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

The human CD1 locus encodes three nonpolymorphic MHC class I-like cell surface glycoproteins, CD1a-c, which are expressed primarily by immature thymocytes. A mAb and antipeptide antiserum were utilized to determine the tissue distribution of a fourth CD1 molecule, CD1d. Within the lymphoid lineage, CD1d was expressed on B cells but not on thymocytes. Immunoperoxidase staining of fresh frozen intestinal tissues demonstrated that the majority of intestinal epithelial cells, with the exception of cells at the base of some crypts, expressed CD1d. The CD1d staining was observed in the cytoplasm and along the basolateral membranes of the epithelial cells. The intestinal epithelial cell expression of CD1d was confirmed by immunoblotting with a CD1d antipeptide antiserum. Further immunoperoxidase studies indicated that CD1d, unlike murine CD1, was also expressed by nonlymphoid tissues outside of the gastrointestinal tract. The expression of CD1d outside the lymphoid and myeloid lineages clearly distinguishes this molecule from CD1a-c and suggests that it may serve a distinct function. The prominent expression of CD1d by intestinal epithelial cells suggests that this molecule may be an important ligand for T lymphocytes within the gut-associated lymphoid tissue.
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PMID:Expression of a nonpolymorphic MHC class I-like molecule, CD1D, by human intestinal epithelial cells. 171 64

The human gut epithelium is a unique immunological compartment, containing substantial amounts of intra-epithelial lymphocytes (IEL) with unknown functions. In this study we show that distinct and unusual subpopulations of IEL are present at different levels of human intestine. IEL phenotypes in normal jejunum, ileum and colon were compared using immunoflow cytometry and immunohistochemistry. The expression of mRNA for recombination-activating gene-1 (RAG-1) in IEL from all three levels was compared using reverse-transcription polymerase chain reaction, and the morphology of IEL in situ was determined using immunoelectron microscopy. Surface marker profiles of isolated intestinal epithelial cells at all three levels were also investigated. On average the proportion of TCR gamma delta IEL was comparable in jejunum than ileum and colon and varied in phenotype with gut level. CD4-CD8-TCR alpha beta IEL dominated in colon but were absent in jejunum. CD8+ TCR alpha beta IEL were present at all levels but only in jejunum did they constitute the majority of all IEL. CD4+ TCR alpha beta IEL were present in similar frequencies at all levels of the gut. In general, the majority of IEL had an activated phenotype (CD45RO+, alpha E beta 7+). Furthermore, IEL exhibited phenotypes which are rare in peripheral blood. The thymocyte markers CD1a and CD1c as well as the NK cell marker CD56 were expressed on a fraction of TCR alpha beta and TCR gamma delta IEL. A small population of 'null' cells (CD45+ TCR/CD#-CD20-CD14-CD15- cells) was also present at equal proportions along the gut. Jejunal but not colonic IEL expressed RAG-1 mRNA suggesting that extrathymic T cell maturation occurs in the epithelium of small intestine. RAG-1 was expressed in CD2+TCR/CD3- and CD3+/TCR-IEL. Ultrastructurally, IEL often formed small clusters and intimate contacts with epithelial cells, suggesting cell cooperation within the epithelium. Some IEL had pseudopodium-like extensions penetrating the epithelial basement membrane suggesting transmigration. Epithelial cells in small intestine but not colon expressed heat shock protein 60 and HLA-DR. CD1a, CD1b and CD1c were not expressed on intestinal epithelial cells at any level. The distinct surface marker profiles of IEL and epithelial cells along small and large intestine suggest functional regional specialization and are compatible with the hypothesis that TCR alpha beta IEL participate in immune reactions to lumenal antigens while TCR gamma delta IEL perform surveillance of the epithelium.
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PMID:Intra-epithelial lymphocytes. Evidence for regional specialization and extrathymic T cell maturation in the human gut epithelium. 749 55

The objective of this study was to investigate CD163+ macrophages in the synovial membrane of patients with spondyloarthropathy (SpA). Immunohistochemistry was performed on synovium of 17 SpA and 18 rheumatoid arthritis (RA) patients, on colonic biopsies of 16 SpA patients and ten healthy controls, and on paired synovial biopsies of eight SpA patients, before and after anti-TNFalpha therapy. Phenotype and cytokine production were analysed by flow cytometry. CD163+ macrophages were increased in the synovial lining and sublining in SpA versus RA, as well as in colonic lamina propria in SpA versus controls. The number of CD163+ macrophages in the synovial sublining correlated with C-reactive protein levels and erythrocyte sedimentation rate. Paralleling the increase of CD163, HLA-DR was increased in the synovial lining and sublining of SpA. In contrast, the co-stimulatory molecules CD80 and CD86 and the dendritic cell markers CD1a and CD83 were scarce in SpA synovium. Flow cytometry indicated that CD163+ macrophages expressed high levels of HLA-DR and could produce in vitro tumour necrosis factor alpha (TNFalpha) but not interleukin-10 (IL-10). Finally, anti-TNFalpha therapy in vivo induced a decrease of CD163+ macrophages in the synovial lining and sublining. In conclusion, macrophages expressing the scavenger receptor CD163 are increased in synovium and in colonic mucosa in SpA, highlighting the relationship between joint and gut in this disease. The correlation with inflammatory parameters, the expression of HLA-DR, the production of TNFalpha but not IL-10, and the reduction by anti-TNFalpha therapy support a role for CD163+ macrophages in the synovial inflammation in SpA.
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PMID:Macrophages expressing the scavenger receptor CD163: a link between immune alterations of the gut and synovial inflammation in spondyloarthropathy. 1185 99

