Regional variation in Langerhans cell distribution and density in normal human oral mucosa determined using monoclonal antibodies against CD1, HLADR, HLADQ and HLADP

Cruchley, A. T.; Williams, Dennis; Farthing, Paula M.; Lesch, Charles; Squier, Christopher A.

doi:10.1111/j.1600-0714.1989.tb01353.x

Cited by 64 publications

(34 citation statements)

References 33 publications

(13 reference statements)

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“…These findings correlate with other established topographical variations, such as the differences detected between regions of the oral mucosa (the initial segment of the stratified epithelium, which also covers the esophagus) (Cruchley et al, 1989). It has been established that LCs change under physiological stimuli, such as during pregnancy or during the ovarian cycle (Cavicchia et al, 1998).…”

Section: Discussionsupporting

confidence: 76%

“…Moreover, a positive correlation has been reported to exist between the number of LCs in the esophageal epithelium and certain pathologies, such as human papilloma virus infection, squamous dysplasia, and invasive carcinoma (Morris and Price, 1986;Matsuda et al, 1990). However, although LC distribution changes topographically in the female oral mucosa (Daniels, 1984;Cruchley et al, 1989), there is a lack of information about the topographical changes of these cells in the esophageal mucosa. The importance of LCs in immune defense, and the paucity of information about regional variations along the esophagus, prompted us to study the population of LCs in two distinct regions of the human esophageal epithelium.…”

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confidence: 92%

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Variation in Langerhans cell number and morphology between the upper and lower regions of the human esophageal epithelium

et al. 2002

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Langerhans cells (LCs) are dendritic components of stratified epithelia, presenting antigens to other cells of the immune system that play a crucial role in local defense. The paucity of information about their significance in the esophageal mucosa was addressed by studying their distribution and morphology in this particular location. LCs were identified by immunohistochemical detection of CD1a, a cell-specific marker, using a monoclonal antibody, as well as by electron microscopic identification of characteristic Birbeck granules, among other typical morphological features. Cell counts carried out at 25 and 35 cm distal to the dental arch demonstrated significant differences in number and size between the two locations. The upper region contained 10.4 Ϯ 0.8 cells (mean Ϯ SEM) vs. 18.4 Ϯ 1.4 cells in the lower region. Also, cells in the lower region were larger and appeared to have longer dendritic processes. To our knowledge this is the first report of regional differences in number and morphology of LCs in human esophageal mucosa. Anat Rec 268: 360 -364, 2002.

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Section: Discussionsupporting

confidence: 76%

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confidence: 92%

Variation in Langerhans cell number and morphology between the upper and lower regions of the human esophageal epithelium

et al. 2002

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“…However, if molecular mimicry between microbial and human cellular HSP was to elicit the damaging immune response, this might be expected to involve a number of tissues, not just the oral mucosa. The high load of micro-organisms that colonize the oral mucosa (such as certain strains of S. sanguis) may initiate the immune response by the microbial HSP 65 or HSP 70 stimulating the numerous Langerhans cells in the oral mucosa [30,31] to generate the CC chemokines RANTES, MIP1a and MIP1 b [27]. These chemokines attract macrophages, dendritic cells, T and B cells which may initiate expansion of the HSP 65-derived peptide 91-105 autoreactive T-cell clones which are also primed to the homologous peptide 116-130.…”

Section: Discussionmentioning

confidence: 99%

Defining a T-cell epitope within HSP 65 in recurrent aphthous stomatitis

Hasan¹,

Shinnick

Mizushima

et al. 2002

Clinical and Experimental Immunology

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Recurrent aphthous stomatitis (RAS) is the most common disease of the oral mucosa, affecting at least 10% of the general population [1]. The onset of RAS usually presents during adolescence, and the course of the disease is characterized by recurrences followed by remissions. The disease may persist for many years and varies from minor ulcers, which may cause transient discomfort, to major ulcers which are associated with pain, inability to eat and loss of weight [2].The aetiology of RAS has not been determined, but Streptococcus sanguis or its L-form [3,4] has been implicated, as has autoimmunity to the oral mucosal homogenate [5][6][7]. A common or cross-reactive antigen between streptococci and oral epithelium has been suggested [6][7][8][9] and demonstrated between the streptococcal 60-65 kD heat shock protein (HSP) and oral mucosal tissue [10]. Significant increase in serum antibodies to HSP has been detected in patients with RAS [10].Heat shock proteins (HSP) are a group of highly conserved proteins found in eukaryotic and prokaryotic cells, including Gram-positive and Gram-negative micro-organisms [11,12]. Viruses can enhance the production of host HSP. The high degree of homology between microbial and human HSP 60 [13] has led to the concept that molecular mimicry between the microbial and self HSP may be involved in the pathogenesis of autoimmune diseases [14]. A comprehensive investigation of T-cell epitopes within the 65 kD mycobacterial-and 60 kD human HSP-derived peptides has identified four T-cell epitopes specific for Behcet's disease, in which oral ulceration is the most consistent manifestation [15]. All but one of the four peptides (amino acids 219-233) showed significantly greater stimulation of lymphocytes from patients with Behcet's disease than those from RAS. However, the investigation raised the possibility that another peptide (amino acids 91-105) might specifically stimulate lymphocytes from RAS and not Behcet's disease. Indeed, specific lymphoproliferative responses are stimulated with peptide 91-105 in RAS [16]. A comparative investigation with the homologous human 60 kD HSP peptide 116-130 also revealed significantly greater lymphoproliferative responses in RAS than in controls.The objectives of this investigation in patients with RAS were to define the critical residues within the T-cell epitope 91-105, and to investigate the role of HLA class I and II restriction elements in the lymphoproliferative response. The possibility that g d T cells may be involved was also explored. 318 Defining a T-cell epitope within HSP 65 in recurrent aphthous stomatitis SUMMARYThe 65 kD heat shock protein (HSP) has been implicated in the aetiology of recurrent aphthous stomatitis (RAS). We have previously demonstrated that peptide 91-105 derived from the sequence of mycobacterial 65 kD HSP stimulates specifically lymphocytes from patients with RAS. In this investigation, we show that both CD4 + and CD8 + T cells were significantly stimulated with mycobacterial peptide 91-105. In contrast, the human h...

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“…In normal humans, the density of Langerhans' cells in nonkeratinized oral mucosa is apparently the same as in the skin, but keratinized oral mucosa has fewer Langerhans' cells (96,103,442). Although murine palate implants are repopulated by Langerhans' cells within 2 weeks (365), the numerical densities of Langerhans' cells in old mice is reduced compared with that in young mice (364).…”

Section: Moreover Il-2 (But Not Gamma Interferon [Ifn-␥])-activated Cd8mentioning

confidence: 99%

“…DCs are thus phenotypically and functionally heterogeneous depending on their specific differentiation pathways (11,468,469). Serving as sentinels for pathogen entry at the epithelium of the skin and mucosa, Langerhans' cells, identified by expression of CD1a, Lag, and langerin, are localized on the basal and suprabasal layers and represent 2 to 4% of the cells in the epithelium (6,34,49,59,96,99,103,216,245,262,351,356,365,390,391,442 (30). The loose interaction of DC-specific, ICAM-3 grabbing, nonintegrin (DC-SIGN) with ICAM-3 establishes the initial contact of the Langerhans' cell with a resting T cell in the apparent absence of foreign antigen (416).…”

Section: Moreover Il-2 (But Not Gamma Interferon [Ifn-␥])-activated Cd8mentioning

confidence: 99%

Immunopathogenesis of Oropharyngeal Candidiasis in Human Immunodeficiency Virus Infection

2004

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Oropharyngeal and esophageal candidiases remain significant causes of morbidity in human immunodeficiency virus (HIV)-infected patients, despite the dramatic ability of antiretroviral therapy to reconstitute immunity. Notable advances have been achieved in understanding, at the molecular level, the relationships between the progression of HIV infection, the acquisition, maintenance, and clonality of oral candidal populations, and the emergence of antifungal resistance. However, the critical immunological defects which are responsible for the onset and maintenance of mucosal candidiasis in patients with HIV infection have not been elucidated. The devastating impact of HIV infection on mucosal Langerhans' cell and CD4+ cell populations is most probably central to the pathogenesis of mucosal candidiasis in HIV-infected patients. However, these defects may be partly compensated by preserved host defense mechanisms (calprotectin, keratinocytes, CD8+ T cells, and phagocytes) which, individually or together, may limit Candida albicans proliferation to the superficial mucosa. The availability of CD4C/HIV transgenic mice expressing HIV-1 in immune cells has provided the opportunity to devise a novel model of mucosal candidiasis that closely mimics the clinical and pathological features of candidal infection in human HIV infection. These transgenic mice allow, for the first time, a precise cause-and-effect analysis of the immunopathogenesis of mucosal candidiasis in HIV infection under controlled conditions in a small laboratory animal

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Regional variation in Langerhans cell distribution and density in normal human oral mucosa determined using monoclonal antibodies against CD1, HLADR, HLADQ and HLADP

Cited by 64 publications

References 33 publications

Variation in Langerhans cell number and morphology between the upper and lower regions of the human esophageal epithelium

Variation in Langerhans cell number and morphology between the upper and lower regions of the human esophageal epithelium

Defining a T-cell epitope within HSP 65 in recurrent aphthous stomatitis

Immunopathogenesis of Oropharyngeal Candidiasis in Human Immunodeficiency Virus Infection

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