Genes and gene pathways in Candida infection

Advances in genetic technology have promoted an explosive increase in our knowledge of genes relevant to Candida infection, and our understanding of their mode of action. Although the major influence on susceptibility to systemic infection is the presence or absence of complement C5, at least two other genes, as yet unidentified, influence the severity of tissue damage. Mice in which specific genes have been deleted (gene-knockout) mice are now readily available, and have been used both in the analysis of receptor interactions with Candida, and to study the role of T cell-derived cytokines in clearance of the infection and the development of host resistance, but results have not always been consistent. Gene profiling studies, in both humans and mice, will no doubt resolve some of the present anomalie

Mycoplasma lipoproteins and Toll-like receptors*

Mycoplasmas, the smallest free-living, self-replicating bacteria with diameters of 200 to 800 nm, have been reported to be associated with human diseases. It is well known that the mycoplasma lipoprotein/peptide is able to modulate the host immune system, whose N-terminal structure is an important factor in inducing immunity and distinguishing Toll-like receptors (TLRs). However, there is still no clear elucidation about the pathogenic mechanism of mycoplasma lipoprotein/peptide and the signaling pathway. Some researchers have focused on understanding the structures of these proteins and the relationships between their structure and biological function. This review provides an update on the research in this field