Cell Host and Microbe Guo Yahui, among others, reveal the body's congenital immune response to tobacco-cranked mold infections.

Fungal infection is an important cause of death in patients with low clinical immune function and deficiency.at present, the types of drugs that can be used to treat invasive fungal infections are very limited, with low specificity, large side effects and high price of broad-spectrum antifungal drugs. Moreover, drug resistance is easy to occur in the process of long-term treatment and repeated drug administration after fungal infection. Most of the fluconazole resistant fungi have cross resistance to other antifungal drugs, which leads to the true invasiveness Bacterial infection can not be cured for a long time, and eventually threaten the life of the infected.innate immune response is the first line of defense against fungal infection. Elucidating the immune response mechanism of antifungal infection can help us to further understand the interaction between fungi and host, and provide new strategies and targets for the prevention and treatment of fungal infection.on June 1, 2020, Tobias M. Hohl research team of memorial Katherine Cancer Research Center (MSKCC) published an online article entitled "during Aspergillus infection, neutrophil, Monocyte Derived DC" in Cell Host & amp; microbe journal, And plasmacytoid DC enhance endogenous defense through CXCR3 dependent crosstalk, which elucidates the role of neutrophils (NF), monocyte derived dendritic cells (Mo DC) and plasma cell like dendritic cells (PMDCs) in acute lung infection with Aspergillus fumigatus DC, PDC) regulates innate immune response to Aspergillus fumigatus infection through CXCR3 signal dependent interaction.in this study, researchers found that plasma cell like dendritic cells (pDCs), which are typically involved in anti viral immune response, play an important role in the mucosal immune cell interaction against fungal infection.the researchers found that mice with acute lung infection with Aspergillus fumigatus activated and recruited phagocytes Mo DCS and NF to reach the infection site, and secreted CXCL9 and cxcl0 through the C-type lectin receptor Dectin-1 / CARD9 signaling pathway and ifn-iii receptor signaling pathway of Mo DCS and NF cells, respectively CXCL9 and CXCL10 recruit pDCs expressing CXCR3 receptors to the fungal infection site.at the same time, the researchers found that the conditional knockout mice induced by diphtheria toxin were more susceptible to Aspergillus fumigatus than the control mice. Unlike the traditional phagocytes, PDC could not phagocytize and kill the spores of Aspergillus fumigatus, but PDC could kill the spores of Aspergillus fumigatus by regulating and activating NF to produce NADPH oxidase.in general, this study elucidates that CXCR3 receptor dependent PDC positive feedback regulates the killing and clearance of NF against Aspergillus fumigatus.these findings provide a theoretical basis for further understanding the mechanism of innate immune cell interaction, and provide new molecular targets and therapeutic strategies for the increasingly serious fungal infection diseases.Tobias M. Hohl, MD, PhD of MSKCC is the corresponding author of this paper. He graduated from the research group of Professor Lin Xin, School of medicine, Tsinghua University. Dr. Guo Yahui, who is now a postdoctoral doctor of MSKCC and Dr. Shinji Kasahara, a former postdoctoral doctor of Tobias M. Hohl laboratory, are co authors of this paper.the work was supported by amariliz Rivera of New Jersey medical school, Rutgers biomedical and Health Sciences (rbhs) and Andrew D. luster from Massachusetts General Hospital.original link: