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Article ; Online: Neuroimmune interactions: dendritic cell modulation by the sympathetic nervous system.

Takenaka, Maisa C / Guereschi, Marcia G / Basso, Alexandre S

2017 Volume 39, Issue 2, Page(s) 165–176

Abstract: Dendritic cells are of paramount importance bridging innate and adaptive immune responses. Depending on the context, after sensing environmental antigens, commensal microorganisms, pathogenic agents, or antigens from the diet, dendritic cells may drive ... ...

Abstract	Dendritic cells are of paramount importance bridging innate and adaptive immune responses. Depending on the context, after sensing environmental antigens, commensal microorganisms, pathogenic agents, or antigens from the diet, dendritic cells may drive either different effector adaptive immune responses or tolerance, avoiding tissue damage. Although the plasticity of the immune response and the capacity to regulate itself are considered essential to orchestrate appropriate physiological responses, it is known that the nervous system plays a relevant role controlling immune cell function. Dendritic cells present in the skin, the intestine, and lymphoid organs, besides expressing adrenergic receptors, can be reached by neurotransmitters released by sympathetic fibers innervating these tissues. These review focus on how neurotransmitters from the sympathetic nervous system can modulate dendritic cell function and how this may impact the immune response and immune-mediated disorders.
MeSH term(s)	Animals ; Cytokines/metabolism ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Humans ; Immune System/cytology ; Immune System/physiology ; Intestines/immunology ; Intestines/innervation ; Intestines/metabolism ; Lymphoid Tissue/immunology ; Lymphoid Tissue/innervation ; Lymphoid Tissue/metabolism ; Neuroimmunomodulation ; Norepinephrine/metabolism ; Receptors, Adrenergic/metabolism ; Signal Transduction ; Skin/immunology ; Skin/innervation ; Skin/metabolism ; Sympathetic Nervous System/physiology
Chemical Substances	Cytokines ; Receptors, Adrenergic ; Norepinephrine (X4W3ENH1CV)
Language	English
Publishing date	2017-02
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	2316828-6
ISSN	1863-2300 ; 1863-2297
ISSN (online)	1863-2300
ISSN	1863-2297
DOI	10.1007/s00281-016-0590-0
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Article ; Online: Invariant Natural Killer T cells resilience to paradoxical sleep deprivation-associated stress.

Sousa, Maria E P / Gonzatti, Michelangelo B / Fernandes, Edgar R / Freire, Beatriz M / Guereschi, Márcia G / Basso, Alexandre S / Andersen, Monica L / Rosa, Daniela S / Keller, Alexandre C

Brain, behavior, and immunity

2020 Volume 90, Page(s) 208–215

Abstract: Although several studies demonstrate that stressful situations, such as sleep disturbances, negatively impact the innate and adaptive arms of the immune system, their influence on invariant Natural Killer T (iNKT) cells remains unclear. iNKT cells are ... ...

Abstract	Although several studies demonstrate that stressful situations, such as sleep disturbances, negatively impact the innate and adaptive arms of the immune system, their influence on invariant Natural Killer T (iNKT) cells remains unclear. iNKT cells are CD1d-restricted innate T cells that recognize glycolipid antigens and rapidly produce polarizing cytokines being key players in several immune responses, and a potential target for immunotherapy. iNKT cells differ in several aspects from conventional T lymphocytes, including a unique dependence on CD1d-expressing double-positive (DP) thymocytes for intrathymic maturation. As a consequence of stress, DP thymocytes undergo glucocorticoid-induced apoptosis, which might compromise iNKT developmental pathway. Therefore, we used a paradoxical sleep deprivation (SD) model to determine the impact of sleep disturbance on iNKT cell biology. After 72 h of SD, C57Bl/6 mice exhibited a significant increase in systemic glucocorticoid levels and thymus atrophy. Despite marked decrease in the number of DP thymocytes, the ratio CD1d
MeSH term(s)	Animals ; Cytokines ; Killer Cells, Natural ; Mice ; Mice, Inbred C57BL ; Natural Killer T-Cells ; Sleep, REM ; Spleen
Chemical Substances	Cytokines
Language	English
Publishing date	2020-08-19
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639219-2
ISSN	1090-2139 ; 0889-1591
ISSN (online)	1090-2139
ISSN	0889-1591
DOI	10.1016/j.bbi.2020.08.018
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Zs.A 2276: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: B-1 cells promote immunosurveillance against murine melanoma in host absence of CCR5: new perspective in autologous vaccination therapy.

Vivanco, Bruno C / Viana, Jacqueline D / Perez, Elisabeth C / Konno, Fabiana T C / Guereschi, Marcia G / Xander, Patricia / Keller, Alexandre C / Lopes, José D

Immunobiology

2014 Volume 219, Issue 11, Page(s) 845–849

Abstract: Autologous vaccination with tumor-primed dendritic cells increases immune response against tumor, which seems to be improved in host absence of CCR5. Because B-1 lymphocytes modulate the activity of different immune cells, we decided to study their ... ...

Abstract	Autologous vaccination with tumor-primed dendritic cells increases immune response against tumor, which seems to be improved in host absence of CCR5. Because B-1 lymphocytes modulate the activity of different immune cells, we decided to study their influence in the resistance against murine B16F10 melanoma in a CCR5 deprived environment. Adoptive transfer of peritoneal B-1 CCR5(+/+) lymphocytes to CCR5(-/-) animals inhibited the establishment of lung metastasis and melanoma cell growth, in comparison to saline-treated CCR5(-/-) mice. In loco cell analysis demonstrated that the adoptive transfer of B-1 CCR5(+/+) lymphocytes to CCR5 deficient host was associated with a more intense influx of T CD8(+) to tumor site, indicating that the presence of CCR5(+/+) B-1 cells in the tumor environment induces the migration of T CD8 CCR5(-/-) cells to the implantation site. To corroborate this idea, CCR5(-/-) mice were injected with non B-1 peritoneal cells from wild type (WT) mice before B16F10 inoculation. In this regimen, CCR5(-/-) mice were not protected from tumor growth reinforcing the idea that, in host absence of CCR5, B-1 cells are essential to confer tumor resistance. This work indicates that, in the host absence of CCR5, naive B-1 cells may activate CD8T lymphocytes thereby promoting tumor resistance. Our results strongly suggest that autologous vaccination with B-1 lymphocytes in combination with CCR5 antagonists can be an alternative approach to tumor therapy.
MeSH term(s)	Adoptive Transfer ; Animals ; B-Lymphocyte Subsets/immunology ; B-Lymphocyte Subsets/metabolism ; CD8-Positive T-Lymphocytes/immunology ; Cancer Vaccines/immunology ; Cell Line, Tumor ; Cell Movement/genetics ; Immunotherapy, Adoptive ; Lymphocytes, Tumor-Infiltrating/immunology ; Male ; Melanoma, Experimental/genetics ; Melanoma, Experimental/immunology ; Melanoma, Experimental/mortality ; Melanoma, Experimental/pathology ; Melanoma, Experimental/therapy ; Mice ; Mice, Knockout ; Monitoring, Immunologic ; Receptors, CCR5/deficiency ; Receptors, CCR5/genetics
Chemical Substances	Cancer Vaccines ; Receptors, CCR5
Language	English
Publishing date	2014-11
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	563292-4
ISSN	1878-3279 ; 0171-2985
ISSN (online)	1878-3279
ISSN	0171-2985
DOI	10.1016/j.imbio.2014.07.013
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Article ; Online: GCN2 kinase plays an important role triggering the remission phase of experimental autoimmune encephalomyelitis (EAE) in mice.

Orsini, Heloisa / Araujo, Leandro P / Maricato, Juliana T / Guereschi, Marcia G / Mariano, Mario / Castilho, Beatriz A / Basso, Alexandre S

Brain, behavior, and immunity

2014 Volume 37, Page(s) 177–186

Abstract: Experimental autoimmune encephalomyelitis (EAE) has been widely employed as a model to study multiple sclerosis (MS) and indeed has allowed some important advances in our comprehension of MS pathogenesis. Several pieces of evidence suggest that ... ...

