Repositório Institucional - Unifesp :: Navegando por Palavras-chave "B-1 cells"

Navegando por Palavras-chave "B-1 cells"

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Alteration in Ikaros expression promotes B-1 cell differentiation into phagocytes
(Elsevier Gmbh, Urban & Fischer Verlag, 2018) de Oliveira, Vivian Cristina [UNIFESP]; Pires Sodre, Ana Clara [UNIFESP]; Gomes, Caio Perez [UNIFESP]; Moretti, Nilmar Silvio [UNIFESP]; Pesquero, Joao Bosco; Popi, Ana Flavia [UNIFESP]
Ikaros is a broad transcription factor pointed as a critical regulator of lymphocyte development. Recent reports have emphasized that distinct isoforms of Ikaros control the dichotomy of the hematopoietic system into lymphoid and myeloid lineages. In addition, expression of dominant-negative isoforms of Ikaros is linked to abnormal hematopoiesis, which could culminate in hematological disorders due to loss of function of the protein. B-1 cells are an intriguing subtype of B-lymphocytes that preserves some myeloid characteristics. These cells are able to differentiate into phagocytes (B-1CDP B-1 cell derived phagocytes) in vitro and in vivo. During such process, reprogramming of gene expression occurs: lymphoid genes are turned off, while expression of myeloid genes is increased. This study aims to investigate whether Ikaros could be related to the control of B-1 cell plasticity. Interestingly, Ikaros expression by B-1CDP cells Was found to be relatively low, and the protein is abnormally localized in the cytoplasm. Moreover, the isoforms expressed by B-1 cells are different from those expressed by other lymphocytes, with expression of active isoforms being almost absent in B-1CDP. Based on these findings, Ikaros could be an important factor driving the differentiation and proliferation of B-1 cells.
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B-1 cell participation in T-cell-mediated alloimmune response
(Elsevier B.V., 2010-04-01) Nogueira-Martins, Mauro F. [UNIFESP]; Mariano, Mario [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
B-1 and B cells are important producers of natural antibodies in mice and humans and, therefore, are considered as the first line of defense against pathogens. Because of that, their role in T-cell-mediated immune responses is commonly underrated. However, recent studies have described the participation of B-1 cells in immediate and delayed-type hypersensitivity. the present work assessed the role of B-1 cells in the rejection of allografts in mice, an immune reaction mainly orchestrated by T cells. We have transplanted allogeneic skin and heart to wild-type and B-1-cell-deficient mice, and followed rejection kinetics. Skin graft-infiltrating cells were analyzed by flow cytometry.We observed a delay in rejection kinetics of B-1-cell-deficient mice when compared to wild-type mice. Adoptive transfer of B-1 cells into B-1-cell-deficient mice abrogated this delay. the longer survival observed in the absence of B-I cells correlated with less CD8(+) T cells infiltrating the grafts, as well as with more mast cells. Collectively, our results show the participation of B-1 cells in the allograft rejection process in mice and collaborate to the understanding of B-1 cell biology. (C) 2009 Elsevier GmbH. All rights reserved.
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B-1 cell: the precursor of a novel mononuclear phagocyte with immuno-regulatory properties
(Acad Brasileira De Ciencias, 2009-09-01) Lopes, Jose Daniel [UNIFESP]; Mariano, Mario [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
Characterization of the origin, properties, functions and fate of cells is a fundamental task for the understanding of physiological and pathological phenomena. Despite the bulk of knowledge concerning the diverse characteristics of mammalian cells, some of them, such as B-1 cells, are still poorly understood. Here we report the results obtained in our laboratory on these cells in the last 10 years. After showing that B-1 cells could be cultured and amplified in vitro, a series of experiments were performed with these cells. They showed that B1 cells reside mostly in the peritoneal and pleural cavities, migrate to distant inflammatory foci, coalesce to form giant cells and participate in granuloma formation, both in vitro and in vivo. They are also able to present antigens to immunologically responsive cells and are endowed with regulatory properties. Further, we have also shown that these cells facilitate different types of infection as well as tumor growth and spreading. These data are presently reviewed pointing to a pivotal role that these cells may play in innate and acquired immunity.
