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)

A novel nude mice model of human extranodal nasal type NK/T-cell lymphoma was established by subcutaneously implanting the sample taken from the patient with secondary extranodal nasal type NK/T-cell lymphoma of the stomach into the right axillary region of a BALB/c (nu/nu) nude mouse. This model had been successfully transplanted in vivo for thirty-two generations with a stable growth cycle. The survival rates of both resuscitation and transplantation were 100%. Histologically, the tumor cells were medium to large size and arranged in sheets, with a little mesenchyma, and disseminated almost in all passages of the lymphoma-bearing nude mice. Immunologically, the tumor cells were positive for CD56, cytoplasmic CD3, granzyme B or TIA-1 and LMP1, sometimes for CD8 but negative for surface CD3, CD7, CD20 and CD1a. EBER1/2 was found. No T-cell receptor gamma gene rearrangement was detected in the transplanted tumors. Furthermore, both human sequencing-tagged sites SY14 and Y chromosome were detected by PCR or fluorescent in situ hybridization, respectively, in the transplanted tumor. The transplanted tumor in this novel nude mice model maintained the essential features of human extranodal nasal type NK/T-cell lymphoma, and it would be an ideal tool in vivo for further research of the tumor.
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PMID:A novel nude mice model of human extranodal nasal type NK/T-cell lymphoma. 1785 53

Pulmonary Langerhans' cell histiocytosis (PLCH) is a disease characterized by the occurrence of complex fibro-cellular interstitial lesions dominated by Langerhans' cells (LC), which occurs predominantly in young adult smokers. We undertook this retrospective study to better define the lymphohistiocytic cell populations in PLCH in order to obtain a greater insight into its pathogenesis. Formalin-fixed, paraffin-embedded, surgically excised, archival lung tissue from seven patients (two males, five females; average age 34.9 years) was immunostained with a panel of antibodies for lymphohistiocytic markers: CD1a, CD3, CD4, CD8, CD15, CD20, CD56, TIA-1, CD68-PGM1, Mac387, and mast cell tryptase. Double immunolabeling was performed with CD1a/Mac387. Leder cytochemical stain for chloroacetate esterase was also performed. A moderate number of lymphocytes, predominantly T lymphocytes, were scattered diffusely within the lesions. The mean CD4/CD8 ratio was 0.1/1. The CD3/CD8 ratio (1.18/1) substantiated the CD4/CD8 ratio. The CD8 subset was CD56-negative and TIA-1-positive, indicating a cytotoxic T lymphocyte phenotype. CD68-PGM1 was strongly positive in alveolar macrophages (AM) and weakly stained LC. Mac387, a marker of activated macrophages, weakly stained AM, while highlighting other interstitial cells. These interstitial cells appeared not to be LC (substantiated by CD1a/Mac387 dual labeling) or CD68-PGM-1-positive macrophages. Having excluded mast cells (positive with mast cell tryptase) and neutrophils (positive with CD15 and Leder stains), there appeared to be a residual population of non-Langerhans cell monocytoid cells (NLMC), which were Mac 387+, CD68-PGM1-, Mast cell tryptase-, CD15-, and CD1a-. Our results showed a predominance of CD8+, TIA-1+ cytotoxic T lymphocytes among the lymphocyte subsets which appear to interact with LC and AM in PLCH lesions. A small sub-population of NLMC was also present. Further studies are required to better define and to evaluate the role of cytotoxic T cells and NLMC in the pathogenesis of PLCH.
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PMID:Lymphocyte sub-populations and non-Langerhans' cell monocytoid cells in pulmonary Langerhans' cell histiocytosis. 1833 20

Cardiac allograft vasculopathy (CAV) in heart transplantation (HTx) patients remains the major complication for long-term survival, due to concentric neointima hyperplasia induced by infiltrating mononuclear cells (MNC). Previously, we showed that activated memory T-helper-1 (Th-1) cells are the major component of infiltrating MNC in coronary arteries with CAV. In this study, a more detailed characterization of the MNC in human coronary arteries with CAV (n = 5) was performed and compared to coronary arteries without CAV (n = 5), by investigating MNC markers (CD1a, DRC-1, CD3, CD20, CD27, CD28, CD56, CD68, CD69, FOXP3 and HLA-DR), cytokines (IL-1A, 2, 4, 10, 12B, IFN-gamma, and TGF-beta1), and chemokine receptors (CCR3, CCR4, CCR5, CCR7, CCR8, CXCR3 and CX3CR1) by immunohistochemical double-labeling and quantitative PCR on mRNA isolated from laser microdissected layers of coronary arteries. T cells in the neointima and adventitia of CAV were skewed toward an activated memory Th-1 phenotype, but in the presence of a distinct Th-2 population. FOXP3 positive T cells were not detected and production of most cytokines was low or absent, except for IFN-gamma, and TGF-beta. This typical composition of T-helper cells and especially production of IFN-gamma and TGF-beta may play an important role in the proliferative CAV reaction.
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PMID:T cells in cardiac allograft vasculopathy are skewed to memory Th-1 cells in the presence of a distinct Th-2 population. 1841 40

HIV-1 impairs the production of T cells, through mechanisms that are still unknown. Here, we investigated the effect of the expression of HIV-1 Nef on the T-cell potential of human hematopoietic CD34(+) precursors. Those progenitors were transduced by using lentiviral vectors expressing Nef and cultured on OP9-DL1 cells allowing the differentiation of T cell from human hematopoietic precursors. We demonstrate that Nef impairs the generation of a CD3epsilon(+)CD5(+) CD1a(+) precursor stage that has initiated a D-J rearrangement of the TCRbeta locus. Onward stages of T-cell development were also affected with a quantitative reduction of CD4(+) intraCD3epsilon(+) Immature single positive cells (ISP), Double Positive (DP) CD4(+)CD8(+) TCRalphabeta T cells and CD56(+) NK cells. But B cell production was not affected. Limiting dilution analyses demonstrated a significant reduction in the frequency of T/NK progenitors among Nef-expressing CD34(+) cells. Altogether, these data demonstrate that Nef interferes with the differentiation of a primitive lymphoid human precursor with a T/NK potential.
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PMID:HIV-1 Nef protein expression in human CD34+ progenitors impairs the differentiation of an early T/NK cell precursor. 1855 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

Lymphoepithelioma-like carcinoma (LELC) of the urinary bladder is often mixed with conventional transitional cell carcinoma and/or other histotypes. The pathologist's determination of the morphologic purity of a given LELC at the biopsy stage is a clinically relevant endeavour, because there is some anecdotal evidence suggesting that pure or predominant LELC may be comparatively chemosensitive and have a favorable prognostic profile, which may potentially offer the possibility of effective therapy without bladder resection. The precise degree of cellular pleomorphism that is allowed in a pure LELC is unclear. We describe herein an otherwise conventional and pure LELC that showed, in a localized area that constituted approximately 25% of the overall tumor volume, a two to six fold variation in nuclear size, including multinucleated tumor cells. These pleomorphic areas were set in the same lymphoplasmacytic infiltrate as their conventional counterparts, and similarly displayed cellular syncytia. We performed a detailed immunophenotypic comparison between the conventional areas and the pleomorphic areas. No significant differences were found between the 2 areas in overall lymphoplasmacytic or histiocytic density, lymphocytic CD4/CD8 ratio, and lymphoplasmacytic kappa/lambda ratio. Similarly, both displayed similar qualitative and quantitative staining indices for p53, Ki67, cytokeratin AE1/AE3 and p16(INKa). Scattered cells were cytoplasmically beta-catenin positive exclusively in the pleomorphic areas; however these cells were not notably larger than the cells in the conventional areas. Both components were immunohistochemically negative for HMB-45, CD1a, the estrogen receptor, Epstein-Barr virus, CD117, D2-40, CD56, cytokeratin 20 and chromogranin. Clinicopathologic analysis of a series of cases is required to establish if there is any significance to nuclear pleomorphism in LELC. However, the phenotypic similarity between the 2 areas in this case, the intimate admixture of the pleomorphic cells with the lymphoplasmacytic infiltrate, and their syncytial pattern of growth, all suggest that pure LELC may display marked nuclear pleomorphism, and that this finding may not, in of itself, be a valid basis for removing a case from the "pure" group.
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PMID:Pleomorphic lymphoepithelioma-like carcinoma of the urinary bladder. 1907 56

Tumor-infiltrating leukocytes and other immunohistochemical parameters were evaluated in pretherapeutic biopsies and resection specimens in 73 patients undergoing neoadjuvant chemotherapy with doxorubicin and paclitaxel. Ten patients with pathological complete response had significantly higher p53 expression, CD3(+) lymphocyte and CD83(+) cell counts, and lower progesterone receptor expression. In the remaining 63 patients, a significant decrease in the percentage of Ki-67, vascular endothelial growth factor expression, CD68(+) monocytes, and increased CD31(+), CD34(+), and SMA(+) stromal vessels, maximal CD3(+) and CD56(+) lymphocyte, maximal and mean CD83(+) cell, maximal CD1a(+), and maximal and mean S100(+) cell counts were observed after neoadjuvant chemotherapy.
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PMID:Tumor-infiltrating lymphocytes predict response to neoadjuvant chemotherapy in patients with breast carcinoma. 1909 60

