Interleukin‐33 Triggers <scp>B</scp>1 Cell Expansion and Its Release of Monocyte/Macrophage Chemoattractants and Growth Factors

Ahmed, Ammad; Koma, Mousa Komai

doi:10.1111/sji.12312

Cited by 18 publications

(17 citation statements)

References 32 publications

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“…In mice, IL-33 enhances immunoglobulin (Ig)M synthesis and markedly induces and activates B1 cells in an ST2-dependent manner [18]. Additionally, IL-33 could also induce regulatory B cells to produce IL-10, attenuating mucosal inflammation in the gut [19].…”

Section: Introductionmentioning

confidence: 99%

Serum IL-33, a new marker predicting response to rituximab in rheumatoid arthritis

et al. 2016

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BackgroundRecent works have suggested a possible link between interleukin (IL)-33 and B-cell biology. We aimed to study the possible association between serum IL-33 detection and response to rituximab (RTX) in rheumatoid arthritis (RA) patients in different cohorts with an accurate enzyme-linked immunosorbent assay (ELISA).MethodsSerum IL-33, rheumatoid factor (RF), anti-cyclic citrullinated peptide (anti-CCP), and high serum immunoglobulin (Ig)G levels were assessed in 111 RA patients receiving a first course of 2 g RTX (cohort 1) in an observational study and in 74 RA patients treated with the same schedule in routine care (cohort 2). Univariate and multivariate analyses identified factors associated with a European League Against Rheumatism (EULAR) response at 24 weeks.ResultsAt week 24, 84/111 (76%) and 54/74 (73%) patients reached EULAR response in cohorts 1 and 2, respectively. Serum IL-33 was detectable in only 33.5% of the patients. In the combined cohorts, the presence of RF or anti-CCP (odds ratio (OR) 3.27, 95% confidence interval (CI) 1.13–9.46; p = 0.03), high serum IgG (OR 2.32, 95% CI 1.01–5.33; p = 0.048), and detectable serum IL-33 (OR 2.40, 95% CI 1.01–5.72; p = 0.047) were all associated with RTX response in multivariate analysis. The combination of these three factors increased the likelihood of response to RTX. When serum IL-33 detection was added to seropositivity and serum IgG level, 100% of the patients with the three risk factors (corresponding to 9% of the population) responded to RTX (OR versus patients with none of the three risk factors 29.61, 95% CI 1.30–674.79; p = 0.034).ConclusionDetectable serum IL-33 may predict clinical response to RTX independently of, and synergistically with, auto-antibodies and serum IgG level.Trial registration NCT01126541; 18 May 2010.Electronic supplementary materialThe online version of this article (doi:10.1186/s13075-016-1190-z) contains supplementary material, which is available to authorized users.

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Section: Introductionmentioning

confidence: 99%

Serum IL-33, a new marker predicting response to rituximab in rheumatoid arthritis

et al. 2016

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“…Others have described the ability of IL‐33 to induce the proliferation of B1‐cells, a cell population that makes up a large proportion of the immune cells within the serous cavities . More recently, it has been shown that sorted B1b cells placed into culture with IL‐33 will secrete CSF2 (GM‐CSF) which leads to the alternative possibility that IL‐33 may induce CSF2 from B‐cells within the serous cavities, which then contribute to the proliferation of resident serous macrophages. Future experiments will be required to determine whether the action of IL‐33 on macrophages requires cell‐intrinsic expression of the IL‐33R and whether there is requirement for B‐cell derived CSF2 in the IL‐33 driven macrophage proliferation system.…”

Section: Discussionmentioning

confidence: 99%

IL‐33 delivery induces serous cavity macrophage proliferation independent of interleukin‐4 receptor alpha

et al. 2016

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IL‐33 plays an important role in the initiation of type‐2 immune responses, as well as the enhancement of type 2 effector functions. Engagement of the IL‐33 receptor on macrophages facilitates polarization to an alternative activation state by amplifying IL‐4 and IL‐13 signaling to IL‐4Rα. IL‐4 and IL‐13 also induce macrophage proliferation but IL‐33 involvement in this process has not been rigorously evaluated. As expected, in vivo delivery of IL‐33 induced IL‐4Rα‐dependent alternative macrophage activation in the serous cavities. IL‐33 delivery also induced macrophages to proliferate but, unexpectedly, this was independent of IL‐4Rα signaling. In a filarial nematode infection model in which IL‐4Rα‐dependent alternative activation and proliferation in the pleural cavity is well described, IL‐33R was essential for alternative activation but not macrophage proliferation. Similarly, during Alternaria alternata induced airway inflammation, which provokes strong IL‐33 responses, we observed that both IL‐4Rα and IL‐33R were required for alternative activation, while macrophage proliferation in the pleural cavity was still evident in the absence of either receptor alone. Our data show that IL‐33R and IL‐4Rα promote macrophage proliferation independently of each other, but both are essential for induction of alternative activation.

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“…Komai-Koma et al recently showed that B1 cells proliferate after daily i.p. injection with IL-33 ( Komai-Koma et al, 2011 ) through production of IL-5 that then upregulated ST2 on B1 cells ( Ahmed and Koma, 2015 ). To test the effect of IL-33 on B1 cell IgE production, we injected IL-33 i.p.…”

Section: Resultsmentioning

confidence: 99%

B1 Cell IgE Impedes Mast Cell-Mediated Enhancement of Parasite Expulsion through B2 IgE Blockade

et al. 2018

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SUMMARYHelminth infection is known for generating large amounts of poly-specific IgE. Here we demonstrate that innate-like B1 cells are responsible for this IgE production during infection with the nematode parasites Nippostrongylus brasiliensis and Heligmosomoides polygyrus bakeri. In vitro analysis of B1 cell immunoglobulin class switch recombination to IgE demonstrated a requirement for anti-CD40 and IL-4 that was further enhanced when IL-5 was added or when the B1 source was helminth infected mice. An IL-25-induced upregulation of IgE in B1 cells was also demonstrated. In T cell-reconstituted RAG1−/− mice, N. brasiliensis clearance was enhanced with the addition of B2 cells in an IgE-dependent manner. This enhanced clearance was impeded by reconstitution with IgE sufficient B1 cells. Mucosal mast cells mediated the B2 cell enhancement of clearance in the absence of B1 cells. The data support B1 cell IgE secretion as a regulatory response exploited by the helminth.

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Interleukin‐33 Triggers B1 Cell Expansion and Its Release of Monocyte/Macrophage Chemoattractants and Growth Factors

Cited by 18 publications

References 32 publications

Serum IL-33, a new marker predicting response to rituximab in rheumatoid arthritis

Serum IL-33, a new marker predicting response to rituximab in rheumatoid arthritis

IL‐33 delivery induces serous cavity macrophage proliferation independent of interleukin‐4 receptor alpha

B1 Cell IgE Impedes Mast Cell-Mediated Enhancement of Parasite Expulsion through B2 IgE Blockade

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