Isolation and characterisation of neural progenitor cells from the adult Chx10(orJ/orJ) central neural retina.

Retinal stem cells have been isolated from the ciliary epithelium (CE) of the mammalian retina. However, the central neural retina (CNR) lacks the capability to regenerate, a phenomenon retained by lower vertebrates. Mutations in the Chx10 homeobox gene cause reduced proliferation of retinal progenitor cells during development, leading to microphthalmia. Recently, we showed that in Chx10(orJ/orJ) mice, dividing cells persist in the adult CNR, suggesting the existence of a dormant progenitor population. Here, we show that these cells are proliferative and give rise to neurospheres in vitro, a characteristic of neural stem cells. However, these adult-derived CNR progenitors differ from those of the wildtype CE, leading to de-pigmented, larger and more numerous neurospheres expressing Müller glial cell markers. Our results suggest that lack of Chx10 leads to maintenance of a dormant neural progenitor population in the adult CNR. Furthermore, Chx10 is not required for in vitro proliferation of these progenitors.

Toll-like receptor mRNA expression patterns in human dendritic cells and monocytes.

The innate immune system recognises a wide spectrum of pathogens without a need for prior exposure. The main cells responsible are monocytes, macrophages, dendritic cells (DC) and neutrophils phagocytose microbial pathogens triggering a cytokine network resulting in the development of inflammatory and specific immune responses. Findings in the Toll-like receptor (TLR) family, initially discovered in Drosophila, further elucidated these processes. Toll-like receptors induce activation of an innate immune response and at present ten TLRs have been identified, named TLRs 1-10. In addition to the ignition of the innate immune response, evidence implicates the TLR family in a spectrum of systemic disorders following bacterial infections including sepsis and multiple organ failure, and can be detrimental, leading to tissue injury. In this project, our main goal was to investigate the effects of a TLR4 ligand, lipolysaccharide (LPS) in human DC and monocytes. Our hypothesis is that different professional APCs, express different mRNA TLR transcripts. Our findings indicate that TLR expression patterns change in relation to the pathogen involved and in the case of DC, and the maturation stage the latter are upon challenging. Our results and interpretation showed significant alteration of transcript expression patterns upon LPS challenge in all cell subsets, with DC subsets expressing different TLR mRNA patterns as they go through different maturation stages.