Abstract	Experimental autoimmune encephalomyelitis (EAE) has been widely employed as a model to study multiple sclerosis (MS) and indeed has allowed some important advances in our comprehension of MS pathogenesis. Several pieces of evidence suggest that infiltrating Th1 and Th17 lymphocytes are important players leading to CNS demyelination and lesion during the peak of murine EAE. Subsequently, effector T cell responses rapidly decline and the recovery phase of the disease strongly correlates with the expression of anti-inflammatory cytokines and the enrichment of Foxp3+ regulatory T (Treg) cells within the target organ. However, the mechanisms leading to the increased presence of Treg cells and to the remission phase of the disease are still poorly understood. Recent researches demonstrated that chemically induced amino-acid starvation response might suppress CNS immune activity. Here we verified an important participation of the general control nonrepressible 2 (GCN2), a key regulator kinase of the amino-acid starvation response, in the development of the remission phase of EAE in C57BL/6 mice. By immunizing wild type C57BL/6 (WT) and GCN2 knock-out mice (GCN2 KO) with myelin oligodendrocyte glycoprotein peptide (MOG35-55), it was noticed that GCN2 KO mice did not develop the remission phase of the disease and this was associated with higher levels of CNS inflammation and increased presence of effector T cells (Th1/Th17). These animals also showed lower frequency of Treg cells within the CNS as compared to WT animals. Higher expression of indoleamine 2,3-dioxygenase (IDO) and higher frequency of plasmacytoid dendritic cells (pDCs) were found at the peak of the disease in the CNS of WT animals. Our results suggest that the GCN2 kinase-dependent sensing of IDO activity represents an important trigger to the EAE remission phase. The IDO-mediated immunoregulatory events may include the arresting of effector T cell responses and the differentiation/expansion of Treg cells within the target organ.
MeSH term(s)	Animals ; Cytokines/metabolism ; Encephalomyelitis, Autoimmune, Experimental/enzymology ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Forkhead Transcription Factors/metabolism ; Indoleamine-Pyrrole 2,3,-Dioxygenase/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/physiology ; Remission, Spontaneous ; Spinal Cord/pathology ; Th1 Cells/metabolism ; Th17 Cells/metabolism
Chemical Substances	Cytokines ; Forkhead Transcription Factors ; Foxp3 protein, mouse ; Indoleamine-Pyrrole 2,3,-Dioxygenase ; Eif2ak4 protein, mouse (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2014-03
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639219-2
ISSN	1090-2139 ; 0889-1591
ISSN (online)	1090-2139
ISSN	0889-1591
DOI	10.1016/j.bbi.2013.12.012
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Zs.A 2276: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article: Paracoccidioides brasiliensis GP43-derived peptides are potent modulators of local and systemic inflammatory response

Konno, Fabiana T.C / Maricato, Juliana / Konno, Adriana Y.C / Guereschi, Márcia G / Vivanco, Bruno C / Feitosa, Luciano dos Santos / Mariano, Mário / Lopes, José Daniel

Microbes and Infection. 2012 June, v. 14, no. 6

2012

Abstract: Paracoccidioidomycosis is a systemic granulomatous disease caused by the dimorphic fungus Paracoccidioides brasiliensis. Its major antigen is a 43 kDa glycoprotein whose peptides embody different functions: P10 peptide, a T-cell epitope, induces ... ...

Abstract	Paracoccidioidomycosis is a systemic granulomatous disease caused by the dimorphic fungus Paracoccidioides brasiliensis. Its major antigen is a 43 kDa glycoprotein whose peptides embody different functions: P10 peptide, a T-cell epitope, induces protective response while P4 and P23 peptides inhibit both, macrophage functions and inflammatory reaction, thus facilitating infection. Here we investigated the modulating mechanisms of the immune response exerted by P4 and P23 involved in the latter inhibitory effect on macrophages. Moreover we analyzed the peptides effects in different models in vivo. While evaluating whether P4 and P23 present systemic anti-inflammatory effects in vivo, we showed that their intraperitonial administration decreased footpad swelling in mice infected with either P. brasiliensis or Mycobacterium bovis. Both, qPCR and ELISA assays suggested that this anti-inflammatory effect depended on alterations in the kinetics of production of innate immunity modulators such as TNF-α, IL6, IL10 and TLR2. IL10 seems to be early produced than TNF-α and IL6, produced later in presence of peptides. Higher doses or intravenously given P4 and P23 resulted in earlier and more prolonged anti-inflammatory effects. Moreover, continuous treatment with P4 and P23 sustained the anti-inflammatory activity throughout.
Keywords	Mycobacterium bovis ; Paracoccidioides brasiliensis ; T-lymphocytes ; Toll-like receptor 2 ; anti-inflammatory activity ; enzyme-linked immunosorbent assay ; epitopes ; fungi ; glycoproteins ; immune response ; inflammation ; innate immunity ; interleukin-10 ; interleukin-6 ; intravenous injection ; macrophages ; mice ; models ; peptides ; quantitative polymerase chain reaction ; tumor necrosis factor-alpha
Language	English
Dates of publication	2012-06
Size	p. 517-527.
Publishing place	Elsevier Masson SAS
Document type	Article
ZDB-ID	1465093-9
ISSN	1769-714X ; 1286-4579
ISSN (online)	1769-714X
ISSN	1286-4579
DOI	10.1016/j.micinf.2011.12.012
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Beta2-adrenergic receptor signaling in CD4+ Foxp3+ regulatory T cells enhances their suppressive function in a PKA-dependent manner.

