Number Of Langerhans Cells Research Articles

Quantity and distribution of Langerhans cells and CD8 + T cells in lesions of alopecia areata

Objective To analyze the quantity and distribution of Langerhans cells in lesions of alopecia areata (AA),so as to investigate their role in the pathological process of AA as well as their relationship with T lymphocytes.Methods Tissue specimens were obtained from the scalp lesions of AA in 29 patients,including 16 in active phase and 13 in non-active phase.All the specimens were subjected to immunohistochemical staining for CD1a,and 17 specimens to immunohistochemical staining for CD4 and CD8.Fluorescence-based semi-quantitative reverse transcription (RT)-PCR was performed to determine the mRNA expressions of CD1a and granulocytemacrophage colony stimulating factor (GM-CSF) in the full-thickness skin specimens.Statistical analysis was done using Mann Whitney U test and Pearson correlation analysis.Results There was a significant increase in the quantity of CD1a+ Langerhans cells in the epidermis,perivascular and perifollicular areas in the upper and deep dermis of the AA patients compared with the healthy controls (Z =4.354,2.884,4.640,3.217,3.496,all P ＜ 0.01),and in the epidermis,perivascular and perifollicular areas in the deep dermis of AA patients in active phase compared with those in non-active phase (Z =2.457,2.130,1.954,P ＜ 0.05 or =0.05).The relative mRNA expression levels of CD1a and GM-CSF in the patients were similar to the healthy controls in the upper dermis,but significandy higher than the healthy controls in the deep dermis (Z =2.702,2.941,both P ＜ 0.01).A positive correlation was observed between the quantity of perivascular Langerhans cells in the upper dermis and that of perifollicular CD8+ T lymphocytes in the deep dermis in patients with AA (r =0.618,P ＜ 0.05) and in patients with active AA (r =0.795,P =0.01),but not in patients with inactive AA (r =0.304,P ＞ 0.05).Conclusions The number of Langerhans cells is elevated in patients with AA,especially in patients with active AA.The quantity of perivascular Langerhans cells in the upper dermis is positively correlated with that of perifollicular CD8 + T lymphocytes in the deep dermis of active AA lesions,hinting that Langerhans cells play an important role in the progression of AA. Key words: Alopecia areata; Langerhans cells; T-lymphocytes; CD1a protein

Characterization of diabetic neuropathy in the Zucker diabetic Sprague-Dawley rat: a new animal model for type 2 diabetes.

Recently a new rat model for type 2 diabetes the Zucker diabetic Sprague-Dawley (ZDSD/Pco) was created. In this study we sought to characterize the development of diabetic neuropathy in ZDSD rats using age-matched Sprague-Dawley rats as a control. Rats were examined at 34 weeks of age 12 weeks after the onset of hyperglycemia in ZDSD rats. At this time ZDSD rats were severely insulin resistant with slowing of both motor and sensory nerve conduction velocities. ZDSD rats also had fatty livers, elevated serum free fatty acids, triglycerides, and cholesterol, and elevated sciatic nerve nitrotyrosine levels. The corneas of ZDSD rats exhibited a decrease in subbasal epithelial corneal nerves and sensitivity. ZDSD rats were hypoalgesic but intraepidermal nerve fibers in the skin of the hindpaw were normal compared to Sprague-Dawley rats. However, the number of Langerhans cells was decreased. Vascular reactivity of epineurial arterioles, blood vessels that provide circulation to the sciatic nerve, to acetylcholine and calcitonin gene-related peptide was impaired in ZDSD rats. These data indicate that ZDSD rats develop many of the neural complications associated with type 2 diabetes and are a good animal model for preclinical investigations of drug development for diabetic neuropathy.

