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)

The changes in the number of Langerhans cells within the gingiva during a 21 day experimental gingivitis episode were investigated immunohistochemically. Monoclonal antibodies to CD1a (specific for Langerhans cells and thymocytes) and HLA-DR (class II major histocompatibility antigens - (MHC)) were used to identify Langerhans cells within gingival biopsies taken on days 0, 7, 14 and 21. HLA-DR antibody stained dendritic cells within the oral epithelium which were morphologically identical to the CD1a+ Langerhans cells. Class II MHC LC numbers rose and plateaued between day 7 and 14 then decreased to baseline by day 21. As plaque accumulated and initial inflammation developed there was an increase in the number of CD1a+ Langerhans cells which peaked at day 7 and stayed high (day 14). As inflammation developed there was a statistically significant decrease in the number of CD1a+ Langerhans cells by day 21 (p = 0.028). The initial increase, followed by a decrease in CD1a+ Langerhans cells as inflammation developed, suggests that migration of Langerhans cells occurs within the gingival epithelium and this may represent an important early event in the gingival immune response to plaque.
J Biol Buccale 1992 Sep
PMID:Langerhans cell dynamics in human gingiva during experimentally induced inflammation. 128 8

Histochemical and immunohistochemical studies performed in only a few cases of sinus histiocytosis with massive lymphoadenopathy (SHML) indicated that SHML cells belong to the macrophage--histiocyte system, though their exact origin is still uncertain. We analyzed the morphological, antigenic and enzymatic characteristics of the histiocyte-like cells in one paediatric case of SHML (also named Rosai-Dorfman disease). The SHML cells expressed the S-100 protein, lectins concanavalin A, peanut agglutinin and monocyte-macrophage related antigens CD 11c, CD 14, CD 33, CD 68 and LN 5. Reactivity with other anti-macrophage antibodies (MAC387, lysozyme, alpha-1 anti-chymotrypsin) was variable. The CD1a antigen was present only in scattered cells, whereas HLA-DR and the HLA-DR associated invariant chain were absent. Cytochemistry demonstrated an intense activity of acid phosphatase and non specific esterase of SHML cells. A large amount of medium sized mononuclear cells were located in the sinuses and intersinusoidal tissue. Our findings suggest that SHML cells have intermediate features between phagocytes and Langerhans cells/interdigitating reticulum cells. The heterogeneity of marker expression on SHML cells might be related to the local content of factors (e.g., cytokines), capable of modulating the phenotype of monocyted and derived cells.
Eur J Pediatr 1992 Sep
PMID:Sinus histiocytosis with massive lymphoadenopathy (Rosai-Dorfman disease). Clinico-pathological analysis of a paediatric case. 840 78

Confocal laser scanning microscopy (CLSM) was used for quantitative analysis of CD1a+ cells in epidermis at irritant reactions. Sodium lauryl sulphate (2% and 4%) or non-anoic acid (20% and 80%) were applied to the skin of healthy volunteers under occlusion for 24 h. Skin biopsy specimens were taken after additional 24 h and were snap frozen. Freeze-sections, 25 microns thick, were stained with anti-CD1a antibodies (Leu-6) followed by FITC-labelled rabbit anti-mouse IgG. The sections were viewed and optically sectioned in the CLSM at four depth levels. The data was analysed using a threshold value for the fluorescence. The obtained result is presented as the proportion of specimen area having a fluorescence intensity above the threshold. The result demonstrates that the CLSM is a useful tool for obtaining not only structural information but also quantitative information from a defined tissue volume. In the present investigation it was possible to demonstrate variations in CD1a+ reactivity in epidermis at detergent-induced irritant reactions with a marked decrease in CD1a+ after 80% non-anoic acid exposure and only minor differences in the CD1a+ after 2% and 4% sodium lauryl sulphate exposure.
Acta Derm Venereol 1992 Sep
PMID:Quantitative analysis of Langerhans' cells in epidermis at irritant contact reactions using confocal laser scanning microscopy. 136 Dec 80

Increasing UVB radiation at the earth's surface might have adverse effects on in vivo immunologic responses in humans. We prospectively randomized subjects to test whether epicutaneous immunization is altered by prior administration of biologically equalized doses of UV radiation. Multiple doses of antigens on upper inner arm skin (UV protected) were used to elicit contact sensitivity responses, which were quantitated by measuring increases in skin thickness. If a dose of UVB sufficient to induce redness (erythemagenic) was administered to the immunization site prior to sensitization with dinitrochlorobenzene (DNCB), we noted a marked reduction in the degree of sensitization (P less than 0.0006) that was highly dose responsive (r = 0.98). Even suberythemagenic UV (less than a visible sunburn) resulted in a decreased frequency of strongly positive responses (32%) as compared to controls (73%) (P = 0.019). The rate of immunologic tolerance to DNCB (active suppression of a subsequent repeat immunization) in the groups that were initially sensitized on skin receiving erythemagenic doses of UV was 31% (P = 0.0003). In addition, a localized moderate sunburn appeared to modulate immunization with diphenylcyclopropenone through a distant, unirradiated site (41% weak responses) as compared to the control group (9%) (P = 0.05). Monitoring antigen presenting cell content in the epidermis revealed that erythemagenic regimens induced CD1a-DR+ macrophages and depleted Langerhans cells. In conclusion, relevant and even subclinical levels of UV exposure have significant down modulatory effects on the ability of humans to generate a T-cell-mediated response to antigens introduced through irradiated skin.
Proc Natl Acad Sci U S A 1992 Sep 15
PMID:UV exposure reduces immunization rates and promotes tolerance to epicutaneous antigens in humans: relationship to dose, CD1a-DR+ epidermal macrophage induction, and Langerhans cell depletion. 138 91

Langerhans cells (LC) undergo a variety of phenotypic and functional changes in vitro. To determine the effects of granulocyte macrophage--colony-stimulating factor (GM-CSF), tumor necrosis factor-alpha (TNF-alpha), and interleukin 1-alpha (IL-1) on LC phenotype in vitro, epidermal cell suspensions were enriched for LC by density-gradient centrifugation and cultured in the presence of 10 ng/ml of these cytokines. The percentage of cells expressing the surface protein CD1a was determined by flow cytometry. This percentage typically dropped after 48 h culture in both control and cytokine-treated medium to less than half that of the starting value. By the fifth day, the percentage of cells expressing CD1a in TNF-alpha and IL-1--treated cultures was still near half of the starting value, slightly above that of control cultures. Treatment with GM-CSF caused large and consistent decreases in the percentage of epidermal cells expressing CD1a. Cell viability in each of the three cytokine-treated cultures was identical to the control cultures, with essentially all cells having died by the sixth day after isolation. To determine the functional effects of these cytokines, the cytokine-containing medium was replaced after 72 h with medium containing purified allogeneic T cells and proliferation measured. Preliminary experiments showed no increased proliferation induced by IL-1 or TNF-alpha--treated epidermal cells. GM-CSF-treated epidermal cells induced 2-3 times more T-cell proliferation than epidermal cells cultured without additional cytokines. We conclude that GM-CSF, a cytokine known to be produced by keratinocytes in vitro, decreases CD1a expression by human LC and increases their ability to stimulate proliferation by allogeneic T cells.
J Invest Dermatol 1990 Sep
PMID:Granulocyte macrophage--colony-stimulating factor (GM-CSF) decreases CD1a expression by human Langerhans cells and increases proliferation in the mixed epidermal cell-lymphocyte reaction (MELR). 169 5

This study examined the influence of cytokines on surface antigen expression by gingival Langerhans cells (LC) in organ culture, interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) upregulated the expression of CD1a, HLA-DR and HLA-DP antigens on LC. TNF-alpha, interleukin-4 (IL-4), and transforming growth factor beta (TGF-beta) suppressed CD29 expression, while other cytokines, including interleukin-3 and granulocyte-macrophage colony stimulating factor, were without effect. No cytokines induced CD3, CD4, CD23, CD25 or CD45 RA antigen expression in organ culture. Since TNF-alpha and IL-6 can be secreted by keratinocytes, these molecules, together with interleukin-1, are likely to play a role in the local control of LC number and function within the epithelial milleu. Thus, alterations in cytokine secretion by keratinocytes may at least in part be responsible for variations in LC number and antigen expression which occur in oral mucosal disorders.
J Oral Pathol Med 1990 Sep
PMID:Modulation of Langerhans cell surface antigen expression by recombinant cytokines. 170 Nov 95

