Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Herpes simplex (HSV) and varicella-zoster (VZV) skin infections share so many histological similarities that distinguishing between them may prove to be impossible. We developed and characterized a new monoclonal antibody, VL8, IgG kappa isotype, directed to the VZV envelope glycoprotein gpI. Immunohistochemistry with VL8 appeared highly sensitive and specific on formalin-fixed paraffin-embedded biopsies and a clear-cut distinction between HSV and VZV infections was possible. The pattern of VL8 immunolabelling in VZV infections was strikingly different from that found in HSV infections studied with polyclonal antibodies to HSV I and II. Double immunolabelling revealed the VL8 positivity of sebaceous cells, endothelial cells, Mac 387- and CD68-positive monocyte-macrophages, and factor XIIIa-positive perivascular, perineural and interstitial dendrocytes. Intracytoplasmic VL8 labelling of endothelial cells and perivascular dendrocytes was found at the site of leukocytoclastic vasculitis.
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PMID:Comparative immunohistochemical study of herpes simplex and varicella-zoster infections. 838 79

Fifteen sural nerve biopsies of vasculitic neuropathies have been compared with 11 cases of different non-vasculitic neuropathies and normal nerves from brain-dead organ donors. The APAAP (alkaline phosphatase monoclonal anti-alkaline phosphatase) immunostaining method was applied to cryostat sections from unfixed snap-frozen tissue samples. Immunoglobulins IgG, IgM, IgA, complement factors and light chains were reactive in biopsies of normal nerves as well as of vasculitic and nonvasculitic neuropathies. A strong reaction against IgE in the epineurial vessel walls was only seen in cases of Churg-Strauss-vasculitis. Antibodies against MHC class II (HLA DR) were positive in most of vasculitic infiltrates. Vascular endothelial cells were positive with anti MHC class I in all biopsies. A typical finding in all vasculitic neuropathies was the infiltration of epineurial vessels with CD4 positive and, to a lesser extent, CD8 positive lymphocytes. CD22 positive lymphocytes (B cells) have only been seen in about one third of vasculitic neuropathies. CD16 positive cells (NK-cells or neutrophils) could be demonstrated only in two biopsies. CD68 positive cells (macrophages) are frequently seen in most cases of neuropathy regardless of their etiology. The results support the concept of a primary T-cell mediated process against epineurial vessels as the most important mechanism in the pathogenesis of vasculitic neuropathies. In some cases with small epineurial infiltrates the vasculitic process can only be recognized with antibodies against CD4 or CD8. Therefore, the immunohistochemical evaluation of sural nerve biopsies may be helpful for identifying cases with microvasculitis.
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PMID:Immunohistochemical findings in vasculitic neuropathies. 850 63

Monocyte chemotactic peptide-1 (MCP-1) belongs to a large family of cytokines known as chemokines. It is a potent mediator of inflammatory response and is thought to play a major role in recruiting monocytes into the site of inflammation. Mixed cryoglobulinemia is a systemic vasculitis characterized in 10 to 30% of the cases by renal involvement. Monocyte infiltration into the glomerulus, and in the periglomerular and perivascular areas is a common histopathological feature of this form of glomerulonephritis. We sought to determine, by in situ hybridization and immunohistochemistry, the renal gene and protein expression of MCP-1 in cryoglobulinemic glomerulonephritis compared to normal kidney, and to correlate it with macrophage infiltration. Kidney biopsy specimens were obtained from 9 patients with cryoglobulinemic glomerulonephritis and 9 control kidneys. The distribution and intensity of MCP-1 gene and protein expression, and the macrophage infiltration (CD68 positive cells) were evaluated and quantitated by a computerized image analysis system. In normal kidneys, MCP-1 was weakly expressed, both at the gene as well as at the protein level. In diseased kidneys, a statistically significant (P < 0.001) up-regulation of MCP-1 gene and protein expression was found, particularly within the areas of tubulointerstitial damage and the glomeruli. By means of CD68 positive cells, a significant correlation (P < 0.001) was found between glomerular, tubulointerstitial macrophage infiltration and MCP-1 expression. Moreover, by combining immunohistochemistry and in situ hybridization, we observed the presence of CD68 positive cells mainly, if not exclusively, around the cells expressing MCP-1 mRNA. Interestingly, a striking increase in MCP-1 urinary concentration was found in cryoglobulinemic patients. In conclusion, our data suggest that MCP-1 may play a major role in modulating the inflammatory process observed in cryoglobulinemic glomerulonephritis.
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PMID:Monocyte recruitment in cryoglobulinemic membranoproliferative glomerulonephritis: a pathogenetic role for monocyte chemotactic peptide-1. 899 29

