Lista de obras - Stephen J. Lalor - Dominio Público Uruguay

A population of proinflammatory T cells coexpresses αβ and γδ T cell receptors in mice and humans

artículo científico publicado en 2020

Activation of Human Vδ2+ γδ T Cells by Staphylococcus aureus Promotes Enhanced Anti-Staphylococcal Adaptive Immunity

artículo científico publicado en 2020

Antibodies to the RNA-binding protein hnRNP A1 contribute to neurodegeneration in a model of central nervous system autoimmune inflammatory disease.

scientific article published on 08 July 2016

Caspase-1-processed cytokines IL-1beta and IL-18 promote IL-17 production by gammadelta and CD4 T cells that mediate autoimmunity

artículo científico publicado en 2011

Correction: Staphylococcus aureus Infection of mice expands a population of memory γδ T cells that are protective against subsequent infection.

artículo científico publicado en 2015

Highly polarized Th17 cells induce EAE via a T-bet independent mechanism

scientific article published on 23 August 2013

Infiltration of Th1 and Th17 cells and activation of microglia in the CNS during the course of experimental autoimmune encephalomyelitis

artículo científico publicado en 2010

Inhibition of ERK MAPK Suppresses IL-23- and IL-1-Driven IL-17 Production and Attenuates Autoimmune Disease

artículo científico publicado en 2009

Interleukin-1 and IL-23 induce innate IL-17 production from gammadelta T cells, amplifying Th17 responses and autoimmunity.

artículo científico publicado en 2009

Memory Th1 Cells Are Protective in Invasive Staphylococcus aureus Infection.

artículo científico publicado en 2015

Memory γδ T Cells-Newly Appreciated Protagonists in Infection and Immunity.

artículo científico publicado en 2016

Response: Characteristics of IL-17-Producing γδ T Cells

Staphylococcus aureus infection of mice expands a population of memory γδ T cells that are protective against subsequent infection.

artículo científico publicado en 2014

T cells in multiple sclerosis and experimental autoimmune encephalomyelitis.