B cells and antibodies in the defense against <i><scp>M</scp>ycobacterium tuberculosis</i> infection

Achkar, Jacqueline M.; Chan, John; Casadevall, Arturo

doi:10.1111/imr.12276

Cited by 163 publications

(120 citation statements)

References 190 publications

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“…Serologic testing was restricted to IgG antibodies in our study. IgA and IgM responses to a number of M. tuberculosis antigens have been demonstrated in serum from TB patients and individuals with latent M. tuberculosis infection, 8,24,25 and recent findings suggest that different antibody isotypes may differentially affect infection of cells by M. tuberculosis . 26 Further, our experimental methods did not assess antibody glycosylation, the extent of which has been associated with activity in vitro.…”

Section: Discussionmentioning

confidence: 99%

Serologic Responses in Childhood Pulmonary Tuberculosis

Nicol¹,

Andreas

Rimmele

et al. 2018

Pediatric Infectious Disease Journal

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Background Identification of the Mycobacterium tuberculosis immunoproteome and antigens associated with serologic responses in adults has renewed interest in developing a serologic test for childhood tuberculosis (TB). We investigated IgG antibody responses against M. tuberculosis antigens in children with well-characterized TB. Methods We studied archived sera obtained from hospitalized children with suspected pulmonary TB, and classified as having confirmed TB (culture- confirmed), unlikely TB (clinical improvement without TB treatment), or unconfirmed TB (all others). A multiplexed bead-based assay for IgG antibodies against 119 M. tuberculosis antigens was developed, validated and used to test sera. The area under the curves (AUCs) of the empiric receiver–operator characteristic curves were generated as measures of predictive ability. A cross-validated generalized linear model was used to select the most predictive combinations of antigens. Results For the confirmed TB versus unlikely TB comparison, the maximal single antigen AUC was 0.63, corresponding to sensitivity 0.60 and specificity 0.60. Older (age: 60+ months old) children’s responses were better predictive of TB status than younger (age: 12–59 months old) children’s, with a maximal single antigen AUC of −0.76. For the confirmed TB versus unlikely TB groups, the most predictive combinations of antigens assigned TB risk probabilities of 0.33 and 0.33, respectively, when all ages were considered, and 0.57 (interquartile range: 0.48–0.64) and 0.35 (interquartile range: 0.32–0.40) when only older children were considered. Conclusion An antigen-based IgG test is unlikely to meet the performance characteristics required of a TB detection test applicable to all age groups.

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Section: Discussionmentioning

confidence: 99%

Serologic Responses in Childhood Pulmonary Tuberculosis

Nicol¹,

Andreas

Rimmele

et al. 2018

Pediatric Infectious Disease Journal

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“…Below we will review those aspects of Candida and Mycobacteria -specific T cell activation and effector mechanisms that prevent disease. Although antibody responses to Candida and Mycobacteria are measurable in infected individuals, B cells’ influence on fungal and mycobacterial disease outcome is not reviewed here, but has been recently reviewed elsewhere 180,181 .…”

Section: Acquired Immunity To Candida and Mycobacterial Speciesmentioning

confidence: 99%

The Goldilocks model of immune symbiosis with Mycobacteria and Candida colonizers

Robinson

Huppler

2017

Cytokine

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Mycobacteria and Candida species include significant human pathogens that can cause localized or disseminated infections. Although these organisms may appear to have little in common, several shared pathways of immune recognition and response are important for both control and infection-related pathology. In this article, we compare and contrast the innate and adaptive components of the immune system that pertain to these infections in humans and animal models. We also explore a relatively new concept in the mycobacterial field: biological commensalism. Similar to the well-established model of Candida infection, Mycobacterial species colonize their human hosts in equilibrium with the immune response. Perturbations in the immune response permit the progression to pathologic disease at the expense of the host. Understanding the immune factors required to maintain commensalism may aid with the development of diagnostic and treatment strategies for both categories of pathogens.

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“…The impact of chronic intracellular bacterial infections including that of Mycobacterium tuberculosis (Mtb), on B cells has not been studied in detail in part because there was little evidence for a direct role for antibodies in immunity to these pathogens (57). However, interest in the B cell biology of Mtb infections increased with the demonstration that B cells play key roles in the regulation of T cell responses in TB.…”

Section: Introductionmentioning

confidence: 99%

Atypical memory B cells in human chronic infectious diseases: An interim report

Portugal

Obeng-Adjei

Moir

et al. 2017

Cellular Immunology

165

177

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Immunological memory is a remarkable phenomenon in which survival of an initial infection by a pathogen leads to life-long protection from disease upon subsequent exposure to that same pathogen. For many infectious diseases, long-lived protective humoral immunity is induced after only a single infection in a process that depends on the generation of memory B cells (MBCs) and long-lived plasma cells. However, over the past decade it has become increasingly evident that many chronic human infectious diseases to which immunity is not readily established, including HIV-AIDS, malaria and TB, are associated with fundamental alterations in the composition and functionality of MBC compartments. A common feature of these diseases appears to be a large expansion of what have been termed exhausted B cells, tissue-like memory B cells or atypical memory B cells (aMBCs) that, for simplicity’s sake, we refer to here as aMBCs. It has been suggested that chronic immune activation and inflammation drive the expansion of aMBCs and that in some way aMBCs contribute to deficiencies in the acquisition of immunity in chronic infectious diseases. Although aMBCs are heterogeneous both within individuals and between diseases, they have several features in common including low expression of the cell surface markers that define classical MBCs in humans including CD21 and CD27 and high expression of genes not usually expressed by classical MBCs including T-bet, CD11c and a variety of inhibitory receptors, notably members of the FcRL family. Another distinguishing feature is their greatly diminished ability to be stimulated through their B cell receptors to proliferate, secrete cytokines or produce antibodies. In this review, we describe our current understanding of the phenotypic markers of aMBCs, their specificity in relation to the disease-causing pathogen, their functionality, the drivers of their expansion in chronic infections and their life span. We briefly summarize the features of aMBCs in healthy individuals and in autoimmune disease. We also comment on the possible relationship of human aMBCs and T-bet+, CD11c+ age/autoimmune-associated B cells, also a topic of this review volume.

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B cells and antibodies in the defense against Mycobacterium tuberculosis infection

Cited by 163 publications

References 190 publications

Serologic Responses in Childhood Pulmonary Tuberculosis

Serologic Responses in Childhood Pulmonary Tuberculosis

The Goldilocks model of immune symbiosis with Mycobacteria and Candida colonizers

Atypical memory B cells in human chronic infectious diseases: An interim report

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