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William Fox - One of the best experts on this subject based on the ideXlab platform.
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immunohistochemical expression of CD68 Antigen in human peripheral blood t cells
Human Pathology, 1994Co-Authors: Arif Hameed, Ralph H Hruban, Wes Gage, George Pettis, William FoxAbstract:CD68 Antigen is expressed by tissue macrophages and cells of myeloid/mononuclear lineage. CD68 is recognized by many monoclonal antibodies (mAbs), including KP1, EMB11, Y1/82A, Y2/131, Ki-M6, and Ki-M7. Using the labeled strept-avidin-biotin (LSAB) immunoperoxidase technique, we examined CD68 Antigen expression in human peripheral blood T cells. The anti-CD68 mAbs KP1 and EMB11 stained virtually all fresh isolated gamma/delta T cells and CD3-CD56+ natural killer (NK) cells in a granular cytoplasmic pattern. In contrast, fresh isolated CD4+ and CD8+ T lymphocytes showed no detectable reactivity with these two anti-CD68 mAbs. However, in vitro stimulation with T-cell mitogen or recombinant interleukin-2 (rIL-2) induced expression of CD68 Antigen in activated CD4+ and CD8+ T lymphocytes. Similarly, the lymphokine-activated killer (LAK) cells generated after long-term (14 to 21 days) culture of peripheral blood mononuclear cells (PBMC) in rIL-2 also showed strong granular cytoplasmic staining by the anti-CD68 antibodies. This study shows that the CD68 Antigen is constitutively expressed in NK cells and gamma/delta T cells and that its expression is strongly induced in activated CD4+ and CD8+ T lymphocytes as well as LAK cells.
P Van Der Valk - One of the best experts on this subject based on the ideXlab platform.
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post mortem mri guided sampling of multiple sclerosis brain lesions increased yield of active demyelinating and p reactive lesions
Brain, 2001Co-Authors: C J A De Groot, E Bergers, Wouter Kamphorst, Rivka Ravid, C H Polman, Frederik Barkhof, P Van Der ValkAbstract:Macroscopic sampling of multiple sclerosis lesions in the brain tends to find chronic lesions. For a better understanding of the dynamics of the multiple sclerosis disease process, research into new and developing lesions is of great interest. As MRI in vivo effectively demonstrates lesions in multiple sclerosis patients, we have applied it to unfixed post-mortem brain slices to identify abnormalities, in order to obtain a higher yield of active lesions. The Netherlands Brain Bank organized the rapid autopsy of 29 multiple sclerosis patients. The brain was cut in 1 cm coronal slices. One or two slices were subjected to T(1)- and T(2)-weighted MRI, and then cut at the plane of the MRI scan into 5 mm thick opposing sections. Areas of interest were identified based on the MRI findings and excised. One half was fixed in 10% formalin and paraffin-embedded, and the corresponding area in the adjacent half was snap-frozen in liquid nitrogen. In total, 136 out of 174 brain tissue samples could be matched with the abnormalities seen on T(2)-weighted MRIs. The stage of lesional development was determined (immuno) histochemically. For 54 MRI-detectable samples, it was recorded whether they were macroscopically detectable, i.e. visible and/or palpable. Histopathological analysis revealed that 48% of the hyperintense areas seen on T(2)-weighted images represented active lesions, including lesions localized in the normal appearing white matter, without apparent loss of myelin but nevertheless showing a variable degree of oedema, small clusters of microglial cells with enhanced major histocompatibility complex class II Antigen, CD45 and CD68 Antigen expression and a variable number of perivascular lymphocytes around small blood vessels [designated as (p)reactive lesions]. From the macroscopically not-visible/not-palpable MRI-detected abnormalities, 58% were (p)reactive lesions and 21% contained active demyelinating lesions. In contrast, visible and/or palpable brain tissue samples mainly contained chronic inactive lesions. We conclude that MRI-guided sampling of brain tissue increases the yield of active multiple sclerosis lesions, including active demyelinating and (p)reactive lesions.
Arif Hameed - One of the best experts on this subject based on the ideXlab platform.
