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Citation: Marakalala MJ, Ndlovu H (2017) Signaling C-type lectin receptors in antimycobacterial immunity. PLoS Pathog 13(6): e1006333. Editor: John M. Leong, Tufts Univ School of Medicine, UNITED STATES Published: June 22, 2017 Copyright: © 2017 Marakalala, Ndlovu. This is an open access article distributed under the terms of the, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Funding: The authors acknowledge funding from the South African Medical Research Council (SAMRC) self-initiated research grant () (MJM), The National Research Foundation () (MJM), SAMRC with funding from South African Department of Health (), and the University of Cape Town (HN and MJM). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

We acknowledge Dr. Claire Hoving for useful discussions.

Competing interests: The authors have declared that no competing interests exist. Introduction The mammalian innate immune system is composed of phagocytes such as macrophages and dendritic cells that serve as the first line of defense against microbial infections. These cells express various pattern recognition receptors (PRRs) that recognize specific pathogen-associated molecular patterns (PAMPs) on the surface of or inside microorganisms []. Panasonic toughbook serial number breakdown. PRRs such as Toll-like receptors (TLRs), C-type lectin receptors (CLRs), and Nucleotide-binding Oligomerization Domain (NOD)-like receptors (NLRs) have been widely studied in antimicrobial immunity and homeostasis. These PRRs have also been implicated in antimycobacterial immunity, with CLRs recently receiving considerable attention.

CLRs are a large family of proteins containing at least 1 carbohydrate-recognition domain (CRD) that in most cases binds a range of carbohydrate-based PAMPs, including trehalose 6,6’ dimycolate (TDM), lipoarabinomannan (LAM), lipomannan (LM), and phosphatidylinositol mannosides (PIMs) [–]. Interactions of CLRs with mycobacterial PAMPs induce intracellular signaling that triggers responses ranging from cytokine production to induction of adaptive immunity (). Here, we discuss signaling CLRs that recognize mycobacterial PAMPs and contribute to antimycobacterial immunity. I doser version 45 cracked over 200 doses in adults. We focus on the receptors that signal through the Spleen tyrosine kinase (Syk)/Caspase recruitment domain family member 9 (CARD9) pathway, including Dectin-1, Dectin-2, macrophage-inducible C-type lectin (Mincle), C-type lectin superfamily member 8 (Clecsf8) also called macrophage C-type lectin (MCL), and dendritic cell immunoactivating receptor (DCAR) (). Recognition of mycobacterial pathogen-associated molecular patterns (PAMPs) by C-type lectin receptors (CLRs). Dectin-2 recognizes mannosylated lipoarabinomannan (ManLAM), dendritic cell immunoactivating receptor (DCAR) recognizes phosphatidylinositol mannosides (PIMs), macrophage-inducible C-type lectin (Mincle) and C-type lectin superfamily member 8 (Clecsf8) recognize the glycolipid trehalose 6,6’ dimycolate (TDM), while the mycobacterial ligand of Dectin-1 is yet to be identified. The interaction of the CLRs with mycobacterial PAMPs triggers cytoplasmic signaling and a number of cellular responses.