Correction: Human IgA bind a diverse array of commensal bacteria

Sterlin, Delphine; Fadlallah, Jehane; Adams, Olivia; Fieschi, Claire; Parizot, Christophe; Dorgham, Karim; Rajkumar, Asok; Autaa, Gaëlle; El-Kafsi, Hela; Charuel, Jean‐Luc; Juste, Catherine; Jönsson, Friederike; Candela, Thomas; Wardemann, Hedda; Aubry, Alexandra; Capito, Carmen; Brisson, Hélène; Trésallet, Christophe; Cummings, Richard D.; Larsen, Martin; Yssel, Hans; Gunten, Stephan von; Gorochov, Guy

doi:10.1084/jem.2018163501152020c

Cited by 10 publications

(8 citation statements)

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“…Our follow-up studies on fish sIgT demonstrated that control of microbiota homeostasis by sIgs is a primordial function of specialized mucosal sIgs already found in early vertebrates such as teleosts ( 10 ). However, the current dogma that sIg-dependent microbiota homeostasis is mediated by sIgA or sIgT in vertebrates, has recently been challenged by several studies showing that significant proportions of human and fish microbiota are coated by sIgM in the gut and other mucosal surfaces ( 5, 18, 19 ). Because sIgM does not coat the microbiota of mice under either specific-pathogen-free (SPF) or non-SPF conditions ( 5, 7 ), laboratory mouse models to study the potential role of sIgM in host-microbiome interactions are not suitable to address this question.…”

Section: Discussionmentioning

confidence: 99%

Secretory IgM (sIgM) is an ancient master regulator of microbiota homeostasis and metabolism

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Fernández-Montero

Mani

et al. 2023

Preprint

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The co-evolution between secretory immunoglobulins (sIgs) and microbiota began with the emergence of IgM over half a billion years ago. Yet, IgM function in vertebrates is mostly associated with systemic immunity against pathogens. sIgA and sIgT are the only sIgs known to be required in the control of microbiota homeostasis in warm- and cold-blooded vertebrates respectively. Recent studies have shown that sIgM coats a large proportion of the gut microbiota of humans and teleost fish, thus suggesting an ancient and conserved relationship between sIgM and microbiota early in vertebrate evolution. To test this hypothesis, we temporarily and selectively depleted IgM from rainbow trout, an old bony fish species. IgM depletion resulted in a drastic reduction in microbiota IgM coating levels and losses in gut-associated bacteria. These were accompanied by bacterial translocation, severe gut tissue damage, inflammation and dysbiosis predictive of metabolic shifts. Furthermore, depletion of IgM resulted in body weight loss and lethality in an experimental colitis model. Recovery of sIgM to physiological levels restores tissue barrier integrity, while microbiome homeostasis and their predictive metabolic capabilities are not fully restituted. Our findings uncover a previously unrecognized role of sIgM as an ancient master regulator of microbiota homeostasis and metabolism and challenge the current paradigm that sIgA and sIgT are the key vertebrate sIgs regulating microbiome homeostasis.

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Section: Discussionmentioning

confidence: 99%

Secretory IgM (sIgM) is an ancient master regulator of microbiota homeostasis and metabolism

Ding

Fernández-Montero

Mani

et al. 2023

Preprint

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“…IgG were isolated from serum samples diluted in 1X-PBS as previously described (29). Briefly, serum samples were loaded onto Protein G/Agarose column (Invivogen) after column equilibration.…”

