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)

In this study, we describe human FDF03, a novel member of the Ig superfamily expressed as a monomeric 44-kDa transmembrane glycoprotein and containing a single extracellular V-set Ig-like domain. Two potential secreted isoforms were also identified. The gene encoding FDF03 mapped to chromosome 7q22. FDF03 was mostly detected in hemopoietic tissues and was expressed by monocytes, macrophages, and granulocytes, but not by lymphocytes (B, T, and NK cells), indicating an expression restricted to cells of the myelomonocytic lineage. FDF03 was also strongly expressed by monocyte-derived dendritic cells (DC) and preferentially by CD14+/CD1a- DC derived from CD34+ progenitors. Moreover, flow cytometric analysis showed FDF03 expression by CD11c+ blood and tonsil DC, but not by CD11c- DC precursors. The FDF03 cytoplasmic tail contained two immunoreceptor tyrosine-based inhibitory motif (ITIM)-like sequences. When overexpressed in pervanadate-treated U937 cells, FDF03 was tyrosine-phosphorylated and recruited Src homology-2 (SH2) domain-containing protein tyrosine phosphatase (SHP)-2 and to a lesser extent SHP-1. Like engagement of the ITIM-bearing receptor LAIR-1/p40, cross-linking of FDF03 inhibited calcium mobilization in response to CD32/FcgammaRII aggregation in transfected U937 cells, thus demonstrating that FDF03 can function as an inhibitory receptor. However, in contrast to LAIR-1/p40, cross-linking of FDF03 did not inhibit GM-CSF-induced monocyte differentiation into DC. Thus, FDF03 is a novel ITIM-bearing receptor selectively expressed by cells of myeloid origin, including DC, that may regulate functions other than that of the broadly distributed LAIR-1/p40 molecule.
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PMID:FDF03, a novel inhibitory receptor of the immunoglobulin superfamily, is expressed by human dendritic and myeloid cells. 1090 17

Perivascular epithelioid cell neoplasms comprise a family of rare neoplasms composed of morphologically distinctive perivascular epithelioid cells exhibiting a "myomelanocytic" immunophenotype. The distinction of perivascular epithelioid cell neoplasms from other tumors with melanocytic and smooth muscle differentiation can be difficult. A recent study has suggested that perivascular epithelioid cell neoplasms routinely express CD1a, a Langerhans cell-associated transmembrane glycoprotein involved in antigen presentation and that expression of this marker may be helpful in the distinction of perivascular epithelioid cell neoplasms from various mimics. We evaluated a series of perivascular epithelioid cell neoplasms and potential mimics for CD1a expression. A total of 54 cases (27 perivascular epithelioid cell neoplasms, 11 leiomyosarcomas, 10 melanomas, 6 clear cell sarcomas) were evaluated in 2 laboratories (Mayo Clinic Rochester: 31 cases, Carolinas Medical Center: 23 cases). Selected positive cases were retested at Carolinas Medical Center (11 cases) and Mayo Clinic Rochester (10 cases). Mayo Clinic Rochester methods were as follows: MTB1 clone (1:20, Novocastra, Newcastle-upon-Tyne, UK), heat-induced epitope retrieval in EDTA (pH 8.0), and Dako Advance detection system (Dako Corp, Carpinteria, CA) with background-reducing diluent. Carolinas Medical Center methods were as follows: MTB1 clone (1:30; CellMarque, Rocklin, CA), heat-induced epitope retrieval in Medium Cell Conditioner #1 (pH 8.0-9.0), and streptavidin-biotin detection system with diaminobenzidine chromogen, with and without biotin blocking. Scores were as follows: 1+, 5% to 25%; 2+, 26% to 50%; and 3+, more than 51%. Langerhans cells served as a positive internal control in all tested cases. All Mayo Clinic Rochester cases were negative. Sixteen Carolinas Medical Center perivascular epithelioid cell neoplasms (14 renal angiomyolipomas, 1 soft tissue perivascular epithelioid cell neoplasm, 1 pulmonary clear cell "sugar" tumor) showed CD1a immunopositivity (1+: 7 cases; 2+: 7 cases; 3+: 2 cases) when tested without biotin blocking, 11 of these cases were retested with biotin blocking and were negative. All non-perivascular epithelioid cell neoplasms were negative. All positive perivascular epithelioid cell neoplasms showed cytoplasmic staining only, without membranous staining. Ten Carolinas Medical Center positive perivascular epithelioid cell neoplasms were negative when retested a Mayo Clinic Rochester, using a polymer-based detection system. We conclude that perivascular epithelioid cell neoplasms do not truly express CD1a in a biologically plausible membranous pattern, but may instead show aberrant cytoplasmic immunopositivity in some laboratories. Close inspection of published photomicrographs of previously reported CD1a-positive perivascular epithelioid cell neoplasms shows an identical pattern of cytoplasmic positivity, likely reflecting abundant endogenous biotin within perivascular epithelioid cell neoplasm cells. We do not believe that there is a role for CD1a immunohistochemistry in the differential diagnosis of perivascular epithelioid cell neoplasms.
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PMID:CD1a immunopositivity in perivascular epithelioid cell neoplasms: true expression or technical artifact? A streptavidin-biotin and polymer-based detection system immunohistochemical study of perivascular epithelioid cell neoplasms and their morphologic mimics. 2119 29

Human CD83 is type I transmembrane glycoprotein, mainly expressed on mature dendritic cells (DCs), so it was first described as a molecular marker for mature DC. However, increasing evidence has demonstrated that CD83 is also an immunomodulatory molecule either its membrane-bound CD83 (mCD83) or soluble CD83 (sCD83) released from DCs. Intriguingly, the mCD83 possesses stimulatory effects on immune response, on the contrary, the sCD83 has inhibitory effects. Whether the sCD83 has the inhibitory effects on human monocyte differentiation into DCs is unknown. To this end, we prepared the recombinant human sCD83 in HEK293T cells and treated human monocytes being differentiated into DCs in vitro with the sCD83, and evaluate sCD83 inhibitory effects on immune response by analyzing the surface marker pattern of the cells. The results showed that the sCD83, especially glycosylated sCD83 could bind the monocytes and significantly inhibited the depression of CD14 expressions (P<0.01) and reduced CD1a, CD80, CD86 and MHC II expressions (P<0.01 or P<0.05) during the differentiation, indicating that the sCD83 can inhibit monocyte differentiation into DCs, and suggesting that a negative feedback regulation may exist in monocyte differentiation into DCs based on sCD83 released from the mature DCs.
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PMID:Soluble CD83 inhibits human monocyte differentiation into dendritic cells in vitro. 2524 45