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B-1 cells and concomitant immunity in Ehrlich tumour progression
(Elsevier B.V., 2014-05-01) Azevedo, M. C. [UNIFESP]; Palos, M. C. [UNIFESP]; Osugui, L. [UNIFESP]; Laurindo, M. F. [UNIFESP]; Masutani, D. [UNIFESP]; Nonogaki, S. [UNIFESP]; Bachi, Andre Luis Lacerda [UNIFESP]; Melo, F. H. M. [UNIFESP]; Mariano, M. [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
Concomitant immunity is a phenomenon in which a tumour-bearing host is resistant to the growth of an implanted secondary tumour. Metastases are considered to be secondary tumours that develop spontaneously during primary tumour growth, suggesting the involvement of concomitant immunity in controlling the rise of metastases. It has been demonstrated that B-1 cells, a subset of B-lymphocytes found predominantly in pleural and peritoneal cavities, not only increase the metastatic development of murine melanoma B16F10, but also are capable of differentiating into mononuclear phagocytes, modulating inflammatory responses in wound healing, in oral tolerance and in Paracoccidiose brasiliensis infections. Here, we studied B-1 cells' participation in concomitant immunity during Ehrlich tumour progression. Our results show that B-1 cells obtained from BALB/c mice previously injected with Ehrlich tumour in the footpad were able to protect BALB/c and BALB/Xid mice against Ehrlich tumour challenge. in addition, it was demonstrated that BALB/Xid show faster tumour growth and have lost concomitant immunity, and that this state can be partially restored by reconstituting these animals with B-1 cells. However, further researches are required to establish the mechanism involving B-1 cells in Ehrlich tumour growth. (C) 2014 Elsevier GmbH. All rights reserved.
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B-1 cells are pivotal for in vivo inflammatory giant cell formation
(Blackwell Publishing, 2005-08-01) Bogsan, CSB; Brito, RRNE; Palos, M. D.; Mortara, R. A.; Almeida, SR; Lopes, J. D.; Mariano, M.; Universidade Federal de São Paulo (UNIFESP)
The mechanisms that govern giant cell (GC) formation in inflammatory, neoplastic and physiologic conditions are far from being understood. Here, we demonstrate that B-1 cells are essential for foreign-body GC formation in the mouse. GCs were analysed on the surface of glass cover slips implanted into the subcutaneous tissue of the animals. It was demonstrated that GCs are almost absent on cover slips implanted into the subcutaneous tissue of BALB/c or CBA/N X-linked immunodeficient mice. As these animals do not have B-1 cells in the peritoneal cavity, they were reconstituted with B-1 cells obtained from cultures of adherent mouse peritoneal cells. Results showed that in B-1-reconstituted animals, the number of GCs on the implant surface surpassed the values obtained with preparations from wild animals. in animals selectively irradiated (pleural and peritoneal cavities) to deplete these cavities of B-1 cells, GCs were also not formed. Enriched suspensions of B-1 cells grown in culture were labelled with [H-3]-tymidine and injected into the peritoneal cavity of naive mice before implantation of glass cover slips. After 4 days, about 17% of mononuclear cells had their nuclei labelled, and almost 70% of GCs had one or more of their nuclei labelled when analysed by histoautoradiographic technique. A few GCs expressed an immunoglobulin M when analysed by immunostaining and confocal microscopy. Overall, these data demonstrate that B-1 cells are pivotal in the mechanisms of foreign-body GC formation in the mouse.
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B-1 cells facilitate Paracoccidioides brasiliensis infection in mice via IL-10 secretion
(Elsevier B.V., 2008-06-01) Popi, Ana Flavia [UNIFESP]; Godoy, Luiz Claudio [UNIFESP]; Xander, Patricia [UNIFESP]; Lopes, Jose Daniel [UNIFESP]; Mariano, Mario [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Univ Massachusetts
Protective immunity in paracoccidioidomycosis is mainly mediated by cellular immunity. the role of B cells in this disease, in particular B-1 cells, is poorly understood. the aim of this study was to characterize the participation of B-1 cells in resistance or susceptibility of BALB/c and BALB/Xid mice to P. brasiliensis (Pb) pulmonary infection. BALB/Xid, which lacks B-1 cells, exhibited higher resistance to infection when compared with BALB/c mice. However, adoptive transfer of B-1 cells to BALB/Xid mice drastically increased the susceptibility of these animals to Pb infection. the fungal burden in BALB/c and B-1 -reconstituted BALB/Xid was significantly higher as compared to BALB/Xid strain. Compact, well-organized granulomas were observed in the lungs of BALB/Xid mice, whereas large lesions with necrotic center with a plethora of fungi developed in BALB/c mice. It was also shown that B-1 cells impair phagocytosis of Pb by macrophages in vitro via secretion of IL-10, which was increased upon stimulation with a purified Pb antigen, gp43. Finally, in vivo blockade of IL-10 led to a better control of infection by the highly susceptible B10.A mouse. These findings suggest that B-1 cells play a major role in resistance/susceptibility to Pb infection in murine models, most likely via production of IL-10. (C) 2008 Elsevier Masson SAS. All rights reserved.