A significant proportion of brain tissue specimens from children with AIDS show evidence of vascular inflammation in the form of transmural and/or perivascular mononuclear-cell infiltrates at autopsy. Previous studies have shown that in contrast to inflammatory lesions observed in human immunodeficiency virus type 1 (HIV-1) encephalitis, in which monocytes/macrophages are the prevailing mononuclear cells, these infiltrates consist mostly of lymphocytes. Perivascular mononuclear-cell infiltrates were found in brain tissue specimens collected at autopsy from five of six children with AIDS and consisted of CD3(+) T cells and equal or greater proportions of CD68(+) monocytes/macrophages. Transmural (including endothelial) mononuclear-cell infiltrates were evident in one patient and comprised predominantly CD3(+) T cells and small or, in certain vessels, approximately equal proportions of CD68(+) monocytes/macrophages. There was a clear preponderance of CD3(+) CD8(+) T cells on the endothelial side of transmural infiltrates. In active lesions of transmural vasculitis, CD3(+) T-cell infiltrates exhibited a distinctive zonal distribution. The majority of CD3(+) cells were also CD8(+) and CD45RO+. Scattered perivascular monocytes/macrophages in foci of florid vasculitis were immunoreactive for the p24 core protein. In contrast to the perivascular space, the intervening brain neuropil was dominated by monocytes/macrophages, microglia, and reactive astrocytes, containing only scant CD3(+) CD8(+) cells. Five of six patients showed evidence of calcific vasculopathy, but only two exhibited HIV-1 encephalitis. One patient had multiple subacute cerebral and brainstem infarcts associated with a widespread, fulminant mononuclear-cell vasculitis. A second patient had an old brain infarct associated with fibrointimal thickening of large leptomeningeal vessels. These infiltrating CD3(+) T cells may be responsible for HIV-1-associated CNS vasculitis and vasculopathy and for endothelial-cell injury and the opening of the blood-brain barrier in children with AIDS.
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PMID:Angiocentric CD3(+) T-cell infiltrates in human immunodeficiency virus type 1-associated central nervous system disease in children. 987 73

Inflammation of the arterial wall in giant cell arteritis induces a series of structural changes, including the formation of new vasa vasorum. To study the regulation of neoangiogenesis in giant cell arteritis, temporal arteries were examined for the extent and localization of microvessel generation and for the production of angiogenic factors. In normal arteries, vasa vasorum were restricted to the adventitia, but in inflamed arteries, capillaries emerged in the media and the intima. These capillaries displayed a distinct topography with a circumferential arrangement in the external one-third of the intima. Neovascularization was closely correlated with the formation of lumen-obstructing intima, the fragmentation of the internal elastic lamina, and the presence of multinucleated giant cells. Comparison of tissue cytokine transcription in temporal arteries of giant cell arteritis patients with and without up-regulated neoangiogenesis identified interferon-gamma and vascular endothelial growth factor but not fibroblast growth factor-2 as mediators associated with vasa vasorum proliferation. Giant cells and CD68-positive macrophages at the media-intima junction were found to be the major cellular sources of vascular endothelial growth factor. These data demonstrate that formation of new vasa vasorum in vasculitis is regulated by inflammatory cells and not by arterial wall cells, raising the possibility that it represents a primary disease mechanism and not a secondary hypoxia-induced event. Increased neovascularization in interferon-gamma-rich arteries suggests that the formation of new vasa vasorum is determined by the nature of the immune response in the arterial wall, possibly resulting from the generation and functional activity of multinucleated giant cells.
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PMID:Formation of new vasa vasorum in vasculitis. Production of angiogenic cytokines by multinucleated giant cells. 1048 34

Although there has been extensive research into the mechanisms involved in glomerular crescent formation, it is not yet fully understood how this change may cause renal function impairment. The aim of this study is to identify morphologic changes which may be responsible for this phenomenon. Thirty-eight renal biopsies showing glomerulonephritis with extracapillary proliferation (20 vasculitis-related, 6 idiopathic, 9 due to immune-complex deposition and 3 superimposed on diabetic nephropathy) were considered, and 146 glomeruli in which both crescents and the urinary pole were found at the same time, were studied. The involvement of the urinary pole by cellular crescents was observed in 93.1 and 100% of the glomeruli with segmental or circumferential crescents, respectively. A tridimensional study, for the evaluation of the glomeruli as a whole, was performed on 8 biopsies by means of the step-section technique and disclosed the involvement of the urinary space and a close contact between crescent and tubular cells in all 54 investigated glomeruli. The reported features do not seem to be related to the type of cells which formed the crescent. Indeed, as shown by immunohistochemical study on 10 cases with anti-cytokeratin and anti-CD68 antisera, the crescent localization at the urinary pole had no correlation with the prevalence of epithelial or macrophagic cells. These findings suggest that crescents, due to epithelial proliferation or macrophage clustering, tend to localize at the urinary pole and thus come into close contact with cells of the proximal convoluted tubule: the formation of a sort of plug or a 'glomerular stone' could well explain the block in the urine flow and the consequent impairment of renal function in the acute phase of the disease, even in those cases where crescents are segmental.
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PMID:How glomerular extracapillary proliferation might lead to loss of renal function: light microscopic and immunohistochemical investigation. 1202 22

