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1.
Am J Physiol Lung Cell Mol Physiol ; 326(6): L812-L820, 2024 Jun 01.
Artículo en Inglés | MEDLINE | ID: mdl-38712445

RESUMEN

Chronic obstructive pulmonary disease (COPD) is a condition characterized by chronic airway inflammation and obstruction, primarily caused by tobacco smoking. Although the involvement of immune cells in COPD pathogenesis is well established, the contribution of innate lymphoid cells (ILCs) remains poorly understood. ILCs are a type of innate immune cells that participate in tissue remodeling processes, but their specific role in COPD has not been fully elucidated. During COPD, the breakdown of pulmonary elastin generates elastin peptides that elicit biological activities on immune cells. This study aimed to investigate the presence of ILC in patients with COPD and examine the impact of elastin peptides on their functionality. Our findings revealed an elevated proportion of ILC2 in the peripheral blood of patients with COPD, and a general activation of ILC as indicated by an increase in their cytokine secretion capacity. Notably, our study demonstrated that serum from patients with COPD promotes ILC2 phenotype, likely due to the elevated concentration of IL-5, a cytokine known to favor ILC2 activation. Furthermore, we uncovered that this increase in IL-5 secretion is partially attributed to its secretion by macrophages upon stimulation by elastin peptides, suggesting an indirect role of elastin peptides on ILC in COPD. These findings shed light on the involvement of ILC in COPD and provide insights into the potential interplay between elastin breakdown, immune cells, and disease progression. Further understanding of the mechanisms underlying ILC activation and their interaction with elastin peptides could contribute to the development of novel therapeutic strategies for COPD management.NEW & NOTEWORTHY Elastin-derived peptides, generated following alveolar degradation during emphysema in patients with COPD, are able to influence the response of type 2 innate lymphoid cells. We show that the orientation of innate lymphoid cells in patients with COPD is shifted toward a type 2 profile and that elastin peptides are indirectly participating in that shift through their influence of macrophages, which in turn impact innate lymphoid cells.


Asunto(s)
Elastina , Inmunidad Innata , Linfocitos , Enfermedad Pulmonar Obstructiva Crónica , Humanos , Enfermedad Pulmonar Obstructiva Crónica/inmunología , Enfermedad Pulmonar Obstructiva Crónica/patología , Elastina/metabolismo , Elastina/inmunología , Linfocitos/inmunología , Linfocitos/metabolismo , Linfocitos/efectos de los fármacos , Femenino , Masculino , Anciano , Persona de Mediana Edad , Interleucina-5/metabolismo , Interleucina-5/inmunología , Macrófagos/inmunología , Macrófagos/metabolismo , Péptidos/farmacología , Péptidos/inmunología
2.
Int J Cancer ; 2024 Jul 30.
Artículo en Inglés | MEDLINE | ID: mdl-39077999

RESUMEN

Optimizations are expected in the development of immunotherapy for the treatment of Triple-negative breast cancer (TNBC). We studied the expression of galectin-9 (Gal-9) after irradiation and assessed the differential impacts of its targeting with or without radiotherapy. Tumor resections from TNBC patients who received neoadjuvant radiotherapy revealed higher levels of Gal-9 in comparison to their baseline level, only in non-responder patients. Gal-9 expression was also found to be increased in TNBC tumor biopsies and cell lines after irradiation. We investigated the therapeutic advantage of targeting Gal-9 after radiotherapy in mice. Irradiated 4T1 cells or control non-irradiated 4T1 cells were injected into BALB/c mice. Anti-Gal-9 antibody treatment decreased tumor progression only in mice injected with irradiated 4T1 cells. This proof-of-concept study demonstrates that Gal-9 could be considered as a dynamic biomarker after radiotherapy for TNBC and suggests that Gal-9 induced-overexpression could represent an opportunity to develop new therapeutic strategies for TNBC patients.