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B-1 cells modulate oral tolerance in mice
(Elsevier B.V., 2009-06-04) De-Gennaro, Luiz Antonio [UNIFESP]; Popi, Ana Flavia [UNIFESP]; Almeida, Sandro Rogrio de; Lopes, Jose Daniel [UNIFESP]; Mariano, Mario [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Universidade de São Paulo (USP)
Although the origin and functions of B-1 cells are controversial, they are considered as a cellular element of innate immunity due to their ability to produce natural autoantibodies of the IgM type. These antibodies are encoded by a relatively limited repertoire of V genes, and their resulting diversity is smaller than that produced by conventional B cells. B-1 cells constitute the larger fraction of B cells in the peritoneal cavity and migrate to non-specific inflammation sites. in addition, they contribute to the production of IgA antibodies in the intestinal lamina propria. It has been demonstrated that they participate in the induction and maintenance of peripheral tolerance. Herein, the participation of B-1 cells in inducing oral tolerance is evaluated. Unexpectedly, BALB/Xid mice, the animals deficient in B-1 cells, are not tolerized to OVA but instead are responsive to oral immunization. Conversely, BALB/c mice respond to oral tolerance to this antigen. We used these biological characteristics of these animals to investigate whether BA cells are involved in the induction of oral tolerance to OVA. Results show that B-1 cells from BALB/c mice, treated orally with OVA and adoptively transferred to BALB/Xid mice were able to suppress local hypersensitivity reaction and lymphoproliferative cellular response observed in BALB/.Xid mice. These data demonstrate that B-1 cells have regulatory properties and are involved in the induction of oral tolerance. (C) 2009 Elsevier B.V. All rights reserved.
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B-1 cells modulate the kinetics of wound-healing process in mice
(Elsevier B.V., 2010-03-01) Oliveira, H. C. [UNIFESP]; Popi, A. F. [UNIFESP]; Bachi, Andre Luis Lacerda [UNIFESP]; Nonogaki, S.; Lopes, J. D. [UNIFESP]; Mariano, M. [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Hosp Canc; Univ Paulista
Wound healing is a complex phenomenon whose mechanisms are not fully understood. Although inflammatory cells are recruited to the site of the lesion there are no reports concerning the participation of B lymphocytes in tissue repair. As demonstrated in our laboratory, B-1 cells migrate to a non-specific inflammatory focus and differentiate into a phagocyte. It has been reported that BALB/Xid mice are deficient in B-1 cells. Using this model, here we report that BALB/Xid mice have an increased inflammatory response, a delayed wound-healing process, a prominent neutrophilic infiltration of the lesion, and an increased neovascularization of the lesion as compared with BALB/c and BALB/Xid reconstituted with B-1 cells. the infiltration of B-1 cells into the wound was demonstrated. As B-1 cells secret and use interleukin 10 (IL-10) as an autocrine growth factor, the possible participation of this interleukin in the kinetics of wound healing was investigated. Results show that C57/BL6 IL-10 KO mice had an increased inflammatory response when compared with C57/BL6 and C57/BL6 IL-10 KO mice reconstituted with B-1 cells, thus suggesting that the observed effects of B-1 cells in the healing process is mediated by this interleukin. However, the mechanisms by which IL-10 influence these phenomena remain to be uncovered. (C) 2009 Elsevier GmbH. All rights reserved.