The distribution of specific histiocyte subsets within the human gastrointestinal tract has not been extensively characterized. Our goal was to immunohistochemically evaluate the distribution and location of CD1a-positive, CD68-positive, and Factor XIIIa (FXIIIa)-positive histiocyte subsets within the normal gastrointestinal tract and attempt to relate distribution to possible function. Twenty-nine samples of normal esophagus, stomach, small bowel, large bowel, and anus were routinely processed and immunohistochemically stained with antibodies to CD68, CD1a, and FXIIIa. The distribution and histologic location of histiocyte subsets were qualitatively analyzed. CD1a-positive cells were seen exclusively within anal and esophageal squamous mucosa. CD68 positive histiocytes were present in lamina propria and submucosa throughout the gastrointestinal tract and in Peyer patches. FXIIIa-positive histiocytes were also abundant in lamina propria and submucosa throughout the gastrointestinal tract, particularly around pericryptal sheaths and in parafollicular regions surrounding Peyer patches. Our results showed that there are distinct subpopulations of gastrointestinal histiocytes, and that distribution varies according to both cell type and site. Because Langerhans cells are epidermal antigen processing/presentation cells, their exclusive presence in squamous mucosa suggests an analogous function there. The prominence of both CD68 and FXIIIa-positive cells surrounding glandular pericryptal sheaths suggests that they are important to immune function at this mucosal interface and may play a role in communication between glands and lamina propria. In addition, the presence of specific histiocyte subsets within Peyer patches and para-follicular regions suggests that they are involved in different aspects of antigen processing associated with gut lymphoid tissue. Further studies are needed to explore the relation between specific histiocyte subsets and gastrointestinal disease processes.
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PMID:Histiocytic subpopulations in the gastrointestinal tract: distribution and possible relationship to function. 1553 37

Dendritic cells (DCs) are powerful antigen-presenting cells that have the unique capacity to stimulate naive T-cells (1, 2). DCs are identified by a triad of criteria: Morphologically, they exhibit pronounced cytoplasmic veils that are mobile and can easily be observed under a phase-contrast microscope. These veils become apparent only in the mature state. Phenotypically, they express high levels of major histocompatibility class (MHC) (class I and II), adhesion (CD11c, CD54, CD58), and costimulatory (CD80, CD86, CD40) molecules on their cell surfaces. They also express CD1a and CD83, but lack CD14. On cytocentrifuge smears stained with anti-CD68, a marker of the endocytic system that is abundant in macrophages, DCs display spotlike staining whereas typical macrophages are strongly positive all over the cytoplasm. When looking at forward/side scatter profiles in the fluorescence-activated cell sorter (FACS), DCs show high light scattering and are outside the typical lymphocyte gate. Functionally, they are potent stimulators of resting T lymphocytes in the allogeneic mixed leukocyte reaction. DCs derived from various tissues have been shown to undergo a complex maturation process during which their morphology, phenotype, and function change. DCs are derived from bone marrow progenitors and circulate in the blood as immature precursors before they migrate into peripheral tissues, such as the epidermis, heart, lung, liver, gut, thymus, spleen, and lymph nodes. DCs of myeloid as well as of lymphoid origin have been described (3-5).
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PMID:Dendritic cells in old age. 2235 Dec 83

The Tasmanian devil is under threat of extinction due to the transmissible devil facial tumor disease (DFTD). This fatal tumor is an allograft that does not induce an immune response, raising questions about the activity of Tasmanian devil immune cells. T and B cell analysis has been limited by a lack of antibodies, hence the need to produce such reagents. Amino acid sequence analysis revealed that CD4, CD8, IgM, and IgG were closely related to other marsupials. Monoclonal antibodies were produced against CD4, CD8, IgM, and IgG by generating bacterial fusion proteins. These, and commercial antibodies against CD1a and CD83, identified T cells, B cells and dendritic cells by immunohistochemistry. CD4(+) and CD8(+) T cells were identified in pouch young thymus, adult lymph nodes, spleen, bronchus- and gut-associated lymphoid tissue. Their anatomical distribution was characteristic of mammalian lymphoid tissues with more CD4(+) than CD8(+) cells in lymph nodes and splenic white pulp. IgM(+) and IgG(+) B cells were identified in adult lymph nodes, spleen, bronchus-associated lymphoid tissue and gut-associated lymphoid tissue, with more IgM(+) than IgG(+) cells. Dendritic cells were identified in lymph node, spleen and skin. This distribution is consistent with eutherian mammals and other marsupials, indicating they have the immune cell subsets for an anti-tumor immunity. Devil facial tumor disease tumors contained more CD8(+) than CD4(+) cells, but in low numbers. There were also low numbers of CD1a(+) and MHC class II(+) cells, but no CD83(+) IgM(+) or IgG(+) B cells, consistent with poor immune cell infiltration.
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PMID:Identification of dendritic cells, B cell and T cell subsets in Tasmanian devil lymphoid tissue; evidence for poor immune cell infiltration into devil facial tumors. 2466 54