: host cells attempt to restrict intracellular replication by depriving bacteria of key nutrients or delivering toxic metabolites in a process called nutritional immunity. Here, a cellular genome-wide association study of intracellular replication by S. Typhi in nearly a thousand cell lines from around the world—and extensive follow-up using intracellular S. Typhi transcriptomics and manipulation of magnesium concentrations—demonstrates that the divalent cation channel mucolipin-2 (MCOLN2) restricts S. Typhi intracellular replication through magnesium deprivation. Our results reveal natural diversity in Mg2+ limitation as a key component of nutritional immunity against S. Typhi.One-Sentence SummaryHuman immune cells genetically vary in their ability to use magnesium deprivation to restrict growth of the typhoid fever bacterium.

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Beyond the antibody: B cells as a target for bacterial infection

Cited by 9 publications

References 118 publications

Activation of mucosal immunity as a novel therapeutic strategy for combating brucellosis

Activation of mucosal immunity as a novel therapeutic strategy for combating brucellosis

Immunosuppressive Mechanisms in Brucellosis in Light of Chronic Bacterial Diseases

Human variation impacting MCOLN2 restricts Salmonella Typhi replication by magnesium deprivation

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