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1 of skin langerin-expressing cells (including Langerhans cells).
2 e, overproduction of IFNs, and an absence of Langerhans cells.
3 diated expression of interleukin-6 (IL-6) by Langerhans cells.
4 s (LCH) represents a clonal proliferation of Langerhans cells.
5 facilitate the interaction of M. leprae with Langerhans cells.
6 The latter also included CD1a(bright) Langerhans cells.
7 ts internalization in specific organelles of Langerhans cells.
8 of VIP on TLR regulation in macrophages and Langerhans cells.
9 kin dendritic cell subpopulations, including Langerhans cells.
10 elocalization toward the basal epidermis and Langerhans cells.
11 se T cells recognize CD1a-lipid complexes on Langerhans cells.
12 nterleukin 22 (IL-22) in response to CD1a on Langerhans cells.
13 1c(+)CD1a(+) dermal DCs but not to epidermal Langerhans cells.
14 mice induced in situ maturation of epidermal Langerhans cells.
15 conventional DC subsets and not by epidermal Langerhans cells.
16 s the only other cytokine expressed by human Langerhans cells.
17 al melanocyte hyperplasia and intraepidermal Langerhans cells.
18 DCs, including a population of inflammatory Langerhans cells.
19 ing molecule that is abundantly expressed on Langerhans cells.
20 lation by UVB radiation, because ablation of Langerhans cells abolished the UVB-induced phenotype.
21 particular conventional dendritic cells and Langerhans cells, accounting for the chronic inflammatio
24 ell generation in the presence or absence of Langerhans cells; analysis of BMP versus canonical TGF-b
25 selective expression of RUNX paralogs during Langerhans cell and inducible regulatory T cell differen
26 dent manner, suggesting an essential role of Langerhans cells and dendritic cells in CHQ-provoked pso
27 dermally delivered TLR agonists to stimulate Langerhans cells and dermal DCs in their natural complex
28 he MCs was efficiently taken up by epidermal Langerhans cells and dermal dendritic cells in the vicin
31 oinflammatory cytokines, and accumulation of Langerhans cells and macrophages within 3 days of tamoxi
33 s highly expressed by DC purified from skin (Langerhans cells) and bone marrow, and has been shown to
34 upffer cells), brain (microglia), epidermis (Langerhans cells) and lung (alveolar macrophages) origin
36 cluding ex vivo-generated DCs, skin-isolated Langerhans cells, and blood myeloid DCs and plasmacytoid
37 utrophils, macrophages, dendritic cells, and Langerhans cells, and colocalization of vaccine Ag withi
38 ll populations including endogenous T cells, Langerhans cells, and gammadelta T cells were not requir
39 dressed this in human ex vivo skin, in vitro Langerhans cells, and IDEC models generated from primary
40 tic cells: monocyte-derived dendritic cells, Langerhans cells, and interstitial dermal dendritic cell
41 in regulates the maturation and migration of Langerhans cells, and its ligation prevents the inductio
42 cells, dendritic cells, monocytes, NK cells, Langerhans cells, and leukocytes) had increasing mRNA ex
43 cytes, fibroblasts, melanocytes, mast cells, Langerhans cells, and Meissner's corpuscles, as well as
44 sues, such as liver Kupffer cells, epidermal Langerhans cells, and microglia--cell populations that a
46 r with myeloid cell or with dedifferentiated Langerhans cell antigens, carry the BRAFV600E mutation.
52 pids, whereas DHA abrogated the migration of Langerhans cells, as assessed by immunohistochemistry.
53 migratory dendritic cells and in particular Langerhans cells at governing T follicular helper and ge
55 in the oesophagus, and the relative lack of langerhans cells (CD1a) may indicate this cell type is u
56 cific pattern recognition receptor TLR7, the Langerhans cell chemoattractant CCL20, and proinflammato
57 characterize the dermal T cell and epidermal Langerhans cell components of the skin immune system in
58 R signaling licenses inflammation-associated Langerhans cell/DC to gain an enhanced capacity to promo
59 logical heterogeneity and differentiation of Langerhans cells, delineate the signaling pathways respo
60 No differences were identified in corneal Langerhans cell density (19.84 cells/mm2 for the control
61 corneal nerve fiber tortuosity, and corneal Langerhans cell density between healthy controls and pat
62 ree main cutaneous DC populations: epidermal Langerhans cells, dermal myeloid DCs, and dermal plasmac
63 g cutaneous inflammation when it facilitates Langerhans cell egress from skin and enables the accumul
64 ) mice contained normal numbers of epidermal Langerhans cells (eLC) and increased numbers of CD11b(+)
66 inophils, macrophages, osteoclasts, DCs, and Langerhans cells from human embryonic stem cells (hESCs)
67 ify possible features that can differentiate Langerhans cells from malignant melanocytes to prevent t
68 eric C-type lectin specifically expressed in Langerhans cells, has been reported to be a pathogen rec
70 ations have been observed in 57% of cases of Langerhans cell histiocytosis (LCH) and 54% of cases of
71 novel somatic ARAF mutation in a child with Langerhans cell histiocytosis (LCH) and demonstrate that
72 enesis of 2 of the most common histiocytoses-Langerhans cell histiocytosis (LCH) and Erdheim-Chester
74 have been observed in half of patients with Langerhans cell histiocytosis (LCH) and in 50% to 100% o
79 nase (ERK) signaling pathway is activated in Langerhans cell histiocytosis (LCH) histiocytes, but onl
