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ID PMID Title PublicationDate abstract
2463839 Immunohistologic analysis of the distribution of cell adhesion molecules within the inflam 1989 Jan Antigen-independent binding of T lymphocytes to a variety of cell types has been shown to be mediated by receptor-ligand pairs of adhesion molecules. In forms of inflammatory synovitis (including rheumatoid arthritis), T cells home to synovium, become activated, and participate in the generation of chronic synovitis. Using indirect immunofluorescence assays on synovial frozen tissue sections and on synovial fibroblast cell lines, we studied the distribution of cell adhesion molecules on components of the synovial microenvironment in inflammatory synovitis. We reasoned that analysis of the cell types within synovium that express adhesion molecules might provide clues to lymphocyte-stromal interactions that occur in inflammatory synovitis. We found that antibodies against the lymphocyte function-associated antigen 3 (LFA-3) molecule and the intercellular adhesion molecule 1 (ICAM-1) both reacted with macrophage-like type A synovial cells and synovial fibroblasts, as well as with tissue macrophages and vessel endothelium. Using flow cytometry, we found that anti-LFA-3 and anti-ICAM-1 (but not antibodies against their ligands CD2 and LFA-1) reacted with synovial fibroblast cells cultured in vitro. Thus, these data demonstrate that the ligands for lymphocyte LFA-1 molecules (ICAM-1) and for T cell CD2 molecules (LFA-3) are widely distributed among cell types of the synovial microenvironment and provide numerous cell types with which lymphocytes can interact via these 2 adhesion pathways during the course of inflammatory synovitis.
1725956 Immunological characterization of a low molecular mass polypeptidic antigen of Borrelia bu 1991 Nov The presence of a low molecular mass polypeptidic antigen in Borrelia burgdorferi was described. The protein was exposed at the bacterial surface since it was clearly identified by mAb 3H4 using the immunofluorescence test performed with living bacteria. This antigen was cleaved by proteinase K treatment, whereas it was resistant to the action of chymotrypsin, trypsin and thermolysin. Western blotting analysis of the immunological reactivity of this antigenic structure performed using monoclonal antibody, mouse-immune ascitic fluids raised against B. burgdorferi and other spirochetes, sera from patients with Lyme disease and other infirmities in which false positive results in serological tests for B. burgdorferi have been described, demonstrated that this protein expresses only species-specific epitopes which may be recognized during human B. burgdorferi infections.
2004821 Association between the 65-kilodalton heat shock protein, Streptococcus sanguis, and the c 1991 Apr The etiology of Behcet's syndrome (BS) is unknown, but a number of streptococcal species have been implicated. A hypothesis was postulated that a shared antigen, such as a stress protein, might account for some of these findings. Indeed, a rabbit antiserum against a 65-kDa heat shock protein of Mycobacterium tuberculosis revealed a corresponding 65-kDa band with all six Streptococcus sanguis strains examined and S. pyogenes but not with S. salivarius. By applying a panel of nine monoclonal antibodies to the mycobacterial 65-kDa heat shock protein, an approximately 65-kDa antigen was identified in the uncommon serotypes of S. sanguis ST3 and H.83 and one with a different Mr was identified in KTH-1 and S. pyogenes. Monoclonal antibodies Y1.2, C1.1, II H9, and ML30, which reacted with these streptococci, recognize residues 11 to 27, 88 to 123, 107 to 122, and 276 to 297 of the 65-kDa heat shock protein, respectively, suggesting that these residues are conserved among some uncommon serotypes of S. sanguis and S. pyogenes. Immunoblot analyses of sera from patients with BS for immunoglobulin A (IgA) and IgG antibodies revealed bands of 65 to 70 kDa with the mycobacterial heat shock protein, S. sanguis strains, and S. pyogenes, although these reactivities were also found to a lesser extent in controls. A 65- to 70-kDa band was found more frequently with S. sanguis KTH-2 or KTH-3 and IgA in serum from patients with BS than with serum from controls (P less than 0.02). Antibodies in serum were then studied by a radioimmunoassay, and in patients with BS this revealed significantly raised IgA antibodies to the recombinant 65-kDa mycobacterial heat shock protein and to soluble protein extracts of S. sanguis ST3, KTH-1, KTH-2, and KTH-3. Whereas significant anti-65-kDa heat shock protein and anti-S. sanguis ST3 antibodies were also found in sera from patients with rheumatoid arthritis and recurrent oral ulcers, the anti-S. sanguis KTH-1, KTH-2, and KTH-3 antibodies were confined to BS. The results are consistent with the hypothesis that some of the streptococcal antigens are associated with heat shock or stress proteins, which will need to be formally established by isolating heat shock proteins from streptococci.
