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)

Halo reactions to melanocytic nevi are a well-recognized phenomenon. In contrast, halo reactions to Spitz's nevi have been reported only infrequently. Halo reactions may cause misdiagnosis of an otherwise benign nevus as melanoma because inflammatory cells sometimes obscure the architectural features of the underlying nevus, and may induce cytologic atypia. For Spitz's nevus where the distinction between malignancy and benignancy is already challenging, halo reactions compound the problem. We describe 17 examples of Spitz's nevus with halo reaction, and compare their immunohistochemical features with those of "ordinary" halo nevi. Only 2 of 17 lesions demonstrated clinically apparent halos. Clinical follow-up was available for 12 of 17 cases. None of the 12 has persisted at the biopsy site or metastasized after an average 3.6-year follow-up period. Junctional, compound, intradermal, and combined types of Spitz's nevi were represented. All were characterized by symmetrical lymphocytic infiltrates which permeated the full thickness of the nevus, including junctional nests. Combined Spitz's nevi constituted more than one-half of examples in this series (9/17 cases). The combined Spitz's nevus included a combination of Spitz's nevus with either an ordinary (common, banal) nevus or a superficial congenital type nevus. In these combined Spitz's nevi, the lymphocytic response was often directed exclusively to the Spitz's nevic component. Important distinguishing features from malignant melanoma arising in a pre-existing nevus included symmetry and lateral circumscription of the spitzoid component, no large expansile-appearing aggregates of melanocytes, a decrease in size of nests with increasing dermal depth, a lack of mitotic figures among melanocytes at the base, and a symmetrical and diffusely permeative lymphocytic response. Although the combined Spitz's nevus with halo reaction sometimes appeared asymmetrical at scanning magnification, each component of the combination was symmetrical, when examined independently. Probably because of reactive atypia, nuclear maturation with progressive descent into the dermis was sometimes absent. There were no obvious differences in immunohistochemical staining patterns among 4 Spitz's nevi with halo reaction, 5 regressing melanomas, and 5 benign halo nevi when stained with antibodies to S100, HMB-45, OPD4, CD8, TIA-1, CD1a, CD68, and Ki-67.
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PMID:Spitz's nevi with halo reaction: a histopathologic study of 17 cases. 944 88

The perivascular space (PVS) of human thymus increases in volume during aging as thymopoiesis declines. Understanding the composition of the PVS is therefore vital to understanding mechanisms of thymic atrophy. We have analyzed 87 normal and 31 myasthenia gravis (MG) thymus tissues from patients ranging in age from newborn to 78 years, using immunohistologic and molecular assays. We confirmed that although thymic epithelial space (TES) volume decreases progressively with age, thymopoiesis with active T-cell receptor gene rearrangement continued normally within the TES into late life. Hematopoietic cells present in the adult PVS include T cells, B cells, and monocytes. Eosinophils are prominent in PVS of infants 2 years of age or younger. In the normal adult and the MG thymus, the PVS includes mature single-positive (CD1a(-) and CD4(+) or CD8(+)) T lymphocytes that express CD45RO, and contains clusters of T cells expressing the TIA-1 cytotoxic granule antigen, suggesting a peripheral origin. PBMCs bind in vitro to MECA-79(+) high endothelial venules present in the PVS, suggesting a mechanism for the recruitment of peripheral cells to thymic PVS. Therefore, in both normal subjects and MG patients, thymic PVS may be a compartment of the peripheral immune system that is not directly involved in thymopoiesis.
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PMID:Analysis of the human thymic perivascular space during aging. 1052 41

Hematopoietic neoplasm coexpressing CD4 and CD56 includes a subset of acute myeloid leukemia with myelomonocytic differentiation, plasmacytoid monocyte tumor, and other immature hematopoietic neoplasms of undefined origin. Herein, we report a CD4+CD56+CD68+ hematopoietic tumor that was thought to be a tumor of plasmacytoid monocytes. This case is unique in the absence of accompanying myelomonocytic leukemia and the faint expression of cCD3 on the tumor cells. The patient was a 22-yr old man presented with multiple lymphadenopathy and an involvement of the bone marrow. Tumor cells were large and monomorphic with an angulated eosinophilic cytoplasm of moderate amount. Nuclei of most tumor cells were eccentric and round with one or two prominent nucleoli. Rough endoplasmic reticulum was prominent in electron microscopic examination. Tumor cells expressed CD4, CD7, CD10, CD45RB, CD56, CD68, and HLA-DR and were negative for CD1a, CD2, sCD3, CD5, CD13, CD14, CD20, CD33, CD34, CD43, CD45RA, TIA-1, S-100, and TdT. cCD3 was not detected in the immunostaining using paraffin tissue, but was faintly expressed in flow cytometry and immunostaining using a touch imprint slide. T-cell receptor gene rearrangement analysis and EBV in situ hybridization showed negative results. Cytochemically, myeloperoxidase, Sudan black B, and alpha naphthyl butyrate esterase were all negative.
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PMID:CD4+CD56+CD68+hematopoietic tumor of probable plasmacytoid monocyte derivation with weak expression of cytoplasmic CD3. 1248 12

The pathological role played by T cells infiltrating hair follicles in lesions of alopecia areata (AA) is unknown. We examined the expression in cryostat sections of scalp skin obtained from a total of 28 patients with AA and from five normal control subjects of (1) molecules related to the induction of cell death including Fas, Fas ligand (FasL), perforin, granzyme B (GB), and TIA-1, (2) molecules related to antigen presentation including CD1a, CD40, CD54, CD80, and CD86, and (3) molecules induced by interferon gamma (IFN-gamma) including CD40, CD54, Fas, and HLA-DR. CD3(+) T cells infiltrated perifollicularly, perivascularly and in the hair structure and there was a predominance of CD4(+) over CD8(+) cells. Antigen-presenting cells expressing CD1a, CD40, CD54, or HLA-DR were also seen. Expression of CD40, CD54, HLA-DR and CD95 was also seen in the hair structure including the dermal papilla. Consistent with these observations, IFN-gamma-producing cells were also detected in the perifollicular infiltrate. In contrast, few Fas-L(+), perforin(+), GB(+) or TIA-1(+) cells were found adjacent to the follicles. Apoptotic cells were recognized only in the outer root sheath of catagen hairs. These findings suggest that infiltrating T cells interact with perifollicular or follicular antigen-presenting cells to produce IFN-gamma, which deprives dermal papilla cells of their ability to maintain anagen hair growth.
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PMID:Strong expression of CD40, CD54 and HLA-DR antigen and lack of evidence for direct cellular cytotoxicity are unique immunohistopathological features in alopecia areata. 1262 79

The lymph node is the site of antigen presentation, and dendritic cells are sentinels for anti-tumor immunity. However, little is known about the histological features of lymph nodes and dendritic cells in soft tissue sarcomas. The reactive lymph node and infiltration of dendritic cells or effector cells were studied histologically in 10 soft tissue sarcomas with reactive lymphoid hyperplasia. The cases included four malignant fibrous histiocytomas, two malignant peripheral nerve sheath tumors, one synovial sarcoma, one epithelioid sarcoma, one malignant granular cell tumor, and one liposarcoma. The proportions of the T zone, lymphoid follicle, and lymphoid sinus (which was occupied by cells immunopositive for antibodies against CD3, CD20, or CD68) were 33.4% +/- 11.0%, 6.1% +/- 4.9%, and 13.5% +/- 6.5%, respectively. T zone hyperplasia was observed in all cases, and sinus histiocytosis was found in four. The proportion of the T zone in regional lymph nodes of soft tissue sarcoma patients was significantly higher than that in adult autopsy cases without a cancer history. CD8-, TIA-1-, or granzyme B-positive effector cells were found in each sarcoma tissue. Whereas CD1a-positive dendritic cells were not detected, S-100 protein-positive or CD83-positive dendritic cells were observed in five sarcoma tissues. The coefficient correlation between the numbers of effector cells and dendritic cells positive for CD83 or S-100 protein were demonstrated. Although this is a preliminary report, the present study demonstrated that some soft tissue sarcoma patients showed reactive lymphoid hyperplasia. Furthermore, the association between the infiltration of dendritic cells and that of effector cells was observed in patients with soft tissue sarcomas.
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PMID:Dendritic cell and effector cell infiltration in soft tissue sarcomas with reactive lymphoid hyperplasia. 1455 33

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