Gustavo Martínez

ORCID: 0000-0003-0178-3329
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About
Contact & Profiles
Research Areas
  • Immune Cell Function and Interaction
  • T-cell and B-cell Immunology
  • Educational theories and practices
  • Immunodeficiency and Autoimmune Disorders
  • Immunotherapy and Immune Responses
  • Ovarian function and disorders
  • Immune Response and Inflammation
  • Tuberculosis Research and Epidemiology
  • Psoriasis: Treatment and Pathogenesis
  • Signaling Pathways in Disease
  • Reproductive Biology and Fertility
  • Reproductive System and Pregnancy
  • CAR-T cell therapy research
  • Educational Outcomes and Influences
  • Education and Teacher Training
  • Educational Innovations and Technology
  • Social Skills and Education
  • Educational Research and Science Teaching
  • Education in Rural Contexts
  • Epigenetics and DNA Methylation
  • IL-33, ST2, and ILC Pathways
  • Sperm and Testicular Function
  • Mycobacterium research and diagnosis
  • COVID-19 Impact on Reproduction
  • Developmental and Educational Neuropsychology

Fecunditas Instituto de Medicina Reproductiva
2021-2025

Universidad Nacional de Córdoba
2007-2024

Consejo Nacional de Investigaciones Científicas y Técnicas
2021-2024

Sanatorio Otamendi y Miroli
2019-2024

Rosalind Franklin University of Medicine and Science
2017-2023

Hospital Militar Central
2023

Biology of Infection
2022

University of Buenos Aires
2004-2021

Franklin University
2016-2021

Universidade Federal de Minas Gerais
2021

A fundamental function of CD4+ helper T (T(H)) cells is the regulation B cell-mediated humoral immunity. Development follicular (T(FH)) that provide help to mediated by cytokines interleukin-6 and interleukin-21 but independent TH1, TH2, TH17 effector cell lineages. Here, we characterize Bcl6, a transcription factor selectively expressed in T(FH) cells. Bcl6 expression regulated interleukin-21. overexpression induced T(FH)-related gene inhibited other T(H) lineage differentiation DNA...

10.1126/science.1176676 article EN Science 2009-07-24

Toll-like receptors (TLRs) are critical components of innate immunity and function as rapid pathogen sensors. TLR4 is expressed on CD4 + T cells well, the functional significance which unclear. In this study, we analyzed in but did not find a role promoting helper (Th) cell polarization. Instead, ligation enhanced both T-cell proliferation survival vitro. Using experimental autoimmune encephalomyelitis (EAE) model, found that loss solely almost completely abrogated disease symptoms, mainly...

10.1073/pnas.1120585109 article EN Proceedings of the National Academy of Sciences 2012-07-23

Abstract Protective immunity against Mycobacterium tuberculosis requires the generation of cell-mediated immunity. We investigated expression and role programmed death 1 (PD-1) its ligands, molecules known to modulate T cell activation, in regulation IFN-γ production lytic degranulation during human tuberculosis. demonstrated that specific Ag-stimulation increased CD3+PD-1+ lymphocytes peripheral blood pleural fluid from patients direct correlation with these individuals. Moreover, M....

10.4049/jimmunol.181.1.116 article EN The Journal of Immunology 2008-07-01

Transforming growth factor beta (TGF-beta) is a crucial cytokine with pleiotropic functions on immune cells. In CD4(+) T cells, TGF-beta required for induction of both regulatory and Th17 However, the molecular mechanism underlying this differential cell fate decision remains unclear. study, we have evaluated role Smad3 in development was found to be dispensable natural function. Foxp3 expression by naive cells significantly reduced absence molecule. On contrary, deficiency led enhanced...

10.1074/jbc.c109.078238 article EN cc-by Journal of Biological Chemistry 2009-11-03

Development of Foxp3(+) regulatory T cells and pro-inflammatory Th17 from naive CD4(+) requires transforming growth factor-β (TGF-β) signaling. Although Smad4 Smad3 have been previously shown to regulate Treg cell induction by TGF-β, they are not required in the development cells. Thus, how TGF-β regulates differentiation remains unclear. In this study, we found that TGF-β-induced Foxp3 expression was significantly reduced absence Smad2. More importantly, Smad2 deficiency led vitro vivo....

10.1074/jbc.c110.155820 article EN cc-by Journal of Biological Chemistry 2010-07-29

In the IL-17 family of cytokines, much is known about sources and functions IL-17, IL-17F, IL-25 in host defense against infection inflammatory diseases; however, physiological function IL-17C remains poorly understood. Using mice deficient IL-17C, we demonstrate that this cytokine crucial for regulation an acute experimental colitis elicited by dextran sulfate sodium. model, lacking exhibited exacerbated disease was associated with increased expression γδ T cells Th17 cells. Moreover,...

10.4049/jimmunol.1103014 article EN The Journal of Immunology 2012-10-01

Acquisition of effector properties is a key step in the generation cytotoxic T lymphocytes (CTLs). Here we show that inflammatory signals regulate Dicer expression CTLs, and deletion or depletion mouse human activated CD8(+) cells causes up-regulation perforin, granzymes, cytokines. Genome-wide analysis microRNA (miR, miRNA) changes induced by exposure differentiating CTLs to IL-2 identifies miR-139 miR-150 as components an miRNA network controls eomesodermin, IL-2Rα whose activity modulated...

10.1073/pnas.1317191110 article EN Proceedings of the National Academy of Sciences 2013-10-25

RNA drug targets are pervasive in cells, but methods to design small molecules that target them sparse. Herein, we report a general approach score the affinity and selectivity of motif–small molecule interactions identified via selection. Named High Throughput Structure–Activity Relationships Through Sequencing (HiT-StARTS), HiT-StARTS is statistical nature compares input nucleic acid sequences selected library members bind ligand high throughput sequencing. The allowed facile definition...

10.1021/acscentsci.7b00009 article EN publisher-specific-oa ACS Central Science 2017-03-06

Abstract IL-9 is a proallergic cytokine produced by newly proposed Th cell subset, Th9. Th9 cells can be generated treatment of naive T with TGF-β and IL-4 in vitro. However, it still not clear how signaling regulates differentiation. In this study, we demonstrate that Smad2 Smad4, two transcriptional factors activated signaling, are required for differentiation Deficiency or Smad4 resulted impaired expression, which was coincident enrichment repressive chromatin modification histone H3 K27...

10.4049/jimmunol.1300433 article EN The Journal of Immunology 2013-10-10

Abstract Follicular CD4+ Th (Tfh) cells provide B cell help in germinal center reactions that support class switching, somatic hypermutation, and the generation of high-affinity Abs. In this article, we show deficiency NFAT1 NFAT2 T leads to impaired upon viral infection because reduced Tfh differentiation defective expression proteins involved T/B interactions help, including ICOS, PD-1, SLAM family receptors. Genome-wide chromatin immunoprecipitation data suggest NFAT likely directly...

10.4049/jimmunol.1501841 article EN The Journal of Immunology 2016-02-06

Transforming growth factor–β (TGF-β) regulates reciprocal regulatory T cell (T reg) and helper 17 (Th17) differentiation, the underlying mechanism of which is still not understood. Here, we report that tripartite motif-containing 33 (Trim33), a modulator TGF-β signaling associates with Smad2, proinflammatory function Th17 cells. Trim33 deficiency in cells ameliorated an autoimmune disease vivo. was required for induction vitro Th17, but reg Moreover, Smad4 play contrasting roles regulation...

10.1084/jem.20170779 article EN cc-by-nc-sa The Journal of Experimental Medicine 2018-06-21
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