Langerin, the “Catcher in the Rye”: An important receptor for pathogens on Langerhans cells

Stoitzner, Patrizia; Romani, Nikolaus

doi:10.1002/eji.201141934

Cited by 21 publications

(19 citation statements)

References 31 publications

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“…Lack of plasmacytoid dendritic cells was also confirmed by the absence of CD123 + and CD2AP + cells showing plasmacytoid morphology (not shown). Langerhans cells are the predominant antigen-presenting cells in epithelial tissues and selectively express CD207(Langerin) receptor 34 . The occurrence of Langerhans cells has previously been reported throughout the female reproductive organs, especially in the vagina 35 , cervix 36 and endometrium 37 .…”

Section: Discussionmentioning

confidence: 99%

Characterization of the Immune Cell Repertoire in the Normal Fallopian Tube

Ardighieri¹,

Lonardi²,

Moratto³

et al. 2014

International Journal of Gynecological Pathology

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Recent studies implicating the fallopian tube as the site of putative precursors of ovarian serous carcinoma and the hypothesis that injury, inflammation and repair of the ovarian surface epithelium at the time of ovulation may be contributing factors to ovarian carcinogenesis, prompted us to undertake a comprehensive analysis of the immune cells in the normal fallopian tube. Accordingly, the aim of this study was to provide a base line for future studies exploring the relationship of inflammation to the early events of ovarian carcinogenesis by characterizing the immune cell repertoire in thirteen normal human fallopian tube, combining digital microscopy of immunostained slides and flow cytometry of fresh single cell suspensions, with a panel of markers that identify the most important adaptive and innate immune cells. We found that CD45+ leucocytes are regularly observed in the fallopian tube and are mainly composed of CD163+ macrophages, CD11c+ dendritic cells and CD8+ T-cells. In addition, there are minor populations of CD56+ NK cells, CD4+ T-cells, CD20+ B-cells, TCRγδ+ T-cells, and, among dendritic cells, CD207(Langerin)+ Langerhans cells. The cellular mapping that we performed indicates that the local immune system in the human fallopian tube is composed of a mixture of innate and adaptive immune cells, many of which are recognized as playing a role in cancer immune surveillance. This local immune system could provide a first line of defense against early precancerous lesions and could potentially be exploited for immune-based therapies.

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Section: Discussionmentioning

confidence: 99%

Characterization of the Immune Cell Repertoire in the Normal Fallopian Tube

Ardighieri¹,

Lonardi²,

Moratto³

et al. 2014

International Journal of Gynecological Pathology

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“…Langerin, a C-type lectin receptor, and CD1a, a major histocompatibility complex class I (MHC-I)-type transmembrane glycoprotein, have been shown to be involved in antigen internalization and presentation (15,16). Both E-cadherin and CLA facilitate LC adherence to KC; their downregulation aids in the migration of LC from the epidermis (17,18).…”

Section: Discussionmentioning

confidence: 99%

Quiescent Innate Response to Infective Filariae by Human Langerhans Cells Suggests a Strategy of Immune Evasion

et al. 2013

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bFilarial infection is initiated by mosquito-derived third-stage larvae (L3) deposited on the skin that transit through the epidermis, which contains Langerhans cells (LC) and keratinocytes (KC), among other cells. This earliest interaction between L3 and the LC likely conditions the priming of the immune system to the parasite. To determine the nature of this interaction, human LC (langerin ؉ E-cadherin ؉ CD1a ؉ ) were generated in vitro and exposed to live L3. LC exposed to live L3 for 48 h showed no alterations in the cell surface markers CD14, CD86, CD83, CD207, E-cadherin, CD80, CD40, and HLA-DR or in mRNA expression of inflammation-associated genes, such as those for interleukin 18 (IL-18), IL-18BP, and caspase 1. In contrast to L3, live tachyzoites of Toxoplasma gondii, an intracellular parasite, induced production of CXCL9, IP-10, and IL-6 in LC. Furthermore, preexposure of LC to L3 did not alter Toll-like receptor 3 (TLR3)-or TLR4-mediated expression of the proinflammatory cytokines IL-1␤, gamma interferon (IFN-␥), IL-6, or IL-10. Interestingly, cocultures of KC and LC produced significantly more IL-18, IL-1␣, and IL-8 than did cultures of LC alone, although exposure of the cocultures to live L3 did not result in altered cytokine production. Microarray examination of ex vivo LC from skin blisters that were exposed to live L3 also showed few significant changes in gene expression compared with unexposed blisters, further underscoring the relatively muted response of LC to L3. Our data suggest that failure by LC to initiate an inflammatory response to the invasive stage of filarial parasites may be a strategy for immune evasion by the filarial parasite. L ymphatic filariasis (LF) caused by the parasitic nematodesWuchereria bancrofti, Brugia malayi, and Brugia timori infects approximately 120 million people worldwide in 72 countries. The disfiguring clinical manifestations, such as lymphedema and hydrocele, result in substantial morbidity and social stigma (1). Infection in LF is initiated when mosquito-derived third-stage larvae (L3) are deposited in the skin, an organ containing innate cells, primarily epidermal-resident Langerhans cells (LC) and keratinocytes (KC). Given the parasites' route through the skin, it is likely that the early interaction between L3 and innate cells in the skin-LC in particular-conditions the initiation of the L3-specific immune response, as LC are known to migrate to the draining lymph nodes (LN) soon after antigen internalization.LC are a subset of antigen-presenting dendritic cells (DC) that are located in the epidermal layer of the skin. LC become activated after antigen internalization and mature phenotypically and functionally (reviewed in references 2 and 3). Upon activation, adhesion molecules (such as E-cadherin) are downregulated to allow migration from the skin to the LN, where mature LC can activate naïve T cells and initiate T cell development (reviewed in references 2 and 3).Until recently, LC were considered the major antigen-presenting cells (APC) responsible f...

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“…Langerhans cells (LCs) are a distinct subset of DCs that can be found in the epidermis and oropharyngeal mucosa and are effective APCs capable of inducing T cell responses [82]. LCs express a repertoire of PRRs, including TLRs and CLRs.…”

Section: Myeloid C-type Lectins Receptors—pattern Recognition Recementioning

confidence: 99%

Myeloid C-Type Lectin Receptors in Viral Recognition and Antiviral Immunity

Monteiro

Lepenies

2017

Viruses

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Recognition of viral glycans by pattern recognition receptors (PRRs) in innate immunity contributes to antiviral immune responses. C-type lectin receptors (CLRs) are PRRs capable of sensing glycans present in viral pathogens to activate antiviral immune responses such as phagocytosis, antigen processing and presentation, and subsequent T cell activation. The ability of CLRs to elicit and shape adaptive immunity plays a critical role in the inhibition of viral spread within the host. However, certain viruses exploit CLRs for viral entry into host cells to avoid immune recognition. To block CLR interactions with viral glycoproteins, antiviral strategies may involve the use of multivalent glycan carrier systems. In this review, we describe the role of CLRs in antiviral immunity and we highlight their dual function in viral clearance and exploitation by viral pathogens.

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Langerin, the “Catcher in the Rye”: An important receptor for pathogens on Langerhans cells

Cited by 21 publications

References 31 publications

Characterization of the Immune Cell Repertoire in the Normal Fallopian Tube

Characterization of the Immune Cell Repertoire in the Normal Fallopian Tube

Quiescent Innate Response to Infective Filariae by Human Langerhans Cells Suggests a Strategy of Immune Evasion

Myeloid C-Type Lectin Receptors in Viral Recognition and Antiviral Immunity

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