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immunohistochemical expression of CD68 Antigen in human peripheral blood t cells
Human Pathology, 1994Co-Authors: Arif Hameed, Ralph H Hruban, Wes Gage, George Pettis, William FoxAbstract:CD68 Antigen is expressed by tissue macrophages and cells of myeloid/mononuclear lineage. CD68 is recognized by many monoclonal antibodies (mAbs), including KP1, EMB11, Y1/82A, Y2/131, Ki-M6, and Ki-M7. Using the labeled strept-avidin-biotin (LSAB) immunoperoxidase technique, we examined CD68 Antigen expression in human peripheral blood T cells. The anti-CD68 mAbs KP1 and EMB11 stained virtually all fresh isolated gamma/delta T cells and CD3-CD56+ natural killer (NK) cells in a granular cytoplasmic pattern. In contrast, fresh isolated CD4+ and CD8+ T lymphocytes showed no detectable reactivity with these two anti-CD68 mAbs. However, in vitro stimulation with T-cell mitogen or recombinant interleukin-2 (rIL-2) induced expression of CD68 Antigen in activated CD4+ and CD8+ T lymphocytes. Similarly, the lymphokine-activated killer (LAK) cells generated after long-term (14 to 21 days) culture of peripheral blood mononuclear cells (PBMC) in rIL-2 also showed strong granular cytoplasmic staining by the anti-CD68 antibodies. This study shows that the CD68 Antigen is constitutively expressed in NK cells and gamma/delta T cells and that its expression is strongly induced in activated CD4+ and CD8+ T lymphocytes as well as LAK cells.
Dennis K. Heffner - One of the best experts on this subject based on the ideXlab platform.
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adult rhabdomyoma of the head and neck a clinicopathologic and immunophenotypic study
Human Pathology, 1993Co-Authors: Silloo B. Kapadia, Jeanne M Meis, Dennis M. Frisman, Gary L. Ellis, Dennis K. Heffner, Vincent J HyamsAbstract:Twenty-seven cases of adult rhabdomyoma (ARM) of the head and neck are reported. The 20 male and seven female patients ranged in age from 33 to 80 years (median age, 60 years). Symptoms included airway obstruction and a mass within the mucosa or soft tissue. Median tumor size was 3.0 cm (range, 1.5 to 7.5 cm). Seven patients (26%) presented with multinodular tumors and one tumor was multicentric. Follow-up was available in 19 cases and ranged from 2 months to 18.5 years after diagnosis (median, 6.0 years). Lesions recurred locally in eight cases (42%) 2 to 11 years after diagnosis (median, 6 years). One recurrence was multicentric. Histologically, ARM was composed of closely packed, large polygonal cells having abundant, eosinophilic, granular, or vacuolated glycogen-rich cytoplasm with focal cross-striations. Immunohistochemical stains confirmed skeletal muscle differentiation; the majority of tumors stained for myoglobin (21 of 21 tumors), muscle-specific actin (21 of 21 tumors), and desmin (19 of 21 tumors). Focal or rare immunoreactivity for vimentin (six of 17 cases), alpha-smooth muscle actin (17 of 20 cases), S-100 protein (14 of 21 cases), and Leu-7 (10 of 20 cases) also was detected. Cytokeratin, epithelial membrane Antigen, glial fibrillary acidic protein, and CD68 Antigen (with KP1) were not found. The characteristic histology and immunophenotype distinguish ARM from other lesions with which it is frequently confused, including granular cell tumor, hibernoma, oncocytoma, and paraganglioma. The expression of alpha-smooth muscle actin has not been reported previously in ARM; its presence could reflect aberrant expression of smooth muscle actin in skeletal muscle or possibly be a recapitulation of early skeletal muscle embryogenesis.