3.
Proc Natl Acad Sci U S A ; 115(29): E6826-E6835, 2018 07 17.
Artículo en Inglés | MEDLINE | ID: mdl-29967180

RESUMEN

Antibody-secreting plasma cells (PCs) arise rapidly during adaptive immunity to control infections. The early PCs are retained within the reactive lymphoid organ where their localization and homeostasis rely on extrinsic factors, presumably produced by local niche cells. While myeloid cells have been proposed to form those niches, the contribution by colocalizing stromal cells has remained unclear. Here, we characterized a subset of fibroblastic reticular cells (FRCs) that forms a dense meshwork throughout medullary cords of lymph nodes (LNs) where PCs reside. This medullary FRC type is shown to be anatomically, phenotypically, and functionally distinct from T zone FRCs, both in mice and humans. By using static and dynamic imaging approaches, we provide evidence that medullary FRCs are the main cell type in contact with PCs guiding them in their migration. Medullary FRCs also represent a major local source of the PC survival factors IL-6, BAFF, and CXCL12, besides also producing APRIL. In vitro, medullary FRCs alone or in combination with macrophages promote PC survival while other LN cell types do not have this property. Thus, we propose that this FRC subset, together with medullary macrophages, forms PC survival niches within the LN medulla, and thereby helps in promoting the rapid development of humoral immunity, which is critical in limiting early pathogen spread.


Asunto(s)
Formación de Anticuerpos , Homeostasis/inmunología , Ganglios Linfáticos/inmunología , Células Plasmáticas/inmunología , Animales , Factor Activador de Células B/inmunología , Quimiocina CXCL12/inmunología , Interleucina-6/inmunología , Ganglios Linfáticos/citología , Masculino , Ratones , Células Plasmáticas/citología , Células del Estroma/citología , Células del Estroma/inmunología
4.
J Immunol ; 193(12): 5914-23, 2014 Dec 15.
Artículo en Inglés | MEDLINE | ID: mdl-25381435

RESUMEN

CD4 regulatory T cells (Tregs) can be subdivided into two subsets according to Ly-6C expression in the periphery. Phenotypic analysis, imaging, and adoptive-transfer experiments of peripheral Ly-6C(-) and Ly-6C(+) Tregs reveal that the nonexpression of Ly-6C by ∼70% of peripheral Tregs depends on TCR signaling events. Interestingly, Ly-6C(-) Tregs express higher surface amounts of key immunosuppressive molecules than do Ly-6C(+) Tregs and produce constitutively anti-inflammatory cytokines. In line with their phenotype, Ly-6C(+) Tregs exhibit poor suppressive capacities in vitro and in vivo. Finally, although Ly-6C(-) Tregs maintain their numbers with age, Ly-6C(+) Tregs gradually disappear. Altogether, our data strongly suggest that both the survival and suppressive functions of peripheral CD4 Tregs rely on their ability to receive strong TCR signals.


Asunto(s)
Inmunomodulación , Receptores de Antígenos de Linfocitos T/metabolismo , Transducción de Señal , Subgrupos de Linfocitos T/inmunología , Subgrupos de Linfocitos T/metabolismo , Linfocitos T Reguladores/inmunología , Linfocitos T Reguladores/metabolismo , Factores de Edad , Envejecimiento/inmunología , Animales , Antígenos Ly/genética , Antígenos Ly/metabolismo , Antígenos de Superficie/genética , Antígenos de Superficie/metabolismo , Expresión Génica , Inmunofenotipificación , Ganglios Linfáticos/inmunología , Ganglios Linfáticos/metabolismo , Activación de Linfocitos/genética , Activación de Linfocitos/inmunología , Ratones , Ratones Transgénicos , Fenotipo
5.
Proc Natl Acad Sci U S A ; 110(32): 13085-90, 2013 Aug 06.
Artículo en Inglés | MEDLINE | ID: mdl-23878221

RESUMEN

The present study evaluates the impact of immune cell populations on metastatic development in a model of spontaneous melanoma [mice expressing the human RET oncogene under the control of the metallothionein promoter (MT/ret mice)]. In this model, cancer cells disseminate early but remain dormant for several weeks. Then, MT/ret mice develop cutaneous metastases and, finally, distant metastases. A total of 35% of MT/ret mice develop a vitiligo, a skin depigmentation attributable to the lysis of normal melanocytes, associated with a delay in tumor progression. Here, we find that regulatory CD4(+) T cells accumulate in the skin, the spleen, and tumor-draining lymph nodes of MT/ret mice not developing vitiligo. Regulatory T-cell depletion and IL-10 neutralization led to increased occurrence of vitiligo that correlated with a decreased incidence of melanoma metastases. In contrast, inflammatory monocytes/dendritic cells accumulate in the skin of MT/ret mice with active vitiligo. Moreover, they inhibit tumor cell proliferation in vitro through a reactive oxygen species-dependent mechanism, and both their depletion and reactive oxygen species neutralization in vivo increased tumor cell dissemination. Altogether, our data suggest that regulatory CD4(+) T cells favor tumor progression, in part, by inhibiting recruitment and/or differentiation of inflammatory monocytes in the skin.