The structural similarities of CD1a molecules to major histocompatibility complex (MHC) class I antigens, as well as their expression on epidermal antigen-presenting cells suggest that CD1a molecules might be involved in the cutaneous immune response. In the present study, we investigated the effect of different anti-CD1a monoclonal antibodies (BL6, DMC1, and Na1/34) on T cell proliferation induced by allogeneic epidermal cells in vitro. A significant inhibition of the mixed skin cell-lymphocyte reaction was obtained with BL6 and DMC1 monoclonal antibodies (MoAb), which recognize the same epitope on CD1a molecule. The observed inhibition could not be related to a steric hindrance of MHC class II molecules, because Na1/34 MoAb, which reacts with another epitope on CD1a molecule, had no significant effect. BL6 and DMC1 MoAb interfered with an early event of T-cell activation, as shown by a time-course study. In the presence of these MoAb, the addition of exogenous interleukin 2 did not restore T-cell proliferation. Furthermore, the inhibitory effect of anti-CD1a MoAb was not mediated by a suppressor factor released by Langerhans cells (LC). These present data suggest that CD1a molecule may have an important function in self peptide presentation by human Langerhans cells.
J Invest Dermatol 1991 Sep
PMID:A potential role for CD1a molecules on human epidermal Langerhans cells in allogeneic T-cell activation. 171 29

The population of CD1a+ cells and the quantity of Birbeck granules were evaluated in comparison with the population of T lymphocytes in a variety of clinical lesions of mycosis fungoides. Anti-CD1a and Lag antibodies that specifically react with Birbeck granules and related structures of human Langerhans cells were used immunohistochemically. CD1a+ cells in the dermis of lesions of mycosis fungoides significantly increased in plaques of the plaque stage and in plaques of the tumor stage. They were most frequent in lesions with CD4+ cells ranging in number from 100 to 150/mm2. These lesions were suspected to be progressing from the plaque to the tumor stage. During the course of the disease, most of the dermal CD1a+ cells had few Lag antigens. These results suggest that dermal CD1a+Lag- cells may promote the progression of mycosis fungoides from the plaque to the tumor stage.
J Am Acad Dermatol 1991 Sep
PMID:A subpopulation of Langerhans cells (CD1a+Lag-) increased in the dermis of plaque lesions of mycosis fungoides. 171 24

Histiocytic cells infiltrating the lesions in eosinophilic granuloma of bone as well as in cutaneous histiocytosis X were studied using a murine monoclonal antibody (MA) produced with proliferating cells from an eosinophilic granuloma of bone. This MA reacts with Langerhans cells (LC) of normal human skin or mucous membranes and with proliferating cells of eosinophilic granuloma of bone and skin lesions of Letter-Siwe disease, as shown by immunohistochemistry and immunogold labelling. As other murine MA's obtained after immunization with human cortical thymocytes, this MA immunoprecipitates the 49-kDa CD1a antigen found on human LC and thymic-cell surfaces but not its breakdown product after treatment with trypsin, as demonstrated by analysis of immunoelectron labelling, cytofluorometry and gel electrophoresis. This first production of a CD1a MA from an eosinophilic granuloma supports the concept of Langerhans-cell histiocytosis.
Clin Exp Dermatol 1991 Sep
PMID:Eosinophilic granuloma of bone and biochemical demonstration of 49-kDa CD1a molecule expression by Langerhans-cell histiocytosis. 172 15

In recent years, several studies have confirmed the clonal elimination of thymocytes with receptors that recognize Ag and MHC molecules present on the membrane of thymic stromal cells, a process that may be relevant to the establishment of self-tolerance. In our work, we show that anti-CD3 treatment of single positive CD4+ or CD8+ human medullary thymocytes (obtained by anti-CD1a plus C) induces their apoptotic death. Some events commonly associated with the early steps of normal activation (IL-2R expression, increase in cytoplasmic Ca2+) are also induced after anti-CD3 treatment. Nevertheless, IL-2 is not secreted by these activated cells. The addition of exogenous IL-2 inhibits the apoptosis induced by anti-CD3. We suggest that the lack of secretion of IL-2 by medullary thymocytes may be a physiologic mechanism implicated in the process of negative selection that leads to tolerance.
J Immunol 1990 Sep 01
PMID:IL-2 protects against anti-CD3-induced cell death in human medullary thymocytes. 197 64


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