Langerhans Cells in Oral Mucosa from Patients with Acquired Immunodeficiency Syndrome

Background: Oral manifestations are common in patients with acquired immunodeficiency syndrome (AIDS). Objectives: Compare the number of Langerhans cells and intensity of anti-CD1a expression in the mucous membranes of the oral cavities of the same patients with AIDS and HIV-negative individuals. Materials and methods: Sixteen autopsied adults were investigated, including 11 with AIDS, and 5 HIV negative. We identified Langerhans cells in three oral regions of the same subject using an anti-CD1a antibody and quantified them in cells/mm2. Were applied normality tests and Mann-Whitney. Results: The numbers of Langerhans cells in the AIDS patient group were less than in the control group, but didn't differ significantly between the two groups. The intensity of anti-CD1a expression was lower in patients with AIDS. Of the three areas, the greater intensity of CD1a cells were found in the masticatory mucosa. Discussion: We observed a reduction of Langerhans cells in the oral mucosa of patients with AIDS and this is the first report, to our knowledge, that evaluate three different oral mucosal membranes in the same subject. Conclusion: Our study suggests that AIDS influences on the depletion of Langerhans’ cells, particularly in the specialized mucosa, and the intensity of expression of anti- CD1a regardless of the type of oral mucosa.

Langerhans cells in lichen planus and lichenoid mucositis an immunohistochemical study.

Aim:The aim of this study is to identify and evaluate Langerhans cell (LC) in lichen planus (LP), lichenoid mucositis (LM) and normal mucosa (NM) using CD1a monoclonal antibody immunohistochemically.Materials and Methods:A total of 15 cases of oral lichen planus and 15 cases of LM were selected based on clinical examination and confirmed by histopathological analysis. The biopsies from the 10 patients were taken from normal buccal mucosa as control. Paraffin blocks of tissue were made, which are used for routine hematoxylin and eosin staining and immunohistochemical staining using biotin streptavidin methods (CD1a monoclonal antibody). Analysis of CD1a expression was performed by evaluating the labeling index (LI) for each slide.Results:The mean CD1a LI for LP was significantly higher than that of LM and NM in the basal and supra basal layer. The mean CD1a positive cells in the connective tissues for LP were higher than that of LM and NM.Conclusion:This study clearly demonstrates a statistically significant increase in number of LC in LP than in LM, indicating the possible different immunopathogenic mechanisms.

Increased number of Langerhans cells in the epidermis of diabetic foot ulcers correlates with healing outcome

Langerhans cells (LCs) are a specialized subset of epidermal dendritic cells. They represent one of the first cells of immunologic barrier and play an important role during the inflammatory phase of acute wound healing. Despite considerable progress in our understanding of the immunopathology of diabetes mellitus and its associated comorbidities such as diabetic foot ulcers (DFUs), considerable gaps in our knowledge exist. In this study, we utilized the human ex vivo wound model and confirmed the increased epidermal LCs at wound edges during early phases of wound healing. Next, we aimed to determine differences in quantity of LCs between normal human and diabetic foot skin and to learn if the presence of LCs correlates with the healing outcome in DFUs. We utilized immunofluorescence to detect CD207+ LCs in specimens from normal and diabetic foot skin and DFU wound edges. Specimens from DFUs were collected at the initial visit and 4 weeks later at the time when the healing outcome was determined. DFUs that decreased in size by >50 % were considered to be healing, while DFUs with a size reduction of <50 % were considered non-healing. Quantitative assessment of LCs showed a higher number of LCs in healing when compared to non-healing DFU's. Our findings provide evidence that LCs are present in higher number in diabetic feet than normal foot skin. Healing DFUs show a higher number of LCs compared to non-healing DFUs. These findings indicate that the epidermal immune barrier plays an important role in the DFU healing outcome and may offer new therapeutic avenues targeting LC in non-healing DFUs.

Identification of bone morphogenetic protein 7 (BMP7) as an instructive factor for human epidermal Langerhans cell differentiation

Human Langerhans cell (LC) precursors populate the epidermis early during prenatal development and thereafter undergo massive proliferation. The prototypic antiproliferative cytokine TGF-β1 is required for LC differentiation from human CD34(+) hematopoietic progenitor cells and blood monocytes in vitro. Similarly, TGF-β1 deficiency results in LC loss in vivo. However, immunohistology studies revealed that human LC niches in early prenatal epidermis and adult basal (germinal) keratinocyte layers lack detectable TGF-β1. Here we demonstrated that these LC niches express high levels of bone morphogenetic protein 7 (BMP7) and that Bmp7-deficient mice exhibit substantially diminished LC numbers, with the remaining cells appearing less dendritic. BMP7 induces LC differentiation and proliferation by activating the BMP type-I receptor ALK3 in the absence of canonical TGF-β1-ALK5 signaling. Conversely, TGF-β1-induced in vitro LC differentiation is mediated via ALK3; however, co-induction of ALK5 diminished TGF-β1-driven LC generation. Therefore, selective ALK3 signaling by BMP7 promotes high LC yields. Within epidermis, BMP7 shows an inverse expression pattern relative to TGF-β1, the latter induced in suprabasal layers and up-regulated in outer layers. We observed that TGF-β1 inhibits microbial activation of BMP7-generated LCs. Therefore, TGF-β1 in suprabasal/outer epidermal layers might inhibit LC activation, resulting in LC network maintenance.

Corneal Langerhans cell and dry eye examinations in ankylosing spondylitis

APCs of the ocular surface, including corneal Langerhans cells (LCs), offer the opportunity to gain insight into the activity of innate immunity. We examined corneal LCs and dry eye parameters in ankylosing spondylitis (AS). Twenty-four AS patients with varying degrees of disease activity and 24 healthy participants were enrolled. Central and peripheral LC numbers, and Langerhans cell morphology (LCM) were assessed with invivo laser confocal microscopy. In addition, ocular surface disease index, lid parallel conjunctival folds, tear break up time, and Schirmer test were evaluated. LC densities and central LCM were greater in AS patients than in the controls. Moreover, LCM was significantly greater in patients with higher systemic inflammation according to elevated C-reactive protein (CRP). Also, tear production was greatly suppressed in patients with more severe onset of the systemic inflammation according to the Bath Ankylosing Spondylitis Disease Activity Index and elevated CRP. Greater corneal LC density and LCM in AS may reflect an increased activation state of the innate immune system of the cornea in AS, which correlates with the systemic activity of AS even without ocular symptoms. Nonetheless, higher systemic inflammation might impair tear production, and it might partly explain the dry eye mechanism.

The immune system of mouse vibrissae follicles: cellular composition and indications of immune privilege

Although vibrissae hair follicles (VHFs) have long been a key research model in the life sciences, their immune system (IS) is essentially unknown. Therefore, we have characterized basic parameters of the VHF-IS of C57BL/6J mice by quantitative (immuno-)histomorphometry. Murine anagen VHF harbour few CD4+ and CD8+ T cells in the distal mesenchyme and sinuses but hardly any gamma-delta T cells in their distal epithelium. MHC class II+ Langerhans cells are seeded in the VHF infundibulum, which is also surrounded by MHC class II+ and CD11b+ cells (macrophages). The number of Langerhans cells then declines sharply in the VHF bulge, and the VHF bulb lacks MHC class II+ cells. Mast cells densely populate the VHF connective tissue sheath, where they strikingly cluster around the bulge. Both the bulge and the bulb of VHF display signs of immune privilege, that is, low MHC class I and MHC class II expression and local immunoinhibitor expression (CD200, TGFβ1). This immunophenotyping study fills an important gap in the immunobiology of murine skin and identifies differences between the IS of VHF, mouse pelage and human terminal HFs. This facilitates utilizing murine VHF as a versatile organ culture model for general immunology and immune privilege research in situ.

Corneal Langerhans cell and dry eye examinations in ankylosing spondylitis

AbstractPurpose To examine the density and the distribution of corneal Langerhans cells (LCs) and to compare the results with dry‐eye related parameters and disease activity in ankylosing spondylitis(AS).Methods Twenty four AS patients (mean age: 41.8±9.8 years) with various degree of disease activity and twenty four healthy subjects (mean age: 47.9 ± 16.4 years) were enrolled. Ocular surface disease index (OSDI), lid parallel conjunctival folds (LIPCOF), tear break up time (TBUT), and Schirmer test (ST) were evaluated. In addition, central and peripheral LCs numbers and Langerhans cell morphology (LCM) were assessed with in vivo laser confocal microscopy.Results Tear production was greatly suppressed in patients with more severe systemic inflammation according to the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and C‐reactive protein (CRP) (BASDAI≤4.0 vs BASDAI&gt;4.0 10.2±8.5 vs 4.0±5.3; CRP≤5.0 vs CRP&gt;5.0 17.2±4.2 vs 3.9±5.5 p&lt;0.05 for all). LCs densities and central LCM were greater in AS patients than in the controls (LC density: 77.5±44.9 vs 23.8±33.8 and central LCM: 1.7±0.7 vs 0.95±0.75 p&lt;0.05 for all).Conclusion Greater corneal LC density and LCM may reflect an increased activation of the corneal innate immune system, which correlates with the systemic activity of AS even without ocular symptoms. Higher systemic inflammation might impair tear production, and it might partly explain the dry eye mechanism.

Mice with heterozygous deficiency of manganese superoxide dismutase (SOD2) have a skin immune system with features of “inflamm-aging”

Dendritic cells (DC) are central in regulating skin immunity. Immunosenescence is associated with a chronic inflammatory state. Little is known about the contribution of DC to "inflamm-aging". When determining langerhans cell (LC) numbers, we found a 60 % reduction of LC in aged epidermis. Reactive oxygen species(ROS) are linked with aging. The mitochondrial manganese superoxide dismutase (SOD2) is in the first line of antioxidant defense. We investigated the function of DC from SOD2 heterozygous mice (SOD2+/-) and found that at 4 months of age LC numbers are not altered, but activated LC have impaired expression of MHC-II and CD44. Immature SOD2+/- DC produced increased proinflammatory IL-6 and chemokines CXCL1 and CXCL2. Upon challenge SOD2+/- DC accumulated ROS. When activating SOD2+/- DC by LPS they less efficiently upregulated MHC-II, CD86 and CD44. Surprisingly, in vivo contact hypersensitivity (CHS) was enhanced in SOD2+/- mice although SOD2+/- DC were less potent in stimulating wt T cells. However, SOD2+/- T cells showed increased proliferation, even when stimulated with SOD2+/- DC, possibly explaining the increased CHS. Our findings suggest that SOD2 is a molecular candidate in the regulation of "inflamm-aging" conveying both immunosuppressive and proinflammatory signals through alteration of DC and T cell functions.

Effect of Laser Thermal Injury on Langerhans Cells in Mouse and Hairless Guinea Pig Epidermis

To examine the effect of laser thermal injury on Langerhans cells (LC) within the epidermis, the dorsal skin of mice and hairless guinea pigs was exposed to varying levels of laser irradiation using a thulium laser at a wavelength of 2.0μm. At 6, 24 and 48h post irradiation, animals were euthanized, skin samples prepared for histology and the epidermis obtained and stained by major histocompatibility complex-II staining (mice) or ATPase assay (hairless guinea pigs) for the enumeration of LC. Mouse skin exhibited histological evidence of thermal damage at 24h post irradiation at even the lowest dose (0.14W) and decreases in the numbers of epidermal LC were observed at all doses and decreases were proportional to dose. In contrast, hairless guinea pig skin only showed consistent histological evidence of thermal damage at the highest dose of irradiation (0.70W) at 24 and 48h post irradiation and exhibited a statistically significant decrease in numbers of epidermal LC only at this dose. Thus, epidermal LC depletion occurred in the skin of both mice and hairless guinea pigs in response to laser treatment and the magnitude of depletion directly correlated with the extent of thermal damage both within and between species.

Immunological and structural remodeling in human papillomavirus-induced warts and Bowen disease.

Human papillomavirus-associated warts (HPV-warts) are persistent, evading host immune surveillance. However, these warts sometimes disappear spontaneously, following inflammation. Non-inflamed HPV-warts demonstrated decreased numbers of epidermal Langerhans cells (LCs), low expression levels of MIP3α and E-cadherin, and no apoptotic cells. In the inflamed HPV-warts, on the other hand, various dendritic cell (DC) subsets and many CD8+ cytotoxic T lymphocytes (CTLs) were recruited in association with epidermal MIP3α expression. Many apoptotic keratinocytes were observed in the dermo-epidermal junction. Cellular events were different in HPV-induced Bowen disease (HPV-Bowen): a few LCs were retained in the lesional epidermis, and considerable numbers of B-cells and plasma cells were also observed in the infiltrates, with little or no infiltration of plasmacytoid DCs or dermal/mature DCs. Multiple HPV16-Bowen diseases in the same individuals showed the presence of different sizes of E6/E7-containing cellular transcripts, which indicated that HPV genomes were integrated into the different sites of chromosomes. Toll-like receptor (TLR) 3 was expressed by the lesional keratinocytes even in the non-inflamed HPV-warts, and type 1 interferons (IFNs) were produced in cultured keratinocytes by TLR3 stimulation. HPV-warts are protected from host immune responses and apoptotic signals because they are surrounded by LC-depleted epidermal walls, and viral anti-apoptotic molecules. The up-regulation of epidermal TLR3 signaling might inhibit further HPV spreading.

Effects of TNF-alpha inhibitors on the number of epidermal Langerhans cells in uninvolved skin of psoriatic patients: A pilot study

Only limited data are available on the effects of TNF-alpha inhibitors on dendritic cells. However, TNF-alpha plays a central role in the biology of dendritic cells, both with regard to their maturity process and mobilization to secondary lymphoid organs. In particular, the effects of TNF-alpha inhibitors on Langerhans cells in healthy skin have never been investigated. In this pilot study, we aimed to assess the change of the density of Langerhans cells within the normal, not photo-exposed, skin of 17 psoriatic patients, before and after 16 weeks of treatment with TNF-alpha inhibitors. Most of the patients (88%) showed an increase or a similar density of Langerhans cells after 16 weeks of therapy with TNF-alpha inhibitors compared with baseline values. Only 2 patients (12%) showed a reduction of these cells following therapy with TNF-alpha inhibitors.

Changes in distribution and ultrastructure of Langerhans cells in condyloma acuminatum tissues, and analysis of the underlying mechanism

To determine the changes in distribution and function of Langerhans cells (LCs) in condyloma acuminatum (CA) tissues, as well as the possible underlying mechanism. The expression of CD1a and E-cadherin in 26 CA lesions and 10 normal prepuce tissues was determined using the streptavidin peroxidase method. The mRNA expression of CD1a and E-cadherin was determined using reverse transcriptase polymerase chain reaction. The ultrastructure of LCs was observed under a transmission electronic microscope (TEM). In the CA tissues, the number of CD1a-positive LCs was significantly decreased (10.66 ± 11.71) compared with the number in normal prepuce tissues ( p < 0.05). The LCs in the CA tissues had smaller cell bodies with fewer and shortened cytodendrites. The CD1a mRNA expression in the CA tissues significantly decreased compared with that in the normal tissues (0.4066 ± 0.2671 vs. 0.7444 ± 0.3667; p < 0.01). The average E-cadherin staining score in the CA tissues was significantly lower than that in the normal tissues (2.36 ± 1.41 vs. 7.67 ± 1.64; p < 0.01). The E-cadherin mRNA expression in the CA tissues was also significantly lower than that in the normal tissues (0.1737 ± 0.1083 vs. 0.3786 ± 0.1460; p < 0.01). A positive correlation was observed between the LC number and E-cadherin expression density ( r = 0.8381, p < 0.05), as well as between the mRNA expression of CD1a and E-cadherin ( r = 0.8381, p < 0.05). TEM observation revealed changes in the morphology and quantity of subcellular organelles (Birbeck granules) in the CA tissues. CA lesions are characterized by a decreased number of LCs and antigen presentation dysfunction. The decrease in the number of LCs may be correlated with reduced E-cadherin expression, which hinders intraepidermal LC retention.

How to Approach A Patient Who Refuses the Recommended Mammoplasty Technique

Objective: To evaluate the changes in the number of Langerhans Cells (LC) observed in the epithelium of smokeless tobacco (SLT-induced) lesions. Methods: Microscopic sections from biopsies carried out in the buccal mucosa of twenty patients, who were chronic users of smokeless tobacco (SLT), were utilized. For the control group, twenty non-SLT users of SLT with normal mucosa were selected. The sections were studied with routine coloring and were immunostained for S-100, CD1a, Ki-67 and p63. These data were statistically analyzed by the Student’s t-test to investigate the differences in the expression of immune markers in ormal mucosa and in SLT-induced leukoplakia lesions. Results: Th re was a significant differenc in the immunolabeling of all markers between normal m cosa and SLT-induced lesions (p<0.001). The leukoplakia lesions in chro i SLT us rs demonstrated a significant increase in the numb r of Langerhans cells and in the absence of epithelial dysplasia. Conclusion: The increase in the n mber of these cells represents t initial stage of leukoplakia. Key w rds: Smokeless tobacco, leukoplakic lesions, cancer, langerhans cells, chewing tobacco.

Authors reply to &amp;#147;Comment on the Day-Care Surgery for Pilonidal Sinus Using Sinotomy Technique and Fibrin Glue Injection&amp;#148;

Objective: To evaluate the changes in the number of Langerhans Cells (LC) observed in the epithelium of smokeless tobacco (SLT-induced) lesions. Methods: Microscopic sections from biopsies carried out in the buccal mucosa of twenty patients, who were chronic users of smokeless tobacco (SLT), were utilized. For the control group, twenty non-SLT users of SLT with normal mucosa were selected. The sections were studied with routine coloring and were immunostained for S-100, CD1a, Ki-67 and p63. These data were statistically analyzed by the Student’s t-test to investigate the differences in the expression of immune markers in normal mucosa and in SLT-induced leukoplakia lesions. Results: There was a significant difference in the immunolabeling of all markers between normal mucosa and SLT-induced lesions (p<0.001). The leukoplakia lesions in chronic SLT users demo strated a significant incr ase in th number of Langerha s cells and in the absenc of epithelial dyspla ia. Conclusion: The increase in the number of these cells represents the initial stag of leukoplakia. Ke words: Smokeless tobacco, leukoplakic lesions, cance , langerhans cells, chewing tobacc .

Association between langerhans cells population and histological grade of oral squamous cell carcinoma

Context:Langerhans cells (LCs) are a unique population of antigen processing cells in the epidermis and mucous membrane, which may play a role in the defence mechanism against epithelial tumors.Aims:To compare the distribution of LCs in oral squamous cell carcinomas (OSCC) and normal oral epithelium; and to determine whether the population of LCs in OSCC has any correlation with histological grading of these malignancies.Settings and Design:A cross-sectional immunohistochemical analysis of OSCC cases.Materials and Methods:Forty-eight randomly selected paraffin tissue blocks of OSCC cases and 30 cases of normal oral epithelium were included. Hematoxylin and eosin-stained sections of the OSCC cases were reviewed and categorized as high-grade malignant tumors or low-grade malignant tumors. Tissue sections were analyzed for density of LCs using CD1a antibody expression.Statistical Analysis Used:Data are expressed as percentages compared by Chi-square statistics; mean ± standard deviation, compared by Mann-Whitney-U test and Spearman's correlation tests.Results:LCs population was significantly higher in normal oral epithelium when compared with OSCC cases (P = 0.001). There was also a significant difference in the number of LCs per millimetre square area of tissue section between well-differentiated tumors and poorly-differentiated tumours (P = 0.03). There was a negative correlation between the population density of LCs and the grade of OSCC.Conclusions:These findings suggest that oral mucosal LCs are involved in immune-surveillance and immunologic impairment may characterize invasive OSCC. In addition, LCs density characterizes histological grades of OSCC, which may be of a prognostic value.

Skin dendritic cells increase in number during early response to wounding.