We describe 3 unusual cases of granuloma annulare with multiple macular lesions in a distribution that simulated mycosis fungoides in patients with no associated underlying diseases. Repeated biopsies showed typical well-formed palisading granulomas and no evidence of an atypical lymphocytic infiltrate. There was no vasculitis, neutrophilic, eosinophilic, or interstitial infiltrate. The patients had no associated underlying diseases. Most of the histiocytes in the palisading granulomas were strongly positive for CD68. The lymphocytes were a minor component of the granulomatous inflammation and were predominantly CD8(+) T-cells. The findings in these cases add to the spectrum of previously defined granulomatous eruptions of the skin.
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PMID:Granuloma annulare with a mycosis fungoides-like distribution and palisaded granulomas of CD68-positive histiocytes. 1524 22

Visceral involvement in systemic lupus erythematosus (SLE) extends beyond renal and cutaneous management. Pleuro-pulmonary lesions have been recognised and diffuse alveolar damage and hemorrhage are the most difficult patterns to control. Pulmonary compromise in clinical evolution of SLE differs from children to adults, both in morphological patterns and in clinical presentation, depending on immunocompetence and the treatment prescribed. A 16-year-old boy presented asthenia, malaise and bilateral cervical painless adenopathies understood as EBV infection as serological EBV IgG, IgM and EBNA were positive. The symptoms persisted for eight months when discrete erythematous and desquamative nasal and malar rash expressed together with persistent fever, dispnoea and bibasilar crackles. Lymph node and pulmonary biopsies were performed. Lymph node presented follicular hyperplasia and LMP1 (EBV) immunostaining was negative. In lung biopsy bronchovascular lesions were consistent with vasculitis and bronchiolitis due to intense macrophage infiltration, validated with CD68 antibody and intra-alveolar macrophages were also present with septal compromise; LMP1 (EBV) positive cells were not visualized. The lung pattern seen in CAT as diffuse micronodules all over the lung parenchyme resolved after corticosteroid therapy. The diagnosis of SLE was confirmed by ANA, anti-dsDNA, anti-nDNA and anti-histones positivity. To the best of our knowledge this is the first reported case of pulmonary SLE involvement with vasculitis and diffuse panbronchiolitis - like pattern as the first clinical sign of the disease.
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PMID:[Vasculitis and diffuse panbronchiolitis-like in systemic lupus erythematosus--case report]. 1749 36

Tsutsugamushi disease is an acute febrile infectious disease caused by Rickettsia tsutsugamushi. An infection is heralded by the presence of an eschar at the site of the inoculating chigger bite and followed by the development of a disseminated erythematous macular rash. CD30 expression is found in anaplastic large cell lymphoma; however, expression in nonneoplastic cutaneous disorders, such as atopic dermatitis, drug reactions, scabies, and various infectious diseases, has also been reported. Study of the cutaneous histopathology of tsutsugamushi disease has been limited. In this study, we performed biopsies of both the eschar and erythematous lesions of 15 cases of tsutsugamushi disease to assess the histopathological changes including the CD3, CD4, CD20, CD30, and CD68 reactivity. Twelve women and 3 men were included with an age range from 21 to 73 years. The most common location of the eschar was the trunk (53.3%). The histological features showed increased leukocytoclastic vasculitis in the eschar (93.3%) compared with the erythematous lesions (33.3%); basal vacuolar changes were more common in the erythematous (100%) than in the eschar lesions (20%). The inflammatory infiltrate had a majority of CD3- and CD68-positive cells. Seven erythematous lesions and 7 eschar lesions showed atypical cells that were CD30-positive cells. Here, we report on the cutaneous histopathology and pattern of inflammatory infiltrates of tsutsugamushi disease. Leukocytoclastic vasculitis and basal vacuolar changes were the characteristic features of the eschar and the erythematous lesions, respectively. In addition, CD30-positive cell infiltration was identified for the first time in this disease.
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PMID:Histopathological features in both the eschar and erythematous lesions of Tsutsugamushi Disease: identification of CD30+ cell infiltration in Tsutsugamushi disease. 1959 Apr 20

Hydroa vacciniforme (HV) is a rare, blistering, childhood photodermatosis that heals with smallpox-like scars, is associated with latent Epstein-Barr virus (EBV) infection, and spontaneously resolves by early adulthood. Cytotoxic T cells are suspected to mediate the histologic hallmark of HV-dense, perivascular, lymphocytic infiltrates and reticular degeneration and necrosis of the epidermis. We report a case of 13-year-old white girl with EBV-associated HV, whose lesional skin harbored a predominate CD68, CD123 infiltrate of plasmacytoid monocytes (PMs). Other significant pathologic attributes included abundant non-neutrophilic nuclear debris, necrosis of adnexal structures, lymphocytic vasculitis, and clusters of CD30 cells. PMs produce large amounts of type I interferon during viral infection, which induces apoptosis of some cell types and promotes the survival of others. This antiviral response can explain these aforementioned pathologic findings representing wide spread cell death and lymphoid proliferation, as well as eventual resolution of HV with time, via elimination of latent EBV-infected cells. The destruction of adnexal structures can account for the depressed circinate scars characteristic of HV. The validity of this proposed mechanism must be evaluated by first examining the prevalence and number of PMs in future case series of HV.
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PMID:Plasmacytoid (CD68+CD123+) monocytes may play a crucial role in the pathogenesis of hydroa vacciniforme: a case report. 1973 83


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