Section: Purification Of Igg From Serummentioning

confidence: 99%

Pre-COVID-19 Immunity to Common Cold Human Coronaviruses Induces a Recall-Type IgG Response to SARS-CoV-2 Antigens Without Cross-Neutralisation

et al. 2022

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The capacity of pre-existing immunity to human common coronaviruses (HCoV) to cross-protect against de novo COVID-19is yet unknown. In this work, we studied the sera of 175 COVID-19 patients, 76 healthy donors and 3 intravenous immunoglobulins (IVIG) batches. We found that most COVID-19 patients developed anti-SARS-CoV-2 IgG antibodies before IgM. Moreover, the capacity of their IgGs to react to beta-HCoV, was present in the early sera of most patients before the appearance of anti-SARS-CoV-2 IgG. This implied that a recall-type antibody response was generated. In comparison, the patients that mounted an anti-SARS-COV2 IgM response, prior to IgG responses had lower titres of anti-beta-HCoV IgG antibodies. This indicated that pre-existing immunity to beta-HCoV was conducive to the generation of memory type responses to SARS-COV-2. Finally, we also found that pre-COVID-19-era sera and IVIG cross-reacted with SARS-CoV-2 antigens without neutralising SARS-CoV-2 infectivity in vitro. Put together, these results indicate that whilst pre-existing immunity to HCoV is responsible for recall-type IgG responses to SARS-CoV-2, it does not lead to cross-protection against COVID-19.

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“…tailoring of immune responses to the situation at hand. In addition to that, the known different antigen-specificities of IgA1 and IgA2 ( 37 – 39 ) will further contribute to pathogen-specific immunity.…”

Section: Discussionmentioning

confidence: 99%

IgA2 immune complexes selectively promote inflammation by human CD103+ dendritic cells

et al. 2023

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While immunoglobulin A (IgA) is well known for its neutralizing and anti-inflammatory function, it is becoming increasingly clear that IgA can also induce human inflammatory responses by various different immune cells. Yet, little is known about the relative role of induction of inflammation by the two IgA subclasses i.e. IgA1, most prominent subclass in circulation, and IgA2, most prominent subclass in the lower intestine. Here, we set out to study the inflammatory function of IgA subclasses on different human myeloid immune cell subsets, including monocytes, and in vitro differentiated macrophages and intestinal CD103+ dendritic cells (DCs). While individual stimulation with IgA immune complexes only induced limited inflammatory responses by human immune cells, both IgA subclasses strongly amplified pro-inflammatory cytokine production upon co-stimulation with Toll-like receptor (TLR) ligands such as Pam3CSK4, PGN, and LPS. Strikingly, while IgA1 induced slightly higher or similar levels of pro-inflammatory cytokines by monocytes and macrophages, respectively, IgA2 induced substantially more inflammation than IgA1 by CD103+ DCs. In addition to pro-inflammatory cytokine proteins, IgA2 also induced higher mRNA expression levels, indicating that amplification of pro-inflammatory cytokine production is at least partially regulated at the level of gene transcription. Interestingly, cytokine amplification by IgA1 was almost completely dependent on Fc alpha receptor I (FcαRI), whilst blocking this receptor only partially reduced cytokine induction by IgA2. In addition, IgA2-induced amplification of pro-inflammatory cytokines was less dependent on signaling through the kinases Syk, PI3K, and TBK1/IKKϵ. Combined, these findings indicate that IgA2 immune complexes, which are most abundantly expressed in the lower intestine, particularly promote inflammation by human CD103+ intestinal DCs. This may serve an important physiological function upon infection, by enabling inflammatory responses by this otherwise tolerogenic DC subset. Since various inflammatory disorders are characterized by disturbances in IgA subclass balance, this may also play a role in the induction or exacerbation of chronic intestinal inflammation.

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Correction: Human IgA bind a diverse array of commensal bacteria

Cited by 10 publications

References 0 publications

Secretory IgM (sIgM) is an ancient master regulator of microbiota homeostasis and metabolism

Secretory IgM (sIgM) is an ancient master regulator of microbiota homeostasis and metabolism

Pre-COVID-19 Immunity to Common Cold Human Coronaviruses Induces a Recall-Type IgG Response to SARS-CoV-2 Antigens Without Cross-Neutralisation

IgA2 immune complexes selectively promote inflammation by human CD103+ dendritic cells

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