Asunto(s)
Inflamación/inmunología , Melanoma/inmunología , Monocitos/inmunología , Linfocitos T Reguladores/inmunología , Animales , Proliferación Celular , Femenino , Citometría de Flujo , Humanos , Inflamación/genética , Inflamación/patología , Ganglios Linfáticos/inmunología , Ganglios Linfáticos/metabolismo , Ganglios Linfáticos/patología , Masculino , Melanoma/genética , Melanoma/patología , Metalotioneína/genética , Ratones , Ratones Endogámicos C57BL , Ratones Noqueados , Ratones Transgénicos , Monocitos/metabolismo , Metástasis de la Neoplasia , Regiones Promotoras Genéticas/genética , Proteínas Proto-Oncogénicas c-ret/genética , Proteínas Proto-Oncogénicas c-ret/inmunología , Especies Reactivas de Oxígeno/inmunología , Especies Reactivas de Oxígeno/metabolismo , Piel/inmunología , Piel/metabolismo , Piel/patología , Bazo/inmunología , Bazo/metabolismo , Linfocitos T Reguladores/metabolismo , Factores de Tiempo , Vitíligo/genética , Vitíligo/inmunología
6.
J Immunol ; 189(7): 3339-46, 2012 Oct 01.
Artículo en Inglés | MEDLINE | ID: mdl-22933631

RESUMEN

Work over the last decades has led to the identification of the factors that influence the survival and homeostasis of conventional T cells. IL-7 and TCR signaling promote the survival of naive CD4(+) and CD8(+) T cells in lymphoreplete mice and their proliferation in a lymphopenic environment, whereas survival and homeostatic proliferation of memory CD4(+) and CD8(+) T cells crucially depend on a combination of IL-7 and IL-15. In contrast, there is little information regarding the factors driving the proliferation of regulatory CD4(+) T cells in response to lymphopenia. In this study, we investigated whether regulatory CD4(+) T cell proliferation in response to lymphopenia was guided by classical homeostatic resources, such as IL-2, IL-7, or TCR-MHC interactions. Altogether, our data suggest that, although homeostatic proliferation of conventional naive CD4(+) T cells is closely related to IL-7 levels, the proliferation of regulatory CD4(+) T cells in response to lymphopenia appears to be primarily controlled by IL-2. The capacity of IL-7 to augment conventional T cell proliferation with minimal concomitant regulatory T cell expansion may be clinically exploitable in the treatment of patients with lymphopenia, especially in the case of chronic viral diseases or cancer immunotherapy.


Asunto(s)
Linfocitos T CD4-Positivos/inmunología , Compartimento Celular/inmunología , Homeostasis/inmunología , Interleucina-2/fisiología , Interleucina-7/fisiología , Animales , Linfocitos T CD4-Positivos/patología , Linfocitos T CD4-Positivos/trasplante , Compartimento Celular/genética , Ciclo Celular/genética , Ciclo Celular/inmunología , Proliferación Celular , Células Cultivadas , Genes Reporteros , Homeostasis/genética , Linfopenia/genética , Linfopenia/inmunología , Linfopenia/patología , Ratones , Ratones Endogámicos C57BL , Ratones Noqueados , Ratones Transgénicos , Linfocitos T Reguladores/citología , Linfocitos T Reguladores/inmunología , Linfocitos T Reguladores/metabolismo
7.
Eur J Immunol ; 42(5): 1237-49, 2012 May.
Artículo en Inglés | MEDLINE | ID: mdl-22539296

RESUMEN

In the periphery, Foxp3 expression is considered sufficient to maintain natural regulatory CD4(+) T-cell suppressive function. In this study, we challenge this model. Indeed, in mouse chimeras in which major histocompatibility complex (MHC) class II expression is restricted to the thymus, peripheral regulatory CD4(+) T cells lack suppressive activity. In addition, regulatory CD4(+) T cells recovered 5 days after transfer into recipient mice lacking expression of MHC class II molecules (self-deprived) are unable to inhibit the proliferative response of conventional CD4(+) T cells both in vitro and in vivo. Disruption of TCR/MHC class II interactions rapidly leads to alterations in the regulatory CD4(+) T-cell phenotype, the ability to respond to stimulation and to produce interleukin-10, and the transcriptional signature. Interestingly, self-deprivation does not affect Foxp3 expression indicating that in regulatory CD4(+) T cells, self-recognition induces unique transcriptional and functional features that do not rely on Foxp3 expression.


Asunto(s)
Factores de Transcripción Forkhead/fisiología , Tolerancia Inmunológica , Linfocitos T Reguladores/inmunología , Animales , Células Cultivadas , Quimera/inmunología , Técnicas de Cocultivo , Antígenos de Histocompatibilidad Clase II/fisiología , Interleucina-10/biosíntesis , Interleucina-10/fisiología , Activación de Linfocitos/inmunología , Ratones , Receptores de Antígenos de Linfocitos T/fisiología , Transcriptoma/inmunología
8.
J Exp Med ; 217(10)2020 10 05.
Artículo en Inglés | MEDLINE | ID: mdl-32667673

RESUMEN

C-C chemokine receptor type 2 (CCR2) is expressed on monocytes and facilitates their recruitment to tumors. Though breast cancer cells also express CCR2, its functions in these cells are unclear. We found that Ccr2 deletion in cancer cells led to reduced tumor growth and approximately twofold longer survival in an orthotopic, isograft breast cancer mouse model. Deletion of Ccr2 in cancer cells resulted in multiple alterations associated with better immune control: increased infiltration and activation of cytotoxic T lymphocytes (CTLs) and CD103+ cross-presenting dendritic cells (DCs), as well as up-regulation of MHC class I and down-regulation of checkpoint regulator PD-L1 on the cancer cells. Pharmacological or genetic targeting of CCR2 increased cancer cell sensitivity to CTLs and enabled the cancer cells to induce DC maturation toward the CD103+ subtype. Consistently, Ccr2-/- cancer cells did not induce immune suppression in Batf3-/- mice lacking CD103+ DCs. Our results establish that CCR2 signaling in cancer cells can orchestrate suppression of the immune response.


Asunto(s)
Inmunidad Adaptativa/inmunología , Tolerancia Inmunológica , Neoplasias Mamarias Experimentales/inmunología , Receptores CCR2/fisiología , Inmunidad Adaptativa/fisiología , Animales , Apoptosis , Antígeno B7-H1/metabolismo , Células Dendríticas/inmunología , Células Dendríticas/fisiología , Femenino , Antígenos de Histocompatibilidad Clase I/metabolismo , Tolerancia Inmunológica/inmunología , Tolerancia Inmunológica/fisiología , Interferones/metabolismo , Ratones , Ratones Endogámicos C57BL , Receptores CCR2/inmunología , Linfocitos T Citotóxicos/inmunología , Linfocitos T Citotóxicos/fisiología
9.
Science ; 364(6446): 1156-1162, 2019 06 21.
Artículo en Inglés | MEDLINE | ID: mdl-31221853

RESUMEN

Glycosylation alterations are indicative of tissue inflammation and neoplasia, but whether these alterations contribute to disease pathogenesis is largely unknown. To study the role of glycan changes in pancreatic disease, we inducibly expressed human fucosyltransferase 3 and ß1,3-galactosyltransferase 5 in mice, reconstituting the glycan sialyl-Lewisa, also known as carbohydrate antigen 19-9 (CA19-9). Notably, CA19-9 expression in mice resulted in rapid and severe pancreatitis with hyperactivation of epidermal growth factor receptor (EGFR) signaling. Mechanistically, CA19-9 modification of the matricellular protein fibulin-3 increased its interaction with EGFR, and blockade of fibulin-3, EGFR ligands, or CA19-9 prevented EGFR hyperactivation in organoids. CA19-9-mediated pancreatitis was reversible and could be suppressed with CA19-9 antibodies. CA19-9 also cooperated with the KrasG12D oncogene to produce aggressive pancreatic cancer. These findings implicate CA19-9 in the etiology of pancreatitis and pancreatic cancer and nominate CA19-9 as a therapeutic target.


Asunto(s)
Antígeno CA-19-9/metabolismo , Carcinoma Ductal Pancreático/metabolismo , Receptores ErbB/metabolismo , Neoplasias Pancreáticas/metabolismo , Pancreatitis/metabolismo , Enfermedad Aguda , Animales , Antígeno CA-19-9/inmunología , Carcinogénesis/metabolismo , Carcinoma Ductal Pancreático/patología , Línea Celular Tumoral , Enfermedad Crónica , Proteínas de la Matriz Extracelular/metabolismo , Fucosiltransferasas/genética , Fucosiltransferasas/metabolismo , Galactosiltransferasas/genética , Galactosiltransferasas/metabolismo , Glicosilación , Humanos , Ratones , Terapia Molecular Dirigida/métodos , Neoplasias Pancreáticas/patología , Pancreatitis/patología
10.
Science ; 360(6394)2018 06 15.
Artículo en Inglés | MEDLINE | ID: mdl-29773669

RESUMEN

The majority of patients with pancreatic ductal adenocarcinoma (PDA) develop metastatic disease after resection of their primary tumor. We found that livers from patients and mice with PDA harbor single disseminated cancer cells (DCCs) lacking expression of cytokeratin 19 (CK19) and major histocompatibility complex class I (MHCI). We created a mouse model to determine how these DCCs develop. Intraportal injection of immunogenic PDA cells into preimmunized mice seeded livers only with single, nonreplicating DCCs that were CK19- and MHCI- The DCCs exhibited an endoplasmic reticulum (ER) stress response but paradoxically lacked both inositol-requiring enzyme 1α activation and expression of the spliced form of transcription factor XBP1 (XBP1s). Inducible expression of XBP1s in DCCs, in combination with T cell depletion, stimulated the outgrowth of macrometastatic lesions that expressed CK19 and MHCI. Thus, unresolved ER stress enables DCCs to escape immunity and establish latent metastases.


Asunto(s)
Carcinoma Ductal Pancreático/secundario , Estrés del Retículo Endoplásmico/inmunología , Neoplasias Hepáticas/secundario , Neoplasias Pancreáticas/patología , Escape del Tumor , Animales , Carcinoma Ductal Pancreático/inmunología , Endorribonucleasas/genética , Endorribonucleasas/metabolismo , Genes MHC Clase I , Ingeniería Genética , Humanos , Queratina-19/metabolismo , Neoplasias Hepáticas/inmunología , Depleción Linfocítica , Ratones , Ratones Endogámicos C57BL , Neoplasias Experimentales/genética , Neoplasias Experimentales/inmunología , Neoplasias Experimentales/secundario , Neoplasias Pancreáticas/inmunología , Proteínas Serina-Treonina Quinasas/genética , Proteínas Serina-Treonina Quinasas/metabolismo , Linfocitos T/inmunología , Proteína 1 de Unión a la X-Box/genética , Proteína 1 de Unión a la X-Box/metabolismo
11.
Science ; 361(6409)2018 09 28.
Artículo en Inglés | MEDLINE | ID: mdl-30262472

RESUMEN

Cancer cells from a primary tumor can disseminate to other tissues, remaining dormant and clinically undetectable for many years. Little is known about the cues that cause these dormant cells to awaken, resume proliferating, and develop into metastases. Studying mouse models, we found that sustained lung inflammation caused by tobacco smoke exposure or nasal instillation of lipopolysaccharide converted disseminated, dormant cancer cells to aggressively growing metastases. Sustained inflammation induced the formation of neutrophil extracellular traps (NETs), and these were required for awakening dormant cancer. Mechanistic analysis revealed that two NET-associated proteases, neutrophil elastase and matrix metalloproteinase 9, sequentially cleaved laminin. The proteolytically remodeled laminin induced proliferation of dormant cancer cells by activating integrin α3ß1 signaling. Antibodies against NET-remodeled laminin prevented awakening of dormant cells. Therapies aimed at preventing dormant cell awakening could potentially prolong the survival of cancer patients.


Asunto(s)
Carcinogénesis/metabolismo , Trampas Extracelulares/enzimología , Laminas/metabolismo , Neoplasias Pulmonares/patología , Neutrófilos/enzimología , Neumonía/patología , Animales , ADN/metabolismo , Humanos , Inflamación/inducido químicamente , Inflamación/microbiología , Integrina alfa3beta1/metabolismo , Elastasa de Leucocito/metabolismo , Lipopolisacáridos , Pulmón/patología , Células MCF-7 , Metaloproteinasa 9 de la Matriz/metabolismo , Ratones , Ratones Endogámicos BALB C , Neoplasias Experimentales/patología , Neumonía/inducido químicamente , Neumonía/microbiología , Neumonía Bacteriana/etiología , Neumonía Bacteriana/patología , Arginina Deiminasa Proteína-Tipo 4 , Desiminasas de la Arginina Proteica/antagonistas & inhibidores , Desiminasas de la Arginina Proteica/metabolismo , Proteolisis , Ratas , Transducción de Señal , Fumar , Nicotiana
12.
Oncoimmunology ; 2(11): e26384, 2013 Nov 01.
Artículo en Inglés | MEDLINE | ID: mdl-24353918

RESUMEN

Although the role of myeloid cells in oncogenesis and tumor progression remains poorly understood, these cells are mainly ascribed with pro-tumor properties. We have recently unveiled a tumoricidal activity of inflammatory monocytes that can be counteracted by CD4+ regulatory T cells.

13.
Nat Commun ; 4: 2209, 2013.
Artículo en Inglés | MEDLINE | ID: mdl-23900386

RESUMEN

Upon activation, naive CD4 T cells differentiate into a variety of T-helper-cell subsets characterized by different cytokine production and functions. Currently, lineage commitment is considered to depend mostly on the environmental context to which naive CD4 T cells are exposed. Here we challenge this model based on the supposed homogeneity of the naive CD4 T-cell compartment. We show that peripheral naive CD4 T cells can be subdivided into two subsets according to Ly-6C expression. Furthermore, the two newly defined subsets (Ly-6C(-) and Ly-6C(+) naive CD4 T cells) are not equal in their intrinsic ability to commit into the induced regulatory T-cell lineage. Finally, phenotypic analysis, imaging and adoptive transfer experiments reveal that Ly-6C expression is modulated by self-recognition, allowing the dichotomization of the naive CD4 T-cell compartment into two cell subsets with distinct self-reactivity. Altogether, our results show that naive CD4 T cells with the highest avidity for self are prone to differentiate into regulatory T cells.


Asunto(s)
Diferenciación Celular/inmunología , Linfocitos T Reguladores/citología , Linfocitos T Reguladores/inmunología , Traslado Adoptivo , Animales , Antígenos Ly/metabolismo , Polaridad Celular/inmunología , Citometría de Flujo , Fluorescencia , Factores de Transcripción Forkhead/metabolismo , Proteínas Fluorescentes Verdes/metabolismo , Antígenos de Histocompatibilidad Clase II/metabolismo , Enfermedades Inflamatorias del Intestino/inmunología , Enfermedades Inflamatorias del Intestino/patología , Ratones , Ratones Endogámicos C57BL , Células Th17/citología , Células Th17/inmunología
14.
PLoS One ; 6(5): e20235, 2011.
Artículo en Inglés | MEDLINE | ID: mdl-21633700

RESUMEN

Tumors affect myelopoeisis and induce the expansion of myeloid cells with immunosuppressive activity. In the MT/ret model of spontaneous metastatic melanoma, myeloid cells are the most abundant tumor infiltrating hematopoietic population and their proportion is highest in the most aggressive cutaneous metastasis. Our data suggest that the tumor microenvironment favors polarization of myeloid cells into type 2 cells characterized by F4/80 expression, a weak capacity to secrete IL-12 and a high production of arginase. Myeloid cells from tumor and spleen of MT/ret mice inhibit T cell proliferation and IFNγ secretion. Interestingly, T cells play a role in type 2 polarization of myeloid cells. Indeed, intra-tumoral myeloid cells from MT/ret mice lacking T cells are not only less suppressive towards T cells than corresponding cells from wild-type MT/ret mice, but they also inhibit more efficiently melanoma cell proliferation. Thus, our data support the existence of a vicious circle, in which T cells may favor cancer development by establishing an environment that is likely to skew myeloid cell immunity toward a tumor promoting response that, in turn, suppresses immune effector cell functions.


Asunto(s)
Melanoma/inmunología , Células Mieloides/inmunología , Linfocitos T/inmunología , Microambiente Tumoral/inmunología , Animales , Antígenos de Diferenciación/inmunología , Antígenos de Diferenciación/metabolismo , Antígeno CD11b/genética , Antígeno CD11b/inmunología , Proliferación Celular , Modelos Animales de Enfermedad , Progresión de la Enfermedad , Femenino , Citometría de Flujo , Humanos , Interferón gamma/inmunología , Interferón gamma/metabolismo , Interleucina-10/genética , Interleucina-10/inmunología , Interleucina-12/inmunología , Interleucina-12/metabolismo , Masculino , Melanoma/genética , Melanoma/patología , Metalotioneína/genética , Metalotioneína/inmunología , Ratones , Ratones Noqueados , Ratones Transgénicos , Células Mieloides/metabolismo , Proteínas Proto-Oncogénicas c-ret/genética , Proteínas Proto-Oncogénicas c-ret/inmunología , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Linfocitos T/metabolismo
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