C-type lectins in immunity and homeostasis

Brown, Gordon D.; Willment, Janet A.; Whitehead, Lauren

doi:10.1038/s41577-018-0004-8

Cited by 521 publications

(460 citation statements)

References 172 publications

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“…Functional analysis suggested that reducing FAMK-1 phosphorylation of one lectin (CLEC-233) resulted in mild phenotypes in embryos analogous to those observed in famk-1Δ. Lectins are increasingly recognized as critical players in diverse aspects of multicellular life (Brown et al, 2018). In particular, there is growing evidence for potential functions for C-type lectins in bone mineralization and/or mineralized structure formation (Wewer et al, 1994;Mann and Siedler, 2006;Yue et al, 2016).…”

Section: Lectins: One Class Of Famk-1 Substratesmentioning

confidence: 98%

Ancestral roles of the Fam20C family of secreted protein kinases revealed in C. elegans

Gerson-Gurwitz

Worby

Lee

et al. 2019

Journal of Cell Biology

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Fam20C is a secreted protein kinase mutated in Raine syndrome, a human skeletal disorder. In vertebrates, bone and enamel proteins are major Fam20C substrates. However, Fam20 kinases are conserved in invertebrates lacking bone and enamel, suggesting other ancestral functions. We show that FAMK-1, the Caenorhabditis elegans Fam20C orthologue, contributes to fertility, embryogenesis, and development. These functions are not fulfilled when FAMK-1 is retained in the early secretory pathway. During embryogenesis, FAMK-1 maintains intercellular partitions and prevents multinucleation; notably, temperature elevation or lowering cortical stiffness reduces requirement for FAMK-1 in these contexts. FAMK-1 is expressed in multiple adult tissues that undergo repeated mechanical strain, and selective expression in the spermatheca restores fertility. Informatic, biochemical, and functional analysis implicate lectins as FAMK-1 substrates. These findings suggest that FAMK-1 phosphorylation of substrates, including lectins, in the late secretory pathway is important in embryonic and tissue contexts where cells are subjected to mechanical strain.

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Section: Lectins: One Class Of Famk-1 Substratesmentioning

confidence: 98%

Ancestral roles of the Fam20C family of secreted protein kinases revealed in C. elegans

Gerson-Gurwitz

Worby

Lee

et al. 2019

Journal of Cell Biology

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“…Alternatively, the ITAM can be present in a receptor-associated signaling subunit. For example, in CD3 chains associated with the T-cell receptor (TCR), the CD79 chains associated with the B-cell receptor (BCR) and the FcRγ chain associating with the myeloid cell receptor Dectin-2 or the natural killer (NK) cell receptors NK1.1/Ly49D/Ly49H/NKG2D (2, 3). Upon receptor triggering, Src family kinases phosphorylate the ITAMs, thereby providing a docking site for Syk family kinases.…”

Section: Various Receptors Signal Via Carma/card Proteins and Malt1mentioning

confidence: 99%

Holding All the CARDs: How MALT1 Controls CARMA/CARD-Dependent Signaling

Juilland

Thome

2018

Front. Immunol.

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The scaffold proteins CARMA1-3 (encoded by the genes CARD11, -14 and -10) and CARD9 play major roles in signaling downstream of receptors with immunoreceptor tyrosine activation motifs (ITAMs), G-protein coupled receptors (GPCR) and receptor tyrosine kinases (RTK). These receptors trigger the formation of oligomeric CARMA/CARD-BCL10-MALT1 (CBM) complexes via kinases of the PKC family. The CBM in turn regulates gene expression by the activation of NF-κB and AP-1 transcription factors and controls transcript stability. The paracaspase MALT1 is the only CBM component having an enzymatic (proteolytic) activity and has therefore recently gained attention as a potential drug target. Here we review recent advances in the understanding of the molecular function of the protease MALT1 and summarize how MALT1 scaffold and protease function contribute to the transmission of CBM signals. Finally, we will highlight how dysregulation of MALT1 function can cause pathologies such as immunodeficiency, autoimmunity, psoriasis, and cancer.

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“…CLRs are a superfamily of more than 1000 secreted and transmembrane proteins that contain one or more C-type lectin domains (CTLDs). Although CTLDs are responsible for the binding of carbohydrates by CLRs, they can also bind several chemically unrelated molecules including proteins, lipids, and inorganic materials [7]. In particular, some CLRs expressed mainly by myeloid cells recognize fungal cell wall polysaccharides.…”

Section: Clr Signaling and Antifungal Innate Immunitymentioning

confidence: 99%

Cellular and molecular mechanisms of antifungal innate immunity at epithelial barriers: The role of C‐type lectin receptors

2020

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Humans are constantly exposed to fungi, either in the form of commensals at epithelial barriers or as inhaled spores. Innate immune cells play a pivotal role in maintaining commensal relationships and preventing skin, mucosal, or systemic fungal infections due to the expression of pattern recognition receptors that recognize fungal cell wall components and modulate both their activation status and the ensuing adaptive immune response. Commensal fungi also play a critical role in the modulation of homeostasis and disease susceptibility at epithelial barriers. This review will outline cellular and molecular mechanisms of anti‐fungal innate immunity focusing on C‐type lectin receptors and their relevance in the context of host‐fungi interactions at skin and mucosal surfaces in murine experimental models as well as patients susceptible to fungal infections.

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C-type lectins in immunity and homeostasis

Cited by 521 publications

References 172 publications

Ancestral roles of the Fam20C family of secreted protein kinases revealed in C. elegans

Ancestral roles of the Fam20C family of secreted protein kinases revealed in C. elegans

Holding All the CARDs: How MALT1 Controls CARMA/CARD-Dependent Signaling

Cellular and molecular mechanisms of antifungal innate immunity at epithelial barriers: The role of C‐type lectin receptors

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