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Query: UMLS:C0027121 (
myositis
)
4,538
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
During the course of a systematic study of T cell lines derived from muscle of patients with various inflammatory myopathies, we identified a new form of polymyositis that is mediated by gamma-delta T cells. In the affected patient's muscle CD3+CD4-
CD8
- gamma-delta T cells surrounded and invaded nonnecrotic muscle fibers in the same way as CD3+CD8+ alpha-beta T cells surround and invade nonnecrotic muscle fibers in inclusion body myositis and other forms of polymyositis. Gamma-delta T cells were extremely rare or absent in muscles and muscle-derived T cell lines in other patients with polymyositis, inclusion-body
myositis
, dermatomyositis or granulomatous myopathy. This new form of polymyositis has provided us with a unique opportunity to study cytotoxic gamma-delta T cells and their muscle-fiber targets in situ. All muscle fibers expressed HLA-class I antigen and the 65-kD heat-shock protein. The autoaggressive behavior of the gamma-delta T cells is consistent with the hypothesis that in some inflammatory myopathies autoinvasive T cells recognize muscle fiber associated antigen(s). Further studies are needed to define the type of gamma-delta T cell receptor used and the antigen(s) recognized by gamma-delta T cells in this rare type of autoimmune muscle disease.
...
PMID:The role of gamma-delta T lymphocytes in inflammatory muscle disease. 153 37
We studied the immunologic correlates of disease activity and differences among subgroups of patients with idiopathic inflammatory myopathy by analysing phenotypic and activation marker expression on peripheral blood mononuclear cells (PBMC). Compared with controls,
myositis
patients with clinically active disease (n = 51) had significantly lower proportions of CD8+ cells and higher proportions of PBMC that expressed DR, CD3- DR, CD14- DR, interleukin-2 receptors, and the late T cell activation markers CD26 and TLiSA1. TLiSA1 expression, a marker for cytotoxic differentiation, correlated significantly with both clinical activity indices and serum levels of muscle-associated enzymes. In serial studies of seven patients, the proportion of PBMC expressing MHC class II antigen and late T cell activation markers decreased as
myositis
disease activity decreased, independent of type of therapy. Among the clinical subgroups, polymyositis (n = 21) and inclusion body myositis (n = 11) were virtually indistinguishable; dermatomyositis patients (n = 19) showed decreased proportions of CD3+DR+ and TLiSA1+ cells, and increased proportions of CD20+ and CD20+DR+ cells compared with the other two groups. Patients with autoantibodies to histidyl-tRNA synthetase (Jo-1 antigen, n = 11) had significantly lower proportions of CD3+ and CD4+ cells, lower CD4/
CD8
ratios, and higher proportions of CD+ cells expressing CD20, compared with patients without anti-Jo-1 antibodies. These findings support the concept that activated lymphocytes, especially cells undergoing anamnestic responses and cytotoxic differentiation, are important in the pathogenesis of idiopathic
myositis
. Moreover, taken together with other studies, these data suggest that groups of patients segregated by clinical or autoantibody status have different mechanisms of systemic immune activation and immunopathology.
...
PMID:Lymphocyte activation markers in idiopathic myositis: changes with disease activity and differences among clinical and autoantibody subgroups. 216 21
To investigate the pathological mechanisms of polymyositis, we performed immunohistochemical analyses with biopsied muscles. Comparative studies using specimens obtained from the same patient enabled us to analyze the pathological alterations at different sequential clinical phases without taking into account each immunogenetic difference. Expression of MHC (major histocompatibility complex) antigens, especially ectopic MHC-class-II antigens, in muscle fibers and infiltrating T-cells were shown to increase concomitantly with the clinically observed exacerbation. Moreover, other observations seem to support the possibilities that 1) administration of steroids lowers the number of invading
CD8
-positive cells, 2) induction of MHC-class-I antigens in muscle fibers precedes the inflammatory cell infiltration and that 3) remaining MHC-class-I antigens in muscle fibers may explain the recurrence of
myositis
often observed in the follow up period.
...
PMID:Temporal alterations of immunohistochemical findings in polymyositis. 794 28
We describe the case of a patient with peripheral gamma/delta T-cell lymphoma (T-ML) with hepatosplenomegaly, generalized lymphadenopathy, and bone marrow involvement. A 44-year-old man had lymphoma, which became clinically apparent 2 months after the onset of
myositis
and insulin-dependent diabetes mellitus. A cervical lymph node biopsy specimen showed diffuse infiltration by large neoplastic cells with vascular proliferation. The neoplastic cells expressed the T-cell receptor (TCR)delta chain detected by TCR delta 1 and delta-TCS1, CD3, CD30, CD45RO, and epithelial membrane antigen, but not the TCR beta chain detected by beta F1, CD1a, CD2, CD4, CD5, CD7,
CD8
, CD25, HLA-DR, and terminal deoxynucleotidyl transferase. The cells had a clonal rearrangement of TCR gamma chain gene and a germ-line configuration of immunoglobulin heavy chain gene and TCR beta chain gene. Despite chemotherapy, the patient died of refractory lymphoma 4 months after diagnosis. Examination at autopsy revealed that the main hepatic and splenic neoplastic infiltration sites were the portal area and white pulp, respectively. Our patient differed from those with gamma/delta T-ML with hepatosplenic involvement reported previously with respect to the hepatic and splenic neoplastic infiltration patterns and the presence of lymphadenopathy.
...
PMID:Gamma/delta T-cell lymphoma with hepatosplenomegaly: report of a case. 836 90
A patient initially presented with sarcoidosis in combination with
myositis
of sarcoid origin and Raynaud's phenomenon. During the course of his disease, he additionally developed scleroderma. Bronchoalveolar lavage, performed because of increase of interstitial markings in the presence of enlarged hilar nodes, showed an increased percentage of granulocytes and a low CD4 to
CD8
ratio of lymphocytes, suggesting a change to scleroderma lung disease.
...
PMID:Interstitial lung disease and myositis in a patient with simultaneously occurring sarcoidosis and scleroderma. 840 19
We present an additional case of focal
myositis
which, after surgical excision of the muscular mass, did not evolve to generalized polymyositis. To our knowledge immunological evaluations of this disease have never before been carried out. Immunohistochemical analysis of the muscular mass showed the presence of activated endothelial cells, CD4 and macrophage cells in the perivascular and endomysial areas, suggesting an immune-mediated mechanism of muscular damage. At the same time the normal distribution of the peripheral blood lymphocyte subpopulations and the normal levels of serum IL-1 beta, IL-6, TNF-alpha, soluble IL-2R and soluble
CD8
underline the non-systemic nature of the disease.
...
PMID:Immunohistochemical analysis of an additional case of focal myositis. 883 51
To characterize the non-caseating granuloma formation in granulomatous
myositis
, we analyzed infiltrating mononuclear cells in 7 patients including 2 sarcoid patients, using monoclonal antibodies with a modified immunoperoxidase method. All granulomas consisting of epithelioid, infiltrating mononuclear cells and multinucleated giant cells had markedly increased numbers of CD45Ro-positive cells. The infiltrating inflammatory cells were mostly T lymphocytes and macrophages. The majority of T lymphocytes behaved as T helper/inducer subtype, expressing CD4 positivity. Although the ratio of CD4- to
CD8
-positive cells in the granuloma in muscle biopsies was not significantly different from that in other organs seen in systemic sarcoidosis, T helper/inducer and T suppressor/cytotoxic cells showed some characteristic distributions: CD4-positive cells accumulated in the center of, and
CD8
-positive cells at the periphery of, the granuloma. The distribution of infiltrating cells did not differ between muscle biopsies from patients with and without systemic sarcoidosis, suggesting that both groups share the same pathogenetic mechanism in granuloma formation.
...
PMID:Granulomatous myositis: pathologic re-evaluation by immunohistochemical analysis of infiltrating mononuclear cells. 907 27
In 14 patients with polymyositis (PM), 5 patients (2 males and 3 females) were positive for anti-hepatitis C virus (HCV) antibody measured by a second generation assay. We analysed the clinical characteristics and histopathological findings of the biopsied muscles from those 5 patients. They aged from 42 to 65 years averaging 53.6 years. Two asymptomatic patients visited our hospital due to elevated muscle enzyme levels, who had slight weakness in their orbicularis oculi and neck muscles on physical examination. The other 3 patients had moderate weakness of the proximal muscles. Anti-nuclear antibody was positive in 2 of the 5 patients and anti-Jo 1 antibody was negative in all patients. The serum enzymes elevated were creatine kinase (215-2, 207 (IU/l)) and glutamate oxaloacetate transaminase (40-119 (KU)). HCV-RNA was positive in the sera of 4 patients examined. All muscle biopsy specimens revealed variation in fiber size with inflammatory cellular infiltration and observed degenerating and regenerating fibers. The scant infiltration type was observed in 2 asymptomatic patients in whom the infiltrated cells were CD4 positive. The endomysial infiltration type was observed in 3 symptomatic patients;
CD8
positive cells were found focally to diffusely in 2 patients examined. The expression of class 1 molecules from the major histocompatibility complex was detected mainly in infiltrated fibers to variable degrees. All of the patients showed a good response to the initial steroid therapy. The present study suggests that autoimmune reaction related to HCV infection causes
myositis
, therefore anti-HCV antibody should be checked in cases of PM.
...
PMID:[Clinical characteristics and muscle histopathology in polymyositis positive anti-hepatitis with C virus antibody]. 921 18
Painful peripheral neuropathies involve both axonal damage and an inflammation of the nerve. The role of the latter by itself was investigated by producing an experimental neuritis in the rat. The sciatic nerves were exposed at mid-thigh level and wrapped loosely in hemostatic oxidized cellulose (Oxycel) that on one side was saturated with an inflammatory stimulus, carrageenan (CARRA) or complete Freund's adjuvant (CFA), and on the other side saturated with saline. In other rats, a
myositis
was created by implanting Oxycel saturated with CFA into a pocket made in the biceps femoris at a position adjacent to where the nerve was treated. Pain-evoked responses from the plantar hind paws were tested before treatment and daily thereafter. Statistically significant heat- and mechano-hyperalgesia, and mechano- and cold-allodynia were present on the side of the inflamed nerve (CARRA or CFA) for 1-5 days after which responses returned to normal. There were no abnormal pain responses on the side of the saline-treated nerve, and none in the rats with the experimental
myositis
. The abnormal pain responses were inhibited by N-methyl-D-aspartate receptor blockade with MK-801, but were relatively resistant to the dose of morphine tested (10 mg/kg). Light microscopic examination of CARRA-treated nerves, harvested at the time of peak symptom severity, revealed that the treated region was mildly edematous and that there was an obvious endoneurial infiltration of immune cells (granulocytes and lymphocytes). There was either a complete absence of degeneration, or the degeneration of no more than a few tens of axons. Immunocytochemical staining for CD4 and
CD8
T-lymphocyte markers revealed that both cell types were present in the epineurial and endoneurial compartments. The endoneurial T-cells appeared to derive from the endoneurial vasculature, rather than from migration across the nerve sheath. We conclude that a focal inflammation of the sciatic nerve produces neuropathic pain sensations in a distant region (the ipsilateral hind paw) and that this is not due to axonal damage. The neuropathic pain is specific to inflammation of the nerve because it was absent in animals with the experimental
myositis
and in those receiving sham-treatment. These results suggest that an acute episode of neuritis-evoked neuropathic pain may contribute to the genesis of chronically painful peripheral neuropathies, and that a chronic (or chronically recurrent) focal neuritis might produce neuropathic pain in the absence of significant (or clinically detectable) structural damage to the nerve. The model that we describe is likely to be useful in the study of the neuroimmune factors that contribute to painful peripheral neuropathies.
...
PMID:Neuropathic pain from an experimental neuritis of the rat sciatic nerve. 1053 88
Recently, it has been shown that inflammatory T-cells in human idiopathic
myositis
only very rarely undergo spontaneous apoptosis. The animal model of experimental autoimmune
myositis
(EAM) in the Lewis rat was chosen to investigate whether similar findings hold true in rat muscle and if glucocorticosteroids act by induction of T-cell apoptosis in inflammatory lesions. The rate of spontaneous T-cell apoptosis in rat EAM was low, even in muscle specimens with extensive inflammation. After intravenous glucocorticosteroid pulse therapy we found a dramatic increase in the rate of apoptotic T-cells in the inflamed muscles. Up to 50% of these apoptotic T-cells were
CD8
positive apoptotic T-cells. T-cell apoptosis was significantly lower in similarly inflamed muscle specimens of the control group. We suggest that glucocorticosteroids induce apoptosis of endomysial T-cells in human idiopathic polymyositis. Glucocorticosteroid-induced apoptosis may be a candidate mechanism in the termination of inflammatory activity.
...
PMID:Experimental autoimmune myositis in the lewis rat: lack of spontaneous T-cell apoptosis and therapeutic response to glucocorticosteroid application. 1080 54
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