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Fetal rhabdomyoma of the head and neck: A clinicopathologic and immunophenotypic study of 24 cases
Human pathology, 1993Co-Authors: Silloo B. Kapadia, Jeanne M Meis, Dennis M. Frisman, Gary L. Ellis, Dennis K. HeffnerAbstract:Abstract Twenty-four fetal rhabdomyomas (FRMs) of the head and neck occurring in 16 male and seven female patients (sex unknown in one), ranging from 3 days to 58 years of age (median, 4.5 years) are reported. Ten patients (42%) were ≤1 year old, six lesions (25%) were congenital, and 11 lesions (46%) occurred in patients ≥ 15 years of age. The median tumor size was 3.0 cm (range, 1.0 to 12.5 cm). The FRMs presented as well-defined, solitary masses arising within the soft tissue or mucosa (2:1) of the head and neck. The median follow-up in 15 cases was 48 months (range, 2 months to 52 years) after diagnosis. With the exception of one patient with a local recurrence, all patients were either alive and well or dead of unrelated causes. Eight cases, regarded as "classic" FRM, consisted predominantly of bland, primitive spindled cells associated with delicate, elongated skeletal muscle cells reminiscent of fetal myotubules that were haphazardly arranged in an abundant fibromyxoid stroma. The remaining 16 cases, designated as "intermediate" FRM, displayed both a greater degree and a greater number of cells with skeletal muscle differentiation as well as a variety of distinctive cytologic and architectural features. These included the presence of large, ganglion cell-like rhabdomyoblasts with vesicular nuclei and prominent nucleoli, interlacing ribbon or strap-like rhabdomyoblasts with deeply acidophilic cytoplasm, broad bundles of more delicate spindled rhabdomyoblasts arranged in fascicles simulating smooth muscle, an occasional plexiform pattern with infiltration of adipose tissue and skeletal muscle, focal intimate association with peripheral nerves, and rare areas of fibroblastic proliferation. Mitoses were not found in 19 of the 24 FRM cases, but in five tumors there were 1 to 14 mitoses/50 high-power fields. Marked nuclear atypia, anaplasia, and a "cambium layer" were uniformly absent. The FRMs typically stained for myoglobin, desmin, and muscle-specific actin with focal or rare staining for vimentin, smooth muscle actin, S-100 protein, glial fibrillary acidic protein, and Leu-7. Cytokeratin, epithelial membrane Antigen, and CD68 Antigen (with KP1) were not detected. This study expands on previous reports of FRM and demonstrates that it has both a broader age range and histologic spectrum than previously recognized. The mitotic rates of FRM as well as certain histologic features overlap with rhabdomyosarcoma; the lack of marked nuclear atypia is an important distinguishing feature. The intimate association of some FRMs with peripheral nerves and a focal fibroblastic proliferation in conjunction with S-100 protein and glial fibrillary acidic protein in some cases raises the possibility that at least some FRMs may be related to neuromuscular hamartoma (benign Triton tumor).
Kunihiko Tamaki - One of the best experts on this subject based on the ideXlab platform.
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increased numbers of CD68 Antigen positive dendritic epidermal cells and upregulation of cla cutaneous lymphocyte associated Antigen expression on these cells in various skin diseases
Journal of Dermatological Science, 1998Co-Authors: Koichiro Nakamura, Nami Yasaka, Akihiko Asahina, Mitsuyasu Kato, Kohei Miyazono, Masutaka Furue, Kunihiko TamakiAbstract:CD68 is a myelomonocytic marker identified in human dermal macrophages. Although the existence of CD68 + dendritic epidermal cells has been reported, their characteristics have not been well elucidated. Cutaneous lymphocyte-associated Antigen (CLA) is a homing receptor of cutaneous inflammatory T cells. Our recent report suggested that CLA was a homing molecule of CD1a+ Langerhans cells (LC) in the skin. In the present study we tested whether CD68 and CLA+ dendritic epidermal cells were present in skin specimens of normal skin and diseased skin such as lichen planus (LP), psoriasis vulgaris (PS), discoid lupus erythematosus (DLE), basal cell epithelioma (BCE), squamous cell carcinoma (SCC), irritated seborrheic keratosis (iSK), and Bowen's disease (BD). CD68+ dendritic epidermal cells were identified in normal skin and consisted of half the population of CD1a+ LC. These data indicate that CD68+ dendritic epidermal cells constitute a subpopulation of CD1a+ LC. CLA was expressed on a small percentage of CD68+ dendritic epidermal cells in normal skin. A remarkably increased number of CD68+ dendritic epidermal cells and upregulation of CLA on CD68+ dendritic epidermal cells were observed in diseased skin. The percentage of CLA+ cells among all CD68+ dendritic epidermal cells was less than that of CLA+ cells among all CD1a+ LC in diseased skin. The percentage of CLA+ cells among all CD68+ dendritic dermal cells was much less than that of CLA+ cells among all CD1a+ dendritic dermal cells. In normal skin, the epidermis showed minimal expression of monocyte chemoattractant protein (MCP)-1 and TGF-beta2, and no expression of TGF-beta1. In diseased skin, the epidermis showed elevated, but still moderate immunoreactivity for MCP-1. Slightly enhanced immunoreactivity for TGF-beta2, but not for TGF-beta1, was observed in the epidermis of diseased skin. Increased epidermal MCP-1 immunohistochemical staining was associated with the increased number of CD68 dendritic epidermal cells. These data suggest the possibility that MCP-1 secretion from the epidermis can affect the migration of CD68; Cutaneous lymphocyte-associated Antigen; Monocyte chemoattractant protein-1; TAF-beta.