Among the cells that may participate to wound response and wound healing, coordinate with other cell types, dendritic cells have been little studied until now and the least so in humans. This issue has been addressed on samples of wounded and control skin taken at autopsy and analyzed by immunohistochemistry and morphometry. Langerhans cell number in the epidermis and the relative volume of MHC II+ cells in the dermis increased transiently upon wounding, with a significant peak in the first and the second half hour after wounding respectively. Dermal MHC II+ cells became part of a perivascular mononuclear cell infiltrate visible in the subpapillary dermis since between 30 and 60 after wounding and which contained also MC. Cells at the periphery of the infiltrates were also DC-SIGN+ and CD11c+, i.e. were well differentiated connective tissue dendritic cells. Mast cells underwent degranulation associated to an increase in number in the first hours after wounding. These modifications of dendritic cells and mast cells and the respective tissue course suggest that epidermal and dermal dendritic cells participate to the early response to wounding in humans, coordinately with mast cells and possibly stimulating the recruitment and activation of the cells involved in injury response at later time points.

Comparison of the Distribution of Dendritic Cells in Peri-implant Mucosa and Healthy Gingiva

The host response to infection differs between peri-implantitis and periodontitis, but the mechanisms underlying these differences are not understood. In this study, the distribution of dendritic cell subpopulations in healthy peri-implant mucosa (HPIM) was compared to that of healthy gingiva (HG). HPIM and HG specimens were obtained from nonsmoking, systemically healthy subjects. Immunohistochemistry was used to quantify the number of Langerhans cells (LCs) (CD1a+) and interstitial dendritic cells (IDCs) (factor XIIIa+) in the oral epithelium, sulcular/junctional epithelia, and lamina propria without inflammatory infiltration and with inflammatory infiltration. Fourteen HPIM and 13 HG specimens were obtained from subjects aged 29 to 55 years. The lamina propria of the HPIM had fewer LCs than that of the HG (HPIM: 7.99 ± 10.76, HG: 25.68 ± 16.98; P = .003). There was no significant difference in the number of CD1a+ cells in the oral epithelium or the sulcular/junctional epithelia between the HPIM and the HG (P ≥ .23). A greater number of IDCs was observed in the lamina propria with inflammatory infiltration of the HPIM compared to the HG (HPIM: 57.02 ± 35.70, HG: 33.89 ± 26.98; P = .06). In the lamina propria of HPIM, fewer LCs and more IDCs were observed. These differences may be associated with reduced stimulation of the innate and acquired immune responses initiated by LCs and the greater matrix remodeling of peri-implant tissue associated with IDCs.

Eczema in Full-Thickness Skin Graft

Eczema is the most common type of dermatitis.1 The term eczema is applied to specific inflammatory reactions of the skin and covers a set of etiologically highly heterogeneous clinical conditions. Typically, the diagnosis is based only on clinical findings. Here, we present a case of unclassified eczema in full-thickness skin graft, which is a rare condition. The case presented here is of a 22-year-old man who was operated elsewhere because of burn contracture on his right hand. The contracture was released, and full-thickness skin graft harvested from his right groin was applied. Three months after the operation, the patient experienced itching and scaling on the graft. We thought this lesion to be an unclassified eczema and prescribed topical steroids. The skin lesions resolved after a week, and patient complaints subsided. In the presented case, there was no history of allergy, and nothing to indicate contact dermatitis. Yoshiki et al,2 in their study about the immunological state of grafted skin on mice, stated that grafted skin provides a specialized immunological status in which T cells do not respond well to external stimuli such as contactants, as a result of skewed function and a reduced number of Langerhans cells. In this context, contact dermatitis cannot easily develop in the grafted skin. Hopkins JG reported a case of exudative dermatitis confined to split-thickness skin graft, but the patient had autogenous as well as heterogenous grafts. 3 Kim et al4 reported a case in which bullous fixed drug eruption developed only at the previous skin graft sites. Harnack et al5 reported eczema in a split-thickness skin graft. To the best of our knowledge, eczema in full-thickness skin graft has not been reported yet. We advise clinicians to remember any kinds of eczema in their minds on all types of grafts.