Liposomes of phosphatidylcholine and cholesterol induce an M2-like macrophage phenotype reprogrammable to M1 pattern with the involvement of B-1 cells

Cruz‐Leal, Yoelys; Laurindo, María Fernanda Lucatelli; Osugui, Lika; Luzardo, Marı́a del Carmen; López‐Requena, Alejandro; Alonso, Mercedes; Álvarez, Carlos; Popi, Ana Flávia; Mariano, Mario; Pérez, Rolando; Lanio, María E.

doi:10.1016/j.imbio.2014.01.006

Cited by 11 publications

(8 citation statements)

References 62 publications

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“…B‐1 cells play a role in the host immune response as natural antibody producers . It is well known that B‐1 cells respond to innate antigen signals, including pathogen‐associated molecules such as lipopolysaccharide . Our previous results showed that PerC B cells are involved in IgM antibody secretion in response to phospholipid antigens.…”

Section: Resultsmentioning

confidence: 95%

“…Cells from the pleural and peritoneal cavities were blocked using anti‐CD16/32 (2.4G2) followed by the addition of anti‐CD19–Cy5PE (1D3), CD90.2–Pacific blue, IgM–APC (331), IgD–Cy7PE, CD43–PE (S7), CD5–biotin (53–7.8) and Streptavidin–Qdot 605 (Life Technologies, Grand Island, NY). After staining, the cells were washed with KDS‐BSS staining medium followed by addition of live/dead violet staining (Invitrogen, Carlsbad, CA).…”

Section: Methodsmentioning

confidence: 99%

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Both B‐1a and B‐1b cells exposed to Mycobacterium tuberculosis lipids differentiate into IgM antibody‐secreting cells

et al. 2018

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Tuberculosis is an infectious disease caused by Mycobacterium tuberculosis. The cellular immune response to mycobacteria has been characterized extensively, but the antibody response remains underexplored. The present study aimed to examine whether host or bacterial phospholipids induce secretion of IgM, and specifically anti-phospholipid IgM, antibodies by B cells and to identify the responsible B-cell subset. Here we show that peritoneal B cells responded to lipid antigens by secreting IgM antibodies. Specifically, stimulation with M. tuberculosis H37Rv total lipids resulted in significant induction of total and anti-phosphatidylcholine IgM. Similarly, IgM antibody production increased significantly with stimulation by whole Mycobacterium bovis bacillus Calmette-Guérin. The B-1 subset was the dominant source of IgM antibodies after exposure to cardiolipin. Both CD5 B-1a and CD5 B-1b cell subsets secreted total IgM antibodies after exposure to M. tuberculosis H37Rv total lipids in vitro. Overall, our results suggest that the poly-reactive B-1 cell repertoire contributes to non-specific anti-phospholipid IgM antibody secretion in response to M. tuberculosis lipids.

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Section: Resultsmentioning

confidence: 95%

Section: Methodsmentioning

confidence: 99%

Both B‐1a and B‐1b cells exposed to Mycobacterium tuberculosis lipids differentiate into IgM antibody‐secreting cells

et al. 2018

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“…Additionally, B1 cells coming from splenocytes could also proliferate under the effect of these Lp. Previous work by our group demonstrated that DPPC-containing Lp encapsulating OVA are internalized by B1 cells and elicit an increase in peritoneal lymphocytes (79, 80). Interestingly, empty DPPC Lp are able to reproduce the effect of those carrying only OVA (80, 81).…”

Section: Discussionmentioning

confidence: 90%

Novel Adjuvant Based on the Pore-Forming Protein Sticholysin II Encapsulated into Liposomes Effectively Enhances the Antigen-Specific CTL-Mediated Immune Response

