Langerhans Cells Phagocytose Vaginal Epithelial Cells Undergoing Apoptosis during the Murine Estrous Cycle1

Parr, Margaret B.; Kepple, Larry; Parr, Earl L.

doi:10.1095/biolreprod45.2.252

Cited by 55 publications

(33 citation statements)

References 10 publications

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“…These results raise a question as to whether such phenotypically mature VEDCs still maintain the capacity to phagocytose pathogens at the frontline of mucosal surface. VEDCs, particularly during late metestrus and early diestrus, have been shown to take up apoptotic keratinocytes (17). Thus, it will be important to examine the role of the three distinct VEDC populations in the context of infectious agents and in the maintenance of immunological tolerance (34) within the reproductive organs.…”

Section: Discussionmentioning

confidence: 99%

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Vaginal epithelial dendritic cells renew from bone marrow precursors

Iijima

Linehan

Saeland³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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Dendritic cells (DCs) represent key professional antigen-presenting cells capable of initiating primary immune responses. A specialized subset of DCs, the Langerhans cells (LCs), are located in the stratified squamous epithelial layer of the skin and within the mucosal epithelial lining of the vaginal and oral cavities. The vaginal mucosa undergoes cyclic changes under the control of sex hormones, and the renewal characteristics of the vaginal epithelial DCs (VEDCs) remain unknown. Here, we examined the origin of VEDCs. In contrast to the skin epidermal LCs, the DCs in the epithelium of the vagina were found to be repopulated mainly by nonmonocyte bone-marrow-derived precursors, with a half-life of 13 days under steady-state conditions. Upon infection with HSV-2, the Gr-1 hi monocytes were found to give rise to VEDCs. Furthermore, flow cytometric analysis of the VEDCs revealed the presence of at least three distinct populations, namely, CD11b ؉ F4/80 hi , CD11b ؉ F4/80 int , and CD11b ؊ F4/80 ؊ . Importantly, these VEDC populations expressed CD207 at low levels and had a constitutively more activated phenotype compared with the skin LCs. Collectively, our results revealed mucosa-specific features of the VEDCs with respect to their phenotype, activation status, and homeostatic renewal potential.Langerhans cell ͉ monocyte ͉ mucosa ͉ viral infection

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Section: Discussionmentioning

confidence: 99%

“…The VEDCs have been found to contain Birbeck granule-like structures that fail to form the typical tennis-racket shape (17). Similar to the skin LCs, VEDCs have been shown to take up transluminally applied FITC-labeled tracers (18).…”

mentioning

confidence: 99%

Vaginal epithelial dendritic cells renew from bone marrow precursors

Iijima

Linehan

Saeland³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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“…Endocytosis of apoptotic vaginal keratinocytes by LCs during the estrus cycle has been described in mice (Parr et al, 1991). Physiological keratinocyte apoptosis in the normal oral mucosa is associated with normal epithelial turnover (Birchall et al, 1995).…”

Section: Keratinocyte Apoptosis and Lc Maturation In Olpmentioning

confidence: 99%

The Pathogenesis of Oral Lichen Planus

Sugerman

Savage²,

Walsh³

et al. 2002

Critical Reviews in Oral Biology & Medicine

645

584

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Both antigen-specific and non-specific mechanisms may be involved in the pathogenesis of oral lichen planus (OLP). Antigen-specific mechanisms in OLP include antigen presentation by basal keratinocytes and antigen-specific keratinocyte killing by CD8 + cytotoxic T-cells. Non-specific mechanisms include mast cell degranulation and matrix metalloproteinase (MMP) activation in OLP lesions. These mechanisms may combine to cause T-cell accumulation in the superficial lamina propria, basement membrane disruption, intra-epithelial T-cell migration, and keratinocyte apoptosis in OLP. OLP chronicity may be due, in part, to deficient antigen-specific TGF-␤1-mediated immunosuppression. The normal oral mucosa may be an immune privileged site (similar to the eye, testis, and placenta), and breakdown of immune privilege could result in OLP and possibly other autoimmune oral mucosal diseases. Recent findings in mucocutaneous graft-versus-host disease, a clinical and histological correlate of lichen planus, suggest the involvement of TNF-␣, CD40, Fas, MMPs, and mast cell degranulation in disease pathogenesis. Potential roles for oral Langerhans cells and the regional lymphatics in OLP lesion formation and chronicity are discussed. Carcinogenesis in OLP may be regulated by the integrated signal from various tumor inhibitors (TGF-␤1, TNF-␣, IFN-␥, IL-12) and promoters (MIF,. We present our recent data implicating antigen-specific and non-specific mechanisms in the pathogenesis of OLP and propose a unifying hypothesis suggesting that both may be involved in lesion development. The initial event in OLP lesion formation and the factors that determine OLP susceptibility are unknown.

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“…Several phagocytic cells are known to be involved in this process including macrophages, fibroblasts, and endothelial cells (1,8,11,12,16). Current assays to measure this process in vitro suffer from their inability to distinguish specific apoptotic cell recognition from adherence mechanisms involved in other cellcell interactions.…”

Section: Discussionmentioning

confidence: 99%

A novel flow cytometric method for quantifying phagocytosis of apoptotic cells

et al. 1997

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Many eukaryotic cell types are capable of specific recognition and phagocytosis of apoptotic cells, and there is increasing interest in the mechanisms involved in this process. To facilitate analysis of these mechanisms, we designed a novel fluorescence‐based method to quantify phagocytosis in vitro using endothelial cell engulfment of apoptotic cells as a model. The B‐cell line WEHI‐231 was labeled with the fluorophore 5‐(&‐6)‐carboxytetramethyl‐rhodamine‐succinimidyl‐ester (TAMRA) and then induced to undergo apoptosis by crosslinking cell surface immunoglobulin: An endothelial cell line was subsequently allowed to ingest these TAMRA‐labeled apoptotic lymphocytes. After 24 h, non‐bound lymphocytes were removed and the monolayers were dissociated. Any nonphagocytosed lymphocytes that remained tightly bound to the endothelial cells were then indirectly immunofluorescein labeled for the pan leukocyte‐specific marker CD45. Flow cytometric analysis of the cells distinguished three endothelial cell populations: 1) endothelial cells with surface bound lymphocytes (TAMRA+ CD45+); 2) endothelial cells containing phagocytosed apoptotic lymphocytes (TAMRA+ CD45‐); and 3) endothelial cells that were not associated with lymphocytes. The identification of these populations was verified by confocal microscopy of sorted cells. The method described herein will facilitate detailed studies on phagocytic recognition of apoptotic cells and should have broad applications to other phagocytic cell systems. Cytometry 27:145–152, 1997. © 1997 Wiley‐Liss, Inc.

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Langerhans Cells Phagocytose Vaginal Epithelial Cells Undergoing Apoptosis during the Murine Estrous Cycle1

Cited by 55 publications

References 10 publications

Vaginal epithelial dendritic cells renew from bone marrow precursors

Vaginal epithelial dendritic cells renew from bone marrow precursors

The Pathogenesis of Oral Lichen Planus

A novel flow cytometric method for quantifying phagocytosis of apoptotic cells

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