97 of two humans from skeletal collections with Langerhans Cell Histiocytosis (LCH), a benign osteolytic
98 ing data to date on a group of patients with Langerhans cell histiocytosis (LCH), which historically
101 9 patients with ECD and ECD overlapping with Langerhans cell histiocytosis (so-called mixed histiocyt
102 hough lymphangioleiomyomatosis and pulmonary Langerhans cell histiocytosis are perhaps more frequentl
103 Erdheim-Chester disease (ECD) is a rare non-Langerhans cell histiocytosis that most commonly affects
104 d eruptive histiocytosis (GEH) is a rare non-Langerhans cell histiocytosis with a benign, self-healin
106 most common histiocytic disorders, including Langerhans cell histiocytosis, Erdheim-Chester disease,
107 Erdheim-Chester disease (ECD) is a rare non-Langerhans cell histiocytosis, to whose pathogenesis neo
114 n the cohort with Erdheim-Chester disease or Langerhans'-cell histiocytosis, the response rate was 43
116 scopy of the t.c. immunization site revealed Langerhans cells in areas of the skin containing the Abe
120 cts with FLG-null mutations have more mature Langerhans cells in nonlesional skin irrespective of whe
121 y an abnormality in corneal nerve fibers and Langerhans cells in patients with and without HIV-SN.
122 IL-10 production by (regulatory) T cells and Langerhans cells in regulating CHS has been established
124 rai and coworkers explore the involvement of Langerhans cells in skin graft rejection and describe fa
125 es, highly significant reductions in CD1a(+) Langerhans cells in the dermis and CD11c(+) dermal dendr
126 ection against HIV infection to skin-derived Langerhans cells in the ex vivo system, suggesting Marav
127 arbohydrate-dependent uptake of pathogens by Langerhans cells in the first step of antigen presentati
129 f Th1 and Th2 polarization in the setting of Langerhans cell (LC) Ag presentation to responsive T cel
130 identify corneal nerve damage and increased Langerhans cell (LC) density in adults with Type 1 diabe
132 Cs in SDLNs, and augmented TRITC/DBP-induced Langerhans cell (LC) migration 72 hours post TRITC treat
133 e required for CCL19 production and adequate Langerhans cell (LC) migration both ex vivo and in vivo.
134 talin1 regulates not only integrin-dependent Langerhans cell (LC) migration, but also MyD88-dependent
137 In this study, the role of the epidermal Langerhans cell (LC) subset of skin dendritic cells in t
139 dritic cells (DC) in the skin and mucosa are Langerhans cells (LC) and interstitial dermal DC (iDDC).
140 1-negative adults and neonates (moDC) and by Langerhans cells (LC) and interstitial, dermal-intestina
141 ransit through the epidermis, which contains Langerhans cells (LC) and keratinocytes (KC), among othe
145 etween these cells and langerin(+) epidermal Langerhans cells (LC) are incompletely characterized.
151 dly, huLangerin-DTA mice (DeltaLC) that lack Langerhans cells (LC) developed increased skin inflammat
153 e literature regarding the role of epidermal Langerhans cells (LC) in promoting skin immune responses
155 isrupted, allowing easier access of HIV-1 to Langerhans cells (LC) in the epidermis and perhaps even
157 plasmacytoid DC (pDC) and in vitro-generated Langerhans cells (LC) obtained from AD patients with HSV
159 ce had multiorgan inflammation, lack of skin Langerhans cells (LC), and a shortened lifespan, consist
160 ll types, including keratinocytes, epidermal Langerhans cells (LC), and dermal dendritic cells (DC).
161 MHD1 is also expressed in epidermis-isolated Langerhans cells (LC), but degradation of SAMHD1 does no
162 There are at least three subsets of skin DC- Langerhans cells (LC), Langerin(+) dermal DCs (dDCs), an
163 Tissue-resident dendritic cells, such as Langerhans cells (LC), normally carry Ags from tissues t
165 During infection, HPV16 also interacts with Langerhans cells (LC), the APC of the epithelium, induci
167 or component of adherens junctions and marks Langerhans cells (LC), the only dendritic cell (DC) popu
173 of TGF-beta1 on the differentiation of human Langerhans cells (LCs) and identified Axl as a key TGF-b
174 he two best-characterized skin-resident DCs, langerhans cells (LCs) and Langerin(+) dermal DCs (dDCs)
175 by heterogeneous lesions containing CD207(+) Langerhans cells (LCs) and lymphocytes that can arise in
178 for all mouse DC subsets revealed that human Langerhans cells (LCs) and the mouse XCR1(+)CD8alpha(+)C
183 eport that dermal dendritic cells (DDCs) and Langerhans cells (LCs) are differentially mobilized duri
187 esident member of the dendritic cell family, Langerhans cells (LCs) are generally regarded to functio
191 We recently reported that human epidermal Langerhans cells (LCs) are more efficient than dermal CD
207 dent DCs remain controversial, and epidermal Langerhans cells (LCs) have been referred to recently as
212 Since their discovery in 1868, the role of Langerhans cells (LCs) in skin immunity has been researc
213 ency virus type 1 (HIV-1) is internalized by Langerhans cells (LCs) in stratified epithelia and trans
214 Although implied by other models, proof that Langerhans cells (LCs) in the human vagina participate i
220 his issue, Su and Igyarto (2019) showed that Langerhans cells (LCs) obtain mRNA from keratinocytes (K
221 assumptions on the identity and functions of Langerhans cells (LCs) of the epidermis have undergone c
225 nfection, we showed that in vivo ablation of Langerhans cells (LCs) resulted in enhanced bone loss.
228 with monocyte-derived DCs (MDDCs) and MUTZ3 Langerhans cells (LCs) to investigate their relevance as
229 In vivo studies questioned the ability of Langerhans cells (LCs) to mediate CD8(+) T cell priming.
230 regulates the outcome of Ag presentation by Langerhans cells (LCs) to T cells through actions on mic
231 To determine the relative contribution of Langerhans cells (LCs) to the ensuing GVHD-like reaction
232 tion of the epidermal mononuclear phagocytes Langerhans cells (LCs) to this phenomenon because of the
234 ited in recent years, and the involvement of Langerhans cells (LCs), a population of epidermal dendri
236 interplay of the C-type lectins, Langerin on Langerhans cells (LCs), and dendritic cell-specific inte
238 ered intradermally are taken up by epidermal Langerhans cells (LCs), dermal Langerin(neg) DCs, and de
239 ts of skin-resident DC have been identified: Langerhans cells (LCs), dermal Langerin+ DC (Lang+ dDC),
241 n two distinct microanatomical compartments: Langerhans cells (LCs), mainly in the epidermis, and der
243 ance in mice critically depends on epidermal Langerhans cells (LCs), which capture DNTB and migrate t
244 ers the morphology and function of epidermal Langerhans cells (LCs), which play a role in UV-induced
245 tigated the age-related changes in epidermal Langerhans cells (LCs), which play a sentinel role in th
252 s; CD1c), plasmacytoid DCs (pDCs; CD303) and Langerhans cells (LCs; CD1a, CD207) in uncinate tissue (
258 -derived IL-1beta alone reduced infection of Langerhans cells, macrophages, and dermal dendritic cell
259 culation led to recruitment and infection of Langerhans cells, macrophages, and dermal dendritic cell
261 NV infected a wide range of cells, including Langerhans cells, macrophages, dermal dendritic cells, m
262 A-DR, CD83, costimulatory molecules, and the Langerhans cell marker CD1a, whereas pDC expressed low l
263 Unconventional immune regulatory roles for Langerhans cells, mast cells, and natural killer T (NKT)
266 response to oxazolone and oxazolone-induced Langerhans cell migration from epidermis were both preve
270 of chronic inflammation, namely macrophages, Langerhans cells, myeloid-derived suppressor cells, and
271 langerin (Lang; CD207)(neg) DCs, but neither Langerhans cells nor Lang(+) DCs were required for CD8(+
273 uman immunodeficiency virus-1) transmission, Langerhans cells of genital mucosa play a protective rol
274 terstitial dendritic cells of the dermis and Langerhans cells of the epidermis, in a dose- and time-d
276 nces in the numbers of T or B lymphocytes or Langerhans cells present in StrataGraft skin substitute
277 utrophils, macrophages, dendritic cells, and Langerhans cells remained in the tissue at least 1 wk.
278 y factors (IRFs) as controllers of the human Langerhans cell response to epidermal cytokines was reve
280 okine for mature DCs) in vitro, and in vivo, Langerhans cells show reduced emigration into draining l
283 1 TCRgammadelta+ intraepithelial T cells and Langerhans cells, swiftly followed by epithelial infiltr
285 ology of the skin, including the function of Langerhans cells, the migration of immune cells in skin,
286 The working theory is that niacin provokes Langerhans cells to produce prostaglandin D2 (PGD2), sti
287 (FLG and other skin barrier gene mutations, Langerhans cells, type 2 innate lymphoid cells, IL-33, T
289 s, mast cells, eosinophils, macrophages, and Langerhans cells; upregulation of chemokine and cytokine
294 DCs were able to cross-prime CD8(+) T cells, Langerhans cells were unexpectedly found to potently cro
295 ted production of prostaglandin D2 and E2 in Langerhans' cells which act on DP1 and EP2/4 receptors i
296 These two markers are mainly expressed by Langerhans cells, which are one of several functionally
297 angerin and the ephrin A2 receptor to infect Langerhans cells, which support full HHV-8 lytic replica
298 S-100-positive cells included CD1a-positive Langerhans cells, while CK20 did not identify any Merkel
300 angerin, the distinguishing C-type lectin of Langerhans cells, would recognize the highly mannosylate