Skip to main content

Dr Mario Labeta

Senior Lecturer

School of Medicine

Comment
Media commentator

Publication

2023

2018

2017

2016

2013

2012

2011

2009

2006

2003

2001

2000

Articles

Research

My research interest and activities have focused on the molecular mechanisms underlying microbial recognition by the innate immune system, in particular by Toll-like receptors (TLR). This family of innate immune receptors plays a pivotal role in infection clearance by mediating a prompt and efficient proinflammatory response to an array of microorganisms and their components, and by controlling the nature and magnitude of the adaptive immune response. My group’s early research focused on the immunobiology of the TLR co-receptor, CD14, which amplifies TLR-mediated responses. Recently, our research focus has been extended to include the regulation of the TLR-mediated inflammatory response to infection, the regulation by TLRs of other innate immune receptors, in particular those for the complement anaphylatoxin C5a, the design and characterisation of a TLR-based novel strategy to boost the immune response, and the role of TLRs in kidney-related pathologies.

Published key findings include: 1) the detection and characterisation of the TLR co-receptor soluble CD14 (sCD14) in human breast milk; 2) demonstration of the differential effect of sCD14 on human B cells; 3) the identification and characterisation of a naturally-occurring soluble form of TLR2 (sTLR2) capable of regulating pro-inflammatory responses; 4) demonstration of the presence of protein components of milk capable of enhancing and inhibiting TLR signalling; 5) the in vitro and in vivo characterisation of the anti-inflammatory capacity of sTLR2; 6) the identification and characterisation of a pro-inflammatory crosstalk between TLRs and complement receptors; 8) the description of a novel TLR2 peptide-based strategy to boost the immune response; 9) the description of the role and therapeutic target potential of TLR2 and TLR4 in peritoneal dialysis-associated fibrosis.