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B-1 cells produce insulin and abrogate experimental streptozotocin-induced diabetes
(Wiley-Blackwell, 2015-05-01) Alvares-Saraiva, Anuska M. [UNIFESP]; Novo, Marilia C. T. [UNIFESP]; Oliveira, Vivian Cristina de [UNIFESP]; Maricato, Juliana Terzi [UNIFESP]; Lopes, Jose Daniel [UNIFESP]; Popi, Ana Flavia [UNIFESP]; Mariano, Mario [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Univ Paulista UNIP
The participation of B-1 cells in a murine model of spontaneous diabetes has been recently reported. Here, we describe the role of B-1 cells in streptozotocin (STZ) induced diabetes in mice. We demonstrated that XID (B-1 cell-deficient) mice are more susceptible to STZ treatment than WT mice, as evidenced by their higher blood glucose level in response to STZ. Unexpectedly, the XID mice that were i.p. transferred with purified B-1 cells, either before or after the STZ treatment, did not develop diabetes. These cell transfers provided long-lasting protection for the XID mice against STZ-induced diabetes, suggesting that B-1 cells play an important role in the experimental diabetes pathobiology. We also showed that B-1 cell culture supernatants were able to regulate the blood glucose level of the diabetic XID mice, and we identified insulin-producing cells when B-1 cells were differentiated in B-1 cell-derived phagocyte in vitro. These findings provide a novel role for B-1 cells in metabolic processes, presenting a new mechanism to explain the pathogenesis of diabetes and a possible therapeutical target.
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B16 melanoma cells increase B-1 cell survival, IL-10 production and radioresistance in vitro
(Elsevier B.V., 2013-04-01) Lucatelli Laurindo, Maria Fernanda [UNIFESP]; Thies, Felipe Garutti [UNIFESP]; Perez, Elizabeth Cristina [UNIFESP]; Novaes e Brito, Ronni Romulo [UNIFESP]; Mariano, Mario [UNIFESP]; Popi, Ana Flavia [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Univ Paulista UNIP
B-1 cells can be differentiated from B-2 cells because they are predominantly located in the peritoneal and pleural cavities and have distinct phenotypic patterns and activation properties. the role of both cell populations in cancer progression is still controversial. Previous studies have indicated that direct contact between B-1 cells and B16 melanoma tumor cells (B16) increases the metastatic potential of the tumor cells. However, cellular changes that are induced in B-1 cells during the interaction between these two cell types have not been evaluated. in the present study, it is hypothesized that B-1 cells are modified after their interaction with tumor cells, leading to both increased cell viability and rate of proliferation. Additionally, soluble factors that were secreted by B16 cells were sufficient to augment B-1 cell viability and to modify the production of IL-10 by B-1 cells. Impressively, after direct or indirect contact with the B16 cells, B-1 cells became resistant to radiation-induced cell death. Thus, future studies that assess the importance of concomitant immunity and other conventional therapies in cancer treatment are needed. (C) 2012 Elsevier GmbH. All rights reserved.
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Blockage of Wnt/beta-catenin signaling by quercetin reduces survival and proliferation of B-1 cells in vitro
(Elsevier B.V., 2015-01-01) Tavares Novo, Marilia Campos [UNIFESP]; Osugui, Lika [UNIFESP]; Reis, Vanessa Oliveira dos [UNIFESP]; Longo-Maugeri, Ieda Maria [UNIFESP]; Mariano, Mario [UNIFESP]; Popi, Ana Flavia [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
The Wnt/beta-catenin signaling pathway has been shown to play an important role in controlling the proliferation, survival and differentiation of hematopoietic cells. Several Wnt/beta-catenin signaling components influence hematopoietic cells fate. B-1 cells are self-renewing and spontaneously express both myeloid and lymphoid restricted transcription factors. B-1 lymphocytes play a major role in autoimmunity and are related to CD5(+) B-cell lymphomas and leukemias, such as CLL (chronic lymphocytic leukemia). Herein, we demonstrate that Wnt/beta-catenin pathway is important to B-1 cell survival in vitro. the loss of Wnt signals by quercetin treatment induces a reduction in the proliferation and survival of B-1 cells. Furthermore, the quercetin treatment diminishes IL-6 production by peritoneal cells, a cytokine important to the maintenance of B-1 cells in vitro. Importantly, the IL-6 addition to B-1 cell culture prevents cells from apoptosis, even in the presence of quercetin. These data suggest that a deregulation in beta-catenin signals could result in alterations in B-1 cell proliferation and differentiation. the correlation between Wnt/beta-catenin and IL-6 could point out a mechanism for the expansion of B-1 cells in autoimmune disease and neoplasia. (C) 2014 Elsevier GmbH. All rights reserved.