Laborde

Sanchez-Ferras

Luzardo

et al. 2017

The Journal of Immunology

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Vaccine strategies to enhance CD8+ CTL responses remain a current challenge because they should overcome the plasmatic and endosomal membranes for favoring exogenous Ag access to the cytosol of APCs. As a way to avoid this hurdle, sticholysin (St) II, a pore-forming protein from the Caribbean Sea anemone Stichodactyla helianthus, was encapsulated with OVA into liposomes (Lp/OVA/StII) to assess their efficacy to induce a CTL response. OVA-specific CD8+ T cells transferred to mice immunized with Lp/OVA/StII experienced a greater expansion than when the recipients were injected with the vesicles without St, mostly exhibiting a memory phenotype. Consequently, Lp/OVA/StII induced a more potent effector function, as shown by CTLs, in vivo assays. Furthermore, treatment of E.G7-OVA tumor-bearing mice with Lp/OVA/StII significantly reduced tumor growth being more noticeable in the preventive assay. The contribution of CD4+ and CD8+ T cells to CTL and antitumor activity, respectively, was elucidated. Interestingly, the irreversibly inactive variant of the StI mutant StI W111C, encapsulated with OVA into Lp, elicited a similar OVA-specific CTL response to that observed with Lp/OVA/StII or vesicles encapsulating recombinant StI or the reversibly inactive StI W111C dimer. These findings suggest the relative independence between StII pore-forming activity and its immuno-modulatory properties. In addition, StII-induced in vitro maturation of dendritic cells might be supporting these properties. These results are the first evidence, to our knowledge, that StII, a pore-forming protein from a marine eukaryotic organism, encapsulated into Lp functions as an adjuvant to induce a robust specific CTL response.

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“…Research groups have also shown that within the tumor microenvironment, liposomes can polarize tumor-associated macrophages (TAMs) [107][108][109]. The reprogramming of classically activated (M1) TAMs, which have a role in eradicating tumor cells in their early stages, to alternatively activated M2-like TAMs has been shown to promote tumor growth and metastasis, as shown in Figure 2 [110,111].…”

Section: Interactions With the Mononuclear Phagocyte Systemmentioning

confidence: 99%

Immunological and Toxicological Considerations for the Design of Liposomes

et al. 2020

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Liposomes hold great potential as gene and drug delivery vehicles due to their biocompatibility and modular properties, coupled with the major advantage of attenuating the risk of systemic toxicity from the encapsulated therapeutic agent. Decades of research have been dedicated to studying and optimizing liposomal formulations for a variety of medical applications, ranging from cancer therapeutics to analgesics. Some effort has also been made to elucidate the toxicities and immune responses that these drug formulations may elicit. Notably, intravenously injected liposomes can interact with plasma proteins, leading to opsonization, thereby altering the healthy cells they come into contact with during circulation and removal. Additionally, due to the pharmacokinetics of liposomes in circulation, drugs can end up sequestered in organs of the mononuclear phagocyte system, affecting liver and spleen function. Importantly, liposomal agents can also stimulate or suppress the immune system depending on their physiochemical properties, such as size, lipid composition, pegylation, and surface charge. Despite the surge in the clinical use of liposomal agents since 1995, there are still several drawbacks that limit their range of applications. This review presents a focused analysis of these limitations, with an emphasis on toxicity to healthy tissues and unfavorable immune responses, to shed light on key considerations that should be factored into the design and clinical use of liposomal formulations.

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Liposomes of phosphatidylcholine and cholesterol induce an M2-like macrophage phenotype reprogrammable to M1 pattern with the involvement of B-1 cells

Cited by 11 publications

References 62 publications

Both B‐1a and B‐1b cells exposed to Mycobacterium tuberculosis lipids differentiate into IgM antibody‐secreting cells

Both B‐1a and B‐1b cells exposed to Mycobacterium tuberculosis lipids differentiate into IgM antibody‐secreting cells

Novel Adjuvant Based on the Pore-Forming Protein Sticholysin II Encapsulated into Liposomes Effectively Enhances the Antigen-Specific CTL-Mediated Immune Response

Immunological and Toxicological Considerations for the Design of Liposomes

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