2789652 Lacrimal and salivary immunoglobulins in Sjögren's syndrome. 1989 Aug The diagnosis of Sjögren's syndrome is sometimes difficult. We have previously demonstrated the diagnostic value of salivary immunoglobulins IgG and IgM in Sjögren's syndrome. In the present study, we assessed both lacrimal immunoglobulins (1 Ig) and salivary Ig (s Ig) in Sjögren's syndrome. We studied 112 patients: 71 had rheumatoid arthritis (57 sero positive), 19 had connective tissue diseases or vasculitis (six Sjögren's syndrome alone, six systemic sclerosis, three mixed connective tissue diseases, three polyarteritis, one relapsing polychondritis), and 22 patients had other inflammatory, metabolic or degenerative joint diseases. Lacrimal Ig and salivary Ig were assessed by double immunodiffusion with antisera specific for IgG, IgM and IgA. Each Ig class was scored on a scale ranging from 0 to 3 plus without knowledge of the patient's diagnosis. The results of factorial analysis demonstrated a strong relationship between xerophtalmia, positive Schirmer's test, s IgG, s IgM, 1 IgG, and 1 IgM in patients with seropositive rheumatoid arthritis or other connective tissue diseases. Analysis of individual parameters showed a significant relationship between 1 IgG and ocular complaints (P less than 0.01), positive Schirmer's test (P less than 0.05), positive rose bengal dye test (P less than 0.05), 1 IgM (P less than 0.01), s IgG (P less than 0.01) and s IgM (P less than 0.05). A significant relationship was also found between s IgG and ocular complaints (P less than 0.02), positive rose bengal dye test (P less than 0.01), positive minor salivary gland biopsy (P less than 0.05), s IgM (P less than 0.01), and 1 IgM (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
3262029 Keratoconjunctivitis sicca in rheumatoid arthritis. 1988 Jun The prevalence of keratoconjunctivitis sicca (KCS) was studied in a randomly selected group of 104 patients with rheumatoid arthritis (RA). Symptoms of KCS were noted in 33 patients (31.7%) and they were studied further. After rose bengal staining, 22 of these patients were found to have KCS which was diagnosed by the presence of corneal or conjunctival desiccation. The overall prevalence of KCS was 21.2%. Although an abnormal Schirmer's test was noted in 21 of the 22 patients with KCS, only 8 patients had values of 5 mm or less while the remainder had a mild abnormality ranging from 6 to 15 mm. A reduced marginal tear film was noted in 15 patients (68.2%) with KCS and 13 patients (59%) had a reduced tear break-up time. The Schirmer's test alone is inadequate to make a definite diagnosis of KCS and it is essential to perform slit lamp examination to detect epithelial staining with rose bengal.
2754790 Functional status and well-being of patients with chronic conditions. Results from the Med 1989 Aug 18 Enhancing daily functioning and well-being is an increasingly advocated goal in the treatment of patients with chronic conditions. We evaluated the functioning and well-being of 9385 adults at the time of office visits to 362 physicians in three US cities, using brief surveys completed by both patients and physicians. For eight of nine common chronic medical conditions, patients with the condition showed markedly worse physical, role, and social functioning; mental health; health perceptions; and/or bodily pain compared with patients with no chronic conditions. Each condition had a unique profile among the various health components. Hypertension had the least overall impact; heart disease and patient-reported gastrointestinal disorders had the greatest impact. Patients with multiple conditions showed greater decrements in functioning and well-being than those with only one condition. Substantial variations in functioning and well-being within each chronic condition group remain to be explained.