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Co-ordinated expression of lymphoid and myeloid specific transcription factors during B-1b cell differentiation into mononuclear phagocytes in vitro
(Wiley-Blackwell, 2009-01-01) Popi, Ana F. [UNIFESP]; Motta, Fabiana L. T. [UNIFESP]; Mortara, Renato A. [UNIFESP]; Schenkman, Sergio [UNIFESP]; Lopes, Jose D. [UNIFESP]; Mariano, Mario [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
We previously demonstrated that B-1b cells can undergo differentiation to acquire a mononuclear phagocyte phenotype upon attachment to substrate in vitro. Here we followed the expression of surface markers and transcription factors during this differentiation. B-1b cells spontaneously express both myeloid and lymphoid restricted transcription factors. When induced to differentiate into a phagocyte, the lymphoid genes E box protein (E2A), early B-cell factor (EBF), paired box 5 (Pax5) are down-modulated, while expression of genes related to myeloid commitment is sustained. Furthermore, B-1b cell-derived phagocytes (B-1CDPs) decrease immunoglobulin M (IgM) expression but retain the expression of the heavy chain variable gene VH11 or VH12, an immunoglobulin gene rearrangement predominantly expressed by B-1 cells. the maintenance of lymphoid characteristics in B-1CDPs characterizes a unique type of phagocyte, not related to monocyte-derived macrophages.
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Crosstalk between B16 melanoma cells and B-1 lymphocytes induces global changes in tumor cell gene expression
(Elsevier B.V., 2013-10-01) Xander, Patricia [UNIFESP]; Novaes e Brito, Ronni Romulo; Perez, Elizabeth Cristina; Pozzibon, Jaqueline Maciel [UNIFESP]; Souza, Camila Ferreira de [UNIFESP]; Pellegrino, Renata [UNIFESP]; Bernardo, Viviane [UNIFESP]; Jasiulionis, Miriam Galvonas [UNIFESP]; Mariano, Mario [UNIFESP]; Lopes, Jose Daniel [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Ctr Univ Sao Camilo
The analysis of gene expression patterns in cancers has improved the understanding of the mechanisms underlying the process of metastatic progression. However, the acquisition of invasive behavior in melanoma is poorly understood. in melanoma, components of the immune system can contribute to tumor progression, and inflammatory cells can influence almost all aspects of cancer progression, including metastasis. Recent studies have attributed an important role to B-1 cells, a subset of B lymphocytes, in melanoma progression. in vitro interactions between B16 melanoma cells and B-1 lymphocytes lead to increased B16 cell metastatic potential, but the molecular changes induced by B-1 lymphocytes on B16 cells have not yet been elucidated. in this study, we used a microarray approach to assess the gene expression profile of B16 melanoma cells following contact with B-1 lymphocytes (B16B1). the microarray analysis identified upregulation in genes involved with metastatic progression, such as ctss, ccl5, cxcl2 and stat3. RT-qPCR confirmed this increase in mRNA expression in B16B1 samples. As previous studies have indicated that the ERK1/2 MAPK cascade is activated in melanoma cells following contact with B-1 lymphocytes, RT-qPCR was performed with RNA from melanoma cells before and after contacting B-1 cells and untreated or treated with ERK phosphorylation inhibitors. the results showed that the expression of stat3, ctss and cxcl2 increased in B16B1 but decreased following ERK1/2 MAPK inhibition. Ccl5 gene expression increased after contacting B-1 cells and was maintained at the same level following inhibitor treatment. Stat3 was verified and validated at the protein level by Western blot analysis. STAT3 expression was also significantly increased in B16B1, suggesting that this pathway can also contribute to the increased metastatic phenotype observed in our model. These results indicated that B-1 cells induce important global gene expression changes in B16 melanoma cells. We also evaluated the relationship of some of the genes identified as differentially expressed and the ERK1/2 MAPK cascade. This work may have important implications for understanding the role of B-1 lymphocytes and the ERK/MAPK cascade in the metastatic process. (C) 2013 Elsevier GmbH. All rights reserved.
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Further insights into B-1 cell biology
(Medicina (buenos Aires), 2007-01-01) Mariano, Mario [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Univ Paulista
The term B-1 cell was originally proposed to describe a subtype of B lymphocytes, which differs from 8 conventional cells by anatomical localization, developmental origin, surface markers expression, antibody repertoire and growth properties. B-1 cells express high levels of surface IgM, low levels of B220 (CD45R) and IgD, but not CD23, whereas conventional B-2 cells express high levels of B220 and IgD, CD23 and low levels of IgM. Besides, typical B-1 cells residing in peritoneal cavity also express low levels of Mac-1 (CD11b). Further, B-1 cells are sub classified in B-1a cells, which express CD5, and their phenotypic CD5(-) twins, B-1b cells. Our laboratory has demonstrated that B-1b cells proliferate in cultures of adherent mouse peritoneal cells and differentiate into a mononuclear phagocyte, provisionally named lymphophage. Yet, that these cells migrate from the peritoneal cavity to a non specific inflammatory lesion. From these observations the origin, differentiation and function of these cells in normal and pathological conditions have been intensively investigated in our laboratory. The morphology of B-1 cells, its participation in giant cell formation and granuloma development in vitro, and facilitation of murine melanoma growth will be presented and discussed.
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Gene Expression in B-1 Cells from Lupus-Prone Mice
(Informa Healthcare, 2014-01-01) Novaes e Brito, Ronni Romulo [UNIFESP]; Xander, Patricia [UNIFESP]; Perez, Elizabeth C. [UNIFESP]; Maricato, Juliana Terzi [UNIFESP]; Laurindo, Maria Fl. [UNIFESP]; De Lorenzo, Beatriz H. P. [UNIFESP]; Pellegrino, Renata [UNIFESP]; Bernardo, Viviane [UNIFESP]; Lopes, Jose Daniel [UNIFESP]; Mariano, Mario [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Ctr Univ Sao Camilo
New Zealand Black X New Zealand White F1 [(NZB/NZW) F1] mice develop an autoimmune condition with similarities to human systemic lupus erythematosus (SLE). in this study, we demonstrate that B-1 cells, which have previously been reported to be involved in several autoimmune diseases, have altered gene expression in these mice. RNA was extracted from purified B-1 cells of disease-free C57BL/6 mice and lupus-prone (NZB/NZW) F1 mice. Gene expression was analysed using DNA microarray techniques and validated by real time reverse transcriptase polymerase chain reaction (RT-PCR). in (NZB/NZW) F1 mice, some genes had altered expression patterns compared to disease-free controls. Specifically, the upregulation of Ifitm1, Pvrl2 and Ifi202b and downregulation of Trp53bp1 mRNA were observed in (NZB/NZW) F1 mice. These genes are known to be associated with autoimmune diseases. This pattern of gene expression in B-1 cells could understanding of the pathogenesis of SLE. Thus, it is reasonable to hypothesise that the altered gene expression observed in B-1 cells in our experimental model is important for SLE prognosis and therapy, and these implications are discussed herein.
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Granuloma formation in vitro requires B-1 cells and is modulated by Paracoccidioides brasiliensis gp43 antigen
(Elsevier B.V., 2006-03-01) Vigna, A. F.; Almeida, SR; Xander, Patricia [UNIFESP]; Freymuller, E.; Mariano, M.; Lopes, J. D.; Universidade Federal de São Paulo (UNIFESP); Universidade de São Paulo (USP)
The mechanisms that determine granuloma formation and the significance of this type of inflammatory response in the pathogenesis of fungal diseases such as paracoccidioidomycosis are far from fully understood. We developed a granuloma model in vitro using beads to evaluate the role of isolated mouse peritoneal macrophages and B-1 cells. We also investigated granuloma formation in the presence of gp43, the main antigenic component of Paracoccidioides brasiliensis, which is secreted exocellularly. To determine whether B-1 cells, macrophages, or both, participate in granuloma formation, peritoneal cells from Xid mice, which lack B-1 cells, were used. Granuloma-like structures were not formed with Xid peritoneal cells or with cells from wild type mice that had their peritoneal and pleural cavities irradiated before the cultures were established. Granulomas were observed either when total adherent peritoneal cells or when isolated B-1 cells were added to macrophage cultures. the data strongly suggest that an interaction of B-1 cells and macrophages plays an important role in granuloma-like formation in this experimental model and that the presence of gp43 strongly stimulates this response. (c) 2005 Elsevier SAS. All rights reserved.