Guereschi, Marcia G / Araujo, Leandro P / Maricato, Juliana T / Takenaka, Maisa C / Nascimento, Vanessa M / Vivanco, Bruno C / Reis, Vanessa O / Keller, Alexandre C / Brum, Patrícia C / Basso, Alexandre S

European journal of immunology

2013 Volume 43, Issue 4, Page(s) 1001–1012

Abstract: Beta2-adrenergic receptor (B2AR) signaling is known to impair Th1-cell differentiation and function in a cAMP-dependent way, leading to inhibition of cell proliferation and decreased production of IL-2 and IFN-γ. CD4(+) Foxp3(+) Treg cells play a key ... ...

Abstract	Beta2-adrenergic receptor (B2AR) signaling is known to impair Th1-cell differentiation and function in a cAMP-dependent way, leading to inhibition of cell proliferation and decreased production of IL-2 and IFN-γ. CD4(+) Foxp3(+) Treg cells play a key role in the regulation of immune responses and are essential for maintenance of self-tolerance. Nevertheless, very little is known about adrenergic receptor expression in Treg cells or the influence of noradrenaline on their function. Here we show that Foxp3(+) Treg cells express functional B2AR. B2AR activation in Treg cells leads to increased intracellular cAMP levels and to protein kinase A (PKA)-dependent CREB phosphorylation. We also found that signaling via B2AR enhances the in vitro suppressive activity of Treg cells. B2AR-mediated increase in Treg-cell suppressive function was associated with decreased IL-2 mRNA levels in responder CD4(+) T cells and improved Treg-cell-induced conversion of CD4(+) Foxp3(-) cells into Foxp3(+) induced Treg cells. Moreover, B2AR signaling increased CTLA-4 expression in Treg cells in a PKA-dependent way. Finally, we found that PKA inhibition totally prevented the B2AR-mediated increase in Treg-cell suppressive function. Our data suggest that sympathetic fibers are able to regulate Treg-cell suppressive activity in a positive manner through B2AR signaling.
MeSH term(s)	Animals ; CD4 Antigens/metabolism ; CTLA-4 Antigen/immunology ; CTLA-4 Antigen/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Forkhead Transcription Factors/metabolism ; Interleukin-2/biosynthesis ; Lymphocyte Activation/immunology ; Mice ; Mice, Knockout ; Receptors, Adrenergic, beta-2/metabolism ; Signal Transduction ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism
Chemical Substances	CD4 Antigens ; CTLA-4 Antigen ; Forkhead Transcription Factors ; Foxp3 protein, mouse ; Interleukin-2 ; Receptors, Adrenergic, beta-2 ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11)
Language	English
Publishing date	2013-04
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.201243005
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Zs.A 489: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article: Exercise Induced Alterations in Rat Monocyte Number, Morphology, and Function.

Guereschi, Marcia G / Prestes, Jonato / Donatto, Felipe F / Dias, Rodrigo / Frollini, Anelena B / Ferreira, Clílton Ko / Cavaglieri, Claudia R / Palanch, Adrianne C

International journal of exercise science

2008 Volume 1, Issue 2, Page(s) 71–78

Abstract: The purpose of this study was to verify the histophysiological alterations in monocytes and macrophages induced by short periods of exercise. Male Wistar rats (age = 2 months, body weight = 200g) were divided into seven groups (N = 6 each): sedentary ... ...