Attempts to establish a concise classification of lymphoblastic lymphomas (LBLs) have gained momentum in recent years, mainly due to the expanding possibilities of immunohistochemical and genetic characterization of different disease entities. Thus, cases of immature lymphoid malignancies with unusual immunopathological features have been reported during the last years, suggesting the need for new LBL classification concepts. To further characterize and demonstrate the extended spectrum of LBL, we present an unusual pediatric case of LBL that could not be categorized into one of the subgroups and exhibited a benign course after surgical treatment and subsequent chemotherapy. A mediastinal tumor of a 6-year-old Caucasian boy was examined by clinical staging, light microscopy, immunohistochemistry and PCR assays. The tumor cells reacted with TdT and had a positive cytoplasmic immunoreactivity for CD3. Further T- aand NK-cell markers CD1a, CD4, CD8, CD10, and CD56 reacted positively, but CD57, CD16 and CD 30 (Ber H2) were all negative. CD34 as a marker for bipotential B/T-precursors was also positive. B cell markers (CD20, CD22, Cd79a and IgM) were all negative. No clonal B cell Ig or T cell gamma chain rearrangements were detectable. Epstein Barr virus and other Herpes Virus DNA were not detected using a sensitive PCR assay. The applied chemotherapy was tolerated well and a complete remission of the tumor was achieved (observation period three years after the initial diagnosis). Localization, morphology, and the expressions markers made the tumor a typical member of the LBL group. However, our case represents a rare pediatric lymphoma derived from a thymic precursor committed to T/NK-cell differentiation and a favourable outcome after chemotherapy.
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PMID:A rare pediatric case of a thymic cytotoxic and lymphoblastic T/NK cell lymphoma. 2049 Mar 34

Organ transplant recipients (OTR) have a greatly increased risk (up to 100 times) of developing squamous cell carcinomas (SCC) in the skin. This is attributed specifically to chronic immunosuppression, causing dysfunctional viral defence and tumour protection. To investigate the possible link between increasing risk of SCCs and type of inflammation in these tumour-prone patients, we analysed the peritumoural infiltrates with regard to cell types and densities. Seven SCCs from immunosuppressed OTR and 14 SCCs from immunocompetent patients were immun-histochemically stained for CD3, CD4, CD8, CD56, CD20, CD138, CD14, CD68, CD1a. Cell counts were performed with the aid of computer-based image analysis of > 100,000 cells. When comparing the percentage distributions, significant differences were detected (outlined as median values (min-max)): T cells (CD3+): OTR 57% (35-78), controls 68% (48-80), p = 0.036; plasma cells (CD138+): OTR 2% (0.7-7), controls 0.2% (0-1.2), p = 0.001; mono-cytes (CD14+): OTR 3.2% (1.1-5.6), controls 9.3% (2.2-17.2), p = 0.014. Surprisingly, no differences in cell densities, i.e. cells/mm2 tumour section area, were detected between the 2 groups. In conclusion, we found that the peritumoural infiltrates in immunosuppressed compared with immunocompetent patients differ in cellular composition, inferring a more tumour-submissive environment in OTR. However, cellular densities were equal, suggesting deviating cellular functionality in OTR.
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PMID:Differences in the peritumoural inflammatory skin infiltrate between squamous cell carcinomas in organ transplant recipients and immunocompetent patients. 2057 3

Decidual antigen-presenting cells including dendritic cells (DCs) and CD14(+) macrophages, as mediators of the first encounter with fetal antigens, appear to be critically involved in the initiation of primary immune response by regulating innate- and adaptive immunity. Interleukin-15, produced by them, permits the proliferation and differentiation of CD3(-)CD16(-)CD94(+)NKG2A(+)CD56(+bright) decidual NK cells that identify trophoblast cells. These cells are able to kill them after Th1 cytokine overstimulation and by increasing the release of preformed cytotoxic mediators. Thus, the local microenvironment is a potent modulator of antigen-presenting cell functions. Tumor associated glycoprotein-72 (TAG-72) and mucine 1 (MUC-1) are glycoproteins secreted by uterine epithelial cells. Our hypothesis is that TAG-72 and MUC-1 are the natural ligands for carbohydrate recognition domains (CRDs) of endocytic mannose receptor (MR or CD206) and DC-specific ICAM non-integrin (DC-SIGN or CD209) expressed on decidual CD14(+) macrophages and CD1a(+) DCs. They might be able to condition antigen-presenting cells to produce distinct profiles of cyto/chemokines with consequential reduction in NK-cell numbers and cytotoxic potential leading to insufficient control over trophoblast growth. This hypothesis could explain the disappearance of MUC-1 beneath the attached embryo during the process of successful implantation when tight regulation of trophoblast invasion is needed. As IL-15 is the earliest and the most important factor in NK-cell proliferation, differentiation, and maturation, we expected primarily an increase of IL-15 expression in antigen-presenting cells concomitant with the disappearance of mucins and the enhancement in NK cells numbers and of cytotoxic potential after their close contact with early pregnancy decidual antigen-presenting cells. If our hypothesis is correct, it would contribute to the understanding of the role of mucins in the redirection of immune response via antigen-presenting cells and could help explain the mechanism of IL-15 regulation at the maternal-fetal interface of normal, ectopic-, and pathological pregnancies with effects on NK-cell proliferation, cytolytic mediator expression, and regulation of trophoblast growth control.
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PMID:Regulation of NK-cell function by mucins via antigen-presenting cells. 2070 48


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