3500229 T lymphocyte control of human eosinophilic granulopoiesis. Clonal analysis in an idiopathi 1987 Dec 1 The idiopathic hypereosinophilic syndrome (HES) comprises a heterogeneous group of disorders with unknown pathogenesis characterized by persistent peripheral blood and bone marrow eosinophilia and eosinophilic infiltrates of multiple organs leading to severe organ dysfunction. In the present study, T lymphocyte clones were randomly established from the blood of a patient with HES and propagated in culture with mitogen and interleukin 2. Whereas 28 of 29 clones were able to stimulate myeloid colony formation when co-cultured with normal bone marrow cells in a double-layer micro-agar culture system, one third of these clones preferentially stimulated pure eosinophil colonies (up to 98% of all colonies). This pattern differed markedly (p less than 0.001) from the pattern of release of hemopoietic factors by 126 T cell clones established from four other individuals. Eosinophil colony stimulation was due to the release of a lineage-specific eosinophilic colony-stimulating factor (Eo-CSF) by these clones after appropriate stimulation. Production of Eo-CSF in vitro was inhibited by hydrocortisone or cyclosporin A. All Eo-CSF-producing clones had the T4+8-phenotype and were capable of producing in addition interleukin 2 and interferon-gamma. Southern blot analysis of the T cell receptor beta-chain rearrangement of the Eo-CSF-producing clones showed a different rearrangement pattern for each clone. These studies suggest a reactive T cell-mediated eosinophilia as the pathogenetic mechanism in this case of HES and, for the first time, point to a biologic relevance of a lymphokine-induced stimulation of hemopoiesis.
2805611 Prediction and evaluation of the effect of iron treatment in anaemic RA patients. 1989 Sep In order to predict a haemoglobin (Hb) rise, in response to treatment with iron from simple erythrocyte and serological parameters, we treated 28 anaemic RA patients with oral iron during 6 weeks. Iron deficiency, present in 57% of patients, was assessed by staining a bone marrow aspirate for iron. Response rate in this group was 81% and median Hb increase was 0.8 mmol/l. After 6 weeks 69% of iron deficient patients were still anaemic. Patients without iron deficiency, considered as having anaemia of chronic disease (ACD), showed no significant Hb rise. The finding of a hypochromic microcytic anaemia was associated with a significant Hb rise. MCV showed highest specificity and predictive value (90 and 88%) and ferritin was the most valid predictor of a Hb rise within 6 weeks. Combination of low MCV and low ferritin resulted in a 100% specificity and predictive value indicating that patients with values below cut off point of these variables will definitely respond to treatment. Disease activity tended to decrease after 6 weeks, but this was not correlated with a Hb rise. It was concluded that a Hb rise can be predicted accurately by blood parameters. Using certain combinations, bone marrow aspiration is rarely necessary. Iron treatment is only useful in iron deficient RA patients, although active RA limits maximal Hb rise. In contrast to earlier findings, iron treatment had no deleterious effects on disease activity.
3303297 Treatment of peptic ulcer induced by non-steroidal anti-inflammatory drugs. 1987 Aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) are often associated with peptic ulcer. A consecutive series of patients with rheumatic disease treated with NSAIDs entered a clinical trial after endoscopic diagnosis of gastric or duodenal ulcer. Three objectives were pursued: comparison between the healing capacities of sucralfate and ranitidine; evaluation of the influence of continuous NSAID administration during ulcer treatment; and determination of the peptic ulcer recurrence rate during a one-year follow-up. Average healing times were identical for 25 patients given sucralfate (4.6 weeks) and 27 patients given ranitidine (4.9 weeks). Ten patients with persistent ulcers after nine weeks of treatment received ulcer therapy for a further 3-9 weeks and healing was obtained in seven cases. Thirty patients continued on NSAID, and the ulcers healed in 23, whereas NSAID was withdrawn in 32 patients, of whom ulcer healing was documented in 29 (p greater than 0.10). 14 symptomatic recurrences were observed during the follow-up period. Adverse reactions were non-significant, and there were no cases of severe gastrointestinal bleeding.
2150567 Endoscopic evaluation of etodolac and naproxen, and their relative effects on gastric and 1990 Etodolac has been shown to have a favorable safety profile in short-term and long-term studies in both osteoarthritis (OA) and rheumatoid arthritis (RA). Two studies were conducted to further assess the gastrointