Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06126 (CD1a)
 2,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Depletion of Langerhans cells (LC) is known to follow bone marrow transplantation (BMT) and is thought to be mainly related to pretransplant radiation and chemotherapy conditioning regimens. We studied sequential biopsies of clinically normal skin of 22 thalassemic and leukemic patients undergoing allogeneic BMT who had received only chemotherapy (busulfan and cyclophosphamide) as conditioning regimen. LC were identified immunohistochemically using antibodies against CD1a and HLA-DR antigens, and their number expressed per square mm of epidermal vertical section, the latter measured by computerized image analysis. After the preparatory regimen, the number of LC decreased progressively in both leukemic and thalassemic patients. CD1a+ and HLA-DR+ epidermal cells were reduced, respectively, to 68.5% and 64.5% of their original number around Day 2, and to 23.1% and to 18.2% around Day 17. By this time, electron microscopic examination of selected biopsies confirmed the depletion of LC. Variable repopulation was observed between Days 40 and 60. Our results indicate that a conditioning regimen based exclusively on high dose chemotherapy depletes epidermal LC early after BMT, and that such depletion is not related to the development of acute graft-versus-host disease.
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PMID:Epidermal Langerhans cells after allogeneic bone marrow transplantation: depletion by chemotherapy conditioning regimen alone. 138 97

Dendritic cells are antigen-presenting cells derived from the hematopoietic stem cell. The dendritic cell family includes Langerhans' cells (CD1a-positive dendritic cells of the skin), and antigen-presenting cells that are found in the lymphoreticular system and throughout the organ parenchyme. Dendritic cells play a key role in both the primary and secondary immune responses. Several studies indicate that these cells participate in antitumor immunity, tumor surveillance, graft-versus-host disease, and in the pathogenesis of clinical syndromes of unknown origin or those induced by viruses, such as the human immunodeficiency virus. Different disorders are characterized by an abnormal proliferation and accumulation of dendritic cells; for example, the Langerhans' histiocytes, which accumulate in Langerhans' cell histiocytosis. In this review the immunophenotypic, morphological, and functional characteristics of the dendritic cell family is described. The clinical and laboratory studies suggesting a unique role for these cells in various syndromes and diseases are reviewed. The Langerhans' cell histiocytoses and the malignant disorders associated with transformation of cells belonging to the dendritic cell family, are discussed.
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PMID:Physiology and pathophysiology of dendritic cells. 949 Feb 85

T-cell dependent immune response is initiated by dendritic cells, which are the only leucocytes able to prime naive CD4-positive T cells. Langerhans cells (LC) are dendritic cells characterized by their localization within the epidermis, their dendritic shape, and their expression of specific markers such as major histocompatibility complex (MHC) class II molecules, CD1a and S100 protein. We retrospectively studied the phenotype of LC in the skin of eight children with MHC class II deficiency (bare lymphocyte syndrome) after allogeneic bone marrow transplantation (BMT). The presence of donor-derived MHC class II positive LC within the epidermis was studied by immunohistochemistry on skin biopsies performed for the determination of graft-versus-host disease. MHC class II positive LC were undetectable in the epidermis of a child who did not engraft and of three children 13-18 d after HLA-mismatched BMT, despite engraftment. However, donor-derived MHC class II positive LC were detected in four children 9-43 d after HLA-identical BMT. Our results demonstrate that LC can differentiate or expand very quickly, as early as within 9 d after BMT.
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PMID:Detection of donor-derived Langerhans cells in MHC class II immunodeficient patients after allogeneic bone marrow transplantation. 926 54

The diagnosis of post-transfusion graft-versus-host disease (GVHD) in early period is critical for the prognosis of the patients. Exanthema and fever are the earliest symptom of the post-transfusion GVHD and usually precede the disturbance of the liver and bone marrow. Snap-frozen, cryostat-sectioned specimens from the lesional and perilesional skin were labeled by monoclonal antibodies against HLA-ABC, HLA- DR, ICAM-1, CD1a and CD8. The reaction was visualized by indirect immunofluorescence. Graft-versus-host reaction (GVHR) was immunopathologically characterized by extensive expression of HLA-DR and ICAM-1 in the epidermal keratinocytes, exocytosis of CD8 positive cytotoxic T-cell and the reduction or disappearance of CD1a expression by epidermal dendritic cells. The other GVHRs such as erythema exudativum multiforme (EEM), fixed drug eruption, toxic epidermal necrolysis (TEN) and lichen planus could not be separated. Our protocol of the immunopathologic examination could be done quickly (within 3 hours) and provides more detailed and useful information for the diagnosis of GVHD in early period compared with conventional histopathology.
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PMID:[Differential diagnosis of post-transfusion graft-versus-host disease (GVHD) by rapid immunopathologic examination of the skin]. 930 Dec 87

Dendritic cells (DC) are the main stimulators of primary T cell responses. Very little is known about DC in cord blood (CB), and whether they are involved in the low incidence and severity of GVHD following CB transplantation. Here, CBDC were identified as a HLA-DR+/lineage marker (lin; CD3, CD11b, CD14, CD16, CD19, CD34, CD56 and glycophorin A antigens) negative population, representing 0.3 +/- 0.1% (mean +/- s.d.; n = 15) of CB mononuclear cells. CBDC expressed the CD4, CD11a, CD18, CD45RA, CD50 and CD54 antigens but revealed no expression of the CD1a, CD11c, CD40, CD45R0, CD58, CD83, CD86 and CD102 antigens. Immunomagnetically enriched CBDC showed potent allostimulatory activity for CB T cells. Thus, CBDC are functionally competent and resemble in their immature/resting state CD11c- DC in peripheral blood.
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PMID:Functional competence of dendritic cells in human umbilical cord blood. 971 87

Dendritic cells (DC) are the main stimulators of primary T-cell responses and, thus, probably play a role in the immune reactions after stem cell transplantation. Very little is known about DC in cord blood (CB) and about their potential involvement in the low incidence and severity of acute graft-versus-host disease after CB transplantation. Here, CBDC were identified as a HLA-DR+ cell population, lacking the CD3, CD11b, CD14, CD16, CD19, CD34, CD56, and glycophorin A lineage markers (lin). This lin-/HLA-DR+ population represented 0.3% +/- 0.1% (mean +/- SD; range, 0.1% to 0. 6%; n = 15) of CB mononuclear cells, and CB contained 5.4 +/- 3.2 x 10(3) CBDC/mL (1.8 to 13.0 x 10(3); n = 15). CBDC expressed CD4, CD11a, CD18, CD45RA, CD50, CD54, and CD123, but showed no expression of CD1a, CD11c, CD33, CD40, CD45R0, CD80, CD83, and CD86 and only limited expression of CD58, CD102, and CD116. Despite this immature phenotype, immunomagnetically lin--enriched CBDC were potent stimulators of allogeneic CB T cells. As few as 266 +/- 107 (193 to 530; n = 10) lin-/HLA-DR+ CBDC stimulated a significant response. However, CBDC failed to take up protein or peptide antigens. Thus, in CB there is a prevalence of a DC subpopulation, resembling the CD11c- DC identified in tonsils, the so-called plasmacytoid T cells, which may exert a function distinct from the CD11c+ DC subpopulation.
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PMID:Identification of cord blood dendritic cells as an immature CD11c- population. 1009 Sep 40

Dendritic cells are critical for the induction of both primary immune responses and immunological tolerance, as well as for the regulation of T-helper 1 (Th1) and 2 (Th2) immune responses. As neonates are notably deficient in Th1 response and cord blood transplantation is noted to result in less graft-versus-host disease (GvHD), we compared the phenotypic and functional characteristics of monocyte-derived dendritic cells (DCs) that favour Th1 development from cord blood and adult peripheral blood to understand the underlying mechanisms of these observations. Our results showed that: (1) after culture for 7 d with interleukin (IL)-4 and granulocyte--macrophage colony-stimulating factor (GM-CSF), cord blood monocytes generated less CD1a(+) cells than adult peripheral blood monocytes, and the CD1a+ cell percentage decreased thereafter; (2) compared with adult blood DCs, cord blood DCs had reduced intensity of expression of CD1a and MHC class II molecules, but the expression levels of CD11c and CD86 were similar; (3) the endocytotic ability of cord blood DCs was reduced compared with adult blood DCs, and this function was related to reduced mannose receptor (MR)-positive cells; (4) furthermore, the ability of cord blood DCs to stimulate CD3(+) T cells in an allogeneic mixed lymphocyte reaction was significantly lower than that of adult blood DCs. These results suggested that the dysfunction of cord blood monocytes in differentiating into professional DCs will affect the activation of naive T cells, especially Th1 development, and may be related to the susceptibility to different infections in the neonates, as well as the lower incidence of GvHD in cord blood transplantation.
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PMID:Decreased yield, phenotypic expression and function of immature monocyte-derived dendritic cells in cord blood. 1132 7

Antigen-presenting cells (APCs) participate in the initiation of the inflammatory process in various immune-mediated dermatoses through the activation of antigen-specific T lymphocytes. The skin contains several different subsets of APCs. To investigate the role of these APCs in T-cell immune-mediated inflammation, we examined the distribution and numbers of epidermal and dermal CD1a(+) dendritic cells (DCs), factor XIIIa(+) dermal DCs, and CD68(+) macrophages in five T-cell-mediated inflammatory skin diseases. Immunohistochemistry of CD1a, factor XIIIa, and CD68 was performed using paraffin-embedded tissue obtained from a total of 51 patients with eczematous dermatitis (histologically spongiotic dermatitis), psoriasis, lichen planus, acute graft-versus-host disease (GVHD), and chronic GVHD. The numbers of positive cells for each staining were compared with those in site-matched normal skin control specimens from aged-matched subjects. In spongiotic dermatitis and lichen planus, the numbers of epidermal and dermal CD1a(+) cells and factor XIIIa(+) cells were significantly greater than in normal control skin, while in psoriasis only factor XIIIa(+) cells were significantly increased in number. Acute and chronic GVHD showed a reduced number of dermal CD1a(+) cells. Interestingly, factor XIIIa(+) cells were decreased in acute GVHD while they were increased in chronic GVHD. There was a significant reduction in epidermal CD1a(+) cells in acute GVHD, but not in chronic GVHD. The differences in the numbers of APCs in lesional skin appeared to reflect differences in the pathophysiology of these inflammatory skin diseases.
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PMID:Comparison of the distribution and numbers of antigen-presenting cells among T-lymphocyte-mediated dermatoses: CD1a+, factor XIIIa+, and CD68+ cells in eczematous dermatitis, psoriasis, lichen planus and graft-versus-host disease. 1237 34

CD1a, an antigen-presenting molecule related to major histocompatibility complex (MHC) class I, is frequently described as nonpolymorphic. In humans it is dimorphic, due to two linked amino acid substitutions in the alpha1 domain (Ile13Thr and Trp51Cys). The CD1a gene on chromosome 1 is not linked to MHC and may be mismatched between human leukocyte antigen-identical siblings. We analyzed 155 donor-recipient pairs of the Eurobank cohort, 141 matched for CD1a and 14 unmatched in the graft-versus-host disease (GVHD) direction. The burden of GVHD was not increased by CD1a mismatching. The incidence of GVHD in matched and unmatched groups was respectively: grade I-IV: 81% and 86% (P = 0.492); II-IV 61% and 57% (P = 0.495); III-IV 23% and 21% (P = 0.608). Adjusting for age, sex mismatch, GVHD prophylaxis, and conditioning did not reveal any significant difference. This suggests that, unlike conventional class I molecules, CD1a does not function as a transplantation antigen and does not require matching in hematopoietic stem cell transplantation.
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PMID:Impact of mismatching CD1a, a dimorphic antigen-presenting molecule, on graft-versus-host disease after hematopoietic stem cell transplantation. 1713 Jul 88

We report 2 patients with plasmacytoid dendritic cell leukemia (pDCL) expressing CD4, CD56, CD33, CD36, HLA-DR, CD123, CD86 and CD83 in the absence of lineage markers (myeloid, B, T or natural killer cells) except for CD33. Culturing leukemic blasts of both cases with IL-3 for 4 days increased the expression of surface molecules associated with antigen presentation, e.g. CD1a and CD40. Leukemic blasts of both cases possessed a considerable level of antigen-presenting ability to allogeneic lymphocytes in mixed leukocyte cultures. Culturing the blasts with IL-3 for 4 days markedly increased allogeneic antigen presenting ability. Combined with data showing evident graft-versus-leukemia effects without graft-versus-host disease in a cord blood stem cell transplanted pDCL case, leukemic cells in pDCL may act as potent antigen presenting cells in vivo, too.
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PMID:Plasmacytoid dendritic cell leukemia with potent antigen-presenting ability. 1894 86


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