Acesso aberto (Open Access)
A Influência de Células B-1 na atividade supressora de células Treg FOXP3+ geradas in vitro
(Universidade Federal de São Paulo, 2017-12-21) Lima, Karina Alcantara de [UNIFESP]; Mariano, Mario [UNIFESP]; Alvares, Anuska Marcelino [UNIFESP]; http://lattes.cnpq.br/2148473770830932; http://lattes.cnpq.br/8301816484338841; http://lattes.cnpq.br/3440256325596611; Universidade Federal de São Paulo (UNIFESP)
The role of B-1 cells in the development of Treg cells has been studied recently. In vitro assays demonstrated that B-1a cells are capable of converting CD4+CD25+ T cells into a cell with regulatory potential without FOXP3 expression. Previously, we demonstrated that B-1 cells could regulate the proliferative activity of FOXP3+ Treg cells in vitro e upregulate Treg cells population in the peritoneal cavity of mice, under physiological and pathogenic conditions. In this study, we aimed to understand the role of B-1 cells in the suppressive activity of FOXP3+ Treg cells generated in vitro with TGF-β stimulation. For this, we performed a co-culture of naive T-cell in the presence of B-1 cells, in order to generate in vitro Treg cells and, after, to evaluate the suppression mechanisms of these cells by effector T cell suppression assay. Thus, in vitro generation of Treg cells is more efficient in cocultures with B-1 cells, which favors the proliferation of Treg cells and modulate the cytokine profile into these cultures. These cells (called iTreg(B-1)) demonstrated suppressive activity similar to the observed in iTregs generated without B-1 cells and also natural Tregs. And we have also shown that B-1 cells can modify the mechanism of suppression in iTreg(B-1) increasing the relative gene expression of CTLA-4. Our results may contribute to future studies aimed therapy with Treg cells and new methodologies for obtaining such cells.
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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
(Elsevier B.V., 2014-06-01) Cruz-Leal, Yoelys; Lucatelli Laurindo, Maria Fernanda [UNIFESP]; Osugui, Lika [UNIFESP]; del Carmen Luzardo, Maria; Lopez-Requena, Alejandro; Eugenia Alonso, Maria; Alvarez, Carlos; Flavia Popi, Ana [UNIFESP]; Mariano, Mario [UNIFESP]; Perez, Rolando; Eliana Lanio, Maria; Univ Havana; Universidade Federal de São Paulo (UNIFESP); Ctr Mol Immunol CIM
Macrophages respond to endogenous and non-self stimuli acquiring the M1 or M2 phenotypes, corresponding to classical or alternative activation, respectively. the role of B-1 cells in the regulation of macrophage polarization through the secretion of interleukin (IL)-10 has been demonstrated. However, the influence of B-1 cells on macrophage phenotype induction by an immunogen that suppress their ability to secrete IL-10 has not been explored. Here, we studied the peritoneal macrophage pattern induced by liposomes comprised of dipalmitoylphosphatidylcholine (DPPC) and cholesterol (Chol) carrying ovalbumin (OVA) (Lp DPPC/OVA), and the involvement of B-1 cells in macrophage polarization. Peritoneal cells from BALB/c, B-1 cells-deficient BALB/xid and C57BL/6 mice immunized with Lp DPPC/OVA and OVA in soluble form (PBS/OVA) were analyzed and stimulated or not in vitro with lipopolysaccharide (LPS). Peritoneal macrophages from BALB/c and C57BL/6 mice immunized with Lp DPPC/OVA showed an M2-like phenotype as evidenced by their high arginase activity without LPS stimulation. Upon stimulation, these macrophages were reprogrammable toward the M1 phenotype with the upregulation of nitric oxide (NO) and a decrease in IL-10 secretion. in addition, high IFN-gamma levels were detected in the culture supernatant of peritoneal cells from BALB/c and C57BL/6 mice immunized with Lp DPPC/OVA. Nevertheless, still high levels of arginase activity and undetectable levels of IL-12 were found, indicating that the switch to a classical activation state was not complete. in the peritoneal cells from liposomes-immunized BALB/xid mice, levels of arginase activity, NO, and IL-6 were below those from wild type animals, but the last two products were restored upon adoptive transfer of B-1 cells, together with an increase in IFN-gamma secretion. Summarizing, we have demonstrated that Lp DPPC/OVA induce an M2-like pattern in peritoneal macrophages reprogrammable to M1 phenotype after LPS stimulation, with the involvement of B-1 cells. (C) 2014 Elsevier GmbH. All rights reserved.