Abstract	The purpose of this study was to verify the histophysiological alterations in monocytes and macrophages induced by short periods of exercise. Male Wistar rats (age = 2 months, body weight = 200g) were divided into seven groups (N = 6 each): sedentary control (C), groups exercised (swimming) at low intensity for 5 (5L), 10 (10L), and 15 minutes (15L), and groups exercised at moderate intensity for 5 (5M), 10 (10M) or 15 minutes (15M). At moderate intensity the animals carried a load of 5% of body weight on their backs. Blood monocytes were evaluated for quantity and morphology, and peritoneal macrophages were analyzed for quantity and phagocytic activity. Data were analyzed using ANOVA and Tukey's post hoc test (p ≤ 0.05). Low intensity groups and 5M exhibited an increase in monocyte levels when compared with the control. There was an increase in monocyte cellular area for the 5L, 10L, 5M and 10M groups; monocyte nuclear area increased for the 10L, 5M and 10M groups in comparison with the control. There was an increase in peritoneal macrophages for the 15L, 10M, 15M and decrease for the 5M group. Macrophage phagocytic capacity increased for low intensity groups and for 10M group. The exercise performed for short periods modulated macrophage levels and function, and monocyte levels and morphology, in an intensity-dependent manner. The sum of acute responses observed in this study may exert a protective effect against sickness and may be used to improve health and lifespan.
Language	English
Publishing date	2008
Publishing country	United States
Document type	Journal Article
ZDB-ID	2411342-6
ISSN	1939-795X
ISSN	1939-795X
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Article: [No title information]

Guereschi, Marcia G / Prestes, Jonato / Donatto, Felipe F / Dias, Rodrigo / Frollini, Anelena B / Ferreira, Clílton Ko / Cavaglieri, Claudia R / Palanch, Adrianne C

International journal of exercise science

2008 Volume 1, Issue 2, Page(s) 71–78

Title translation	Alterações Induzidas Pelo Exercício no Número, Função e Morfologia de Monócitos de Ratos.
Language	Portuguese
Publishing date	2008
Publishing country	United States
Document type	Journal Article
ZDB-ID	2411342-6
ISSN	1939-795X
ISSN	1939-795X
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Paracoccidioides brasiliensis GP43-derived peptides are potent modulators of local and systemic inflammatory response.

Konno, Fabiana T C / Maricato, Juliana / Konno, Adriana Y C / Guereschi, Márcia G / Vivanco, Bruno C / Feitosa, Luciano dos Santos / Mariano, Mário / Lopes, José Daniel

Microbes and infection

2012 Volume 14, Issue 6, Page(s) 517–527

Abstract	Paracoccidioidomycosis is a systemic granulomatous disease caused by the dimorphic fungus Paracoccidioides brasiliensis. Its major antigen is a 43 kDa glycoprotein whose peptides embody different functions: P10 peptide, a T-cell epitope, induces protective response while P4 and P23 peptides inhibit both, macrophage functions and inflammatory reaction, thus facilitating infection. Here we investigated the modulating mechanisms of the immune response exerted by P4 and P23 involved in the latter inhibitory effect on macrophages. Moreover we analyzed the peptides effects in different models in vivo. While evaluating whether P4 and P23 present systemic anti-inflammatory effects in vivo, we showed that their intraperitonial administration decreased footpad swelling in mice infected with either P. brasiliensis or Mycobacterium bovis. Both, qPCR and ELISA assays suggested that this anti-inflammatory effect depended on alterations in the kinetics of production of innate immunity modulators such as TNF-α, IL6, IL10 and TLR2. IL10 seems to be early produced than TNF-α and IL6, produced later in presence of peptides. Higher doses or intravenously given P4 and P23 resulted in earlier and more prolonged anti-inflammatory effects. Moreover, continuous treatment with P4 and P23 sustained the anti-inflammatory activity throughout.
MeSH term(s)	Amino Acid Sequence ; Animals ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use ; Antigens, Fungal/chemistry ; Cytokines/immunology ; Cytokines/metabolism ; Foot/microbiology ; Fungal Proteins/chemistry ; Glycoproteins/chemistry ; Inflammation/drug therapy ; Inflammation/immunology ; Inflammation/microbiology ; Macrophages/drug effects ; Macrophages/immunology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Molecular Sequence Data ; Paracoccidioides/drug effects ; Paracoccidioides/pathogenicity ; Paracoccidioidomycosis/drug therapy ; Paracoccidioidomycosis/immunology ; Paracoccidioidomycosis/microbiology ; Paracoccidioidomycosis/physiopathology ; Peptides/chemical synthesis ; Peptides/chemistry ; Peptides/pharmacology ; Peptides/therapeutic use
Chemical Substances	43 kDa protein, Paracoccidioides ; Anti-Inflammatory Agents ; Antigens, Fungal ; Cytokines ; Fungal Proteins ; Glycoproteins ; Peptides
Language	English
Publishing date	2012-06
Publishing country	France
Document type	Journal Article
ZDB-ID	1465093-9
ISSN	1769-714X ; 1286-4579
ISSN (online)	1769-714X
ISSN	1286-4579
DOI	10.1016/j.micinf.2011.12.012
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