Acesso aberto (Open Access)
An Overview of B-1 Cells as Antigen-Presenting Cells
(Frontiers Media Sa, 2016) Popi, Ana Flavia [UNIFESP]; Longo-Maugéri, Ieda Maria [UNIFESP]; Mariano, Mario [UNIFESP]
The role of B cells as antigen-presenting cells (APCs) has been extensively studied, mainly in relation to the activation of memory T cells. Considering the B cell subtypes, the role of B-1 cells as APCs is beginning to be explored. Initially, it was described that B-1 cells are activated preferentially by T-independent antigens. However, some reports demonstrated that these cells are also involved in a T-dependent response. The aim of this review is to summarize information about the ability of B-1 cells to play a role as APCs and to briefly discuss the role of the BCR and toll-like receptor signals in this process. Furthermore, some characteristics of B-1 cells, such as natural IgM production and phagocytic ability, could interfere in the participation of these cells in the onset of an adaptive response.
Acesso aberto (Open Access)
Papel da via WNT no desenvolvimento de células B-1
(Universidade Federal de São Paulo (UNIFESP), 2016-04-30) Osugui, Lika [UNIFESP]; Popi, Ana Flavia [UNIFESP]; http://lattes.cnpq.br/6073701470193039; http://lattes.cnpq.br/4874492953571723; Universidade Federal de São Paulo (UNIFESP)
Hematopoietic stem cells (HSC) are capable to generate multipotent progenitors that produce all blood cell lineages, and exhibit high proliferative potential and are able to self-renewal. Several molecules has been described to participate in the embryo cells development and commitment. In this context, Wnt proteins have an important role in many biological processes, included participation in different stages of the lymphocyte development and HSC self-renewal. Although B-1 cells are considered mature cells, they express two different programs simultaneously, the lymphoid and myeloid ones, and are self-renewing cells. In order to evaluate the role that Wnt pathway plays in this permissiveness and the self-renewal property, B-1 cells were purified and the Wnt receptors expression were verified by qPCR, showing the Fzd6 are the most expressed Wnt receptor. In co-culture experiments of B-1 and OP9 cells, stimulated or not with Wnt3a or Wnt5a, increased amount of viable and proliferative cells were observed in the Wnt3a treated group. The canonical Wnt signaling activation was assessed by Axin2 expression that was detected in the both treated groups. When the transcription factors related to lymphoid and myeloid lineage were analyzed, the Flt3 gene was upregulated after the both stimuli and IL- 7R was upregulated only when Wnt3a was added to the cultures. Despite of in vitro results indicated the role of canonical Wnt signaling in the B-1 self-renewal, the in vivo assays involving adoptive Wnt-reporter mice (Axin2+/lacZ) derived-B-1 cell transference to RAG-1 mice did not demonstrate increase number of the Wnt activated B-1 cells. Interestingly, B-1 progenitors (B-1P) showed an expressive response when cultivated onto Wnt5a-transduced OP9 cells, expanding their pool 40 times more in relation to the input cell number. Moreover, in the presence of Wnt3a- transduced OP9 cells, B-1P originated a significant population of CD5+ cells. Altogether, these data suggest that mature B-1 cells, and mainly B-1 progenitors are able to respond to Wnt ligands and this signaling could be important to maintenance of this B cell subtype. The pronounced response to Wnt ligands observed in the progenitors suggests that this Wnt pathway could be involved in the B-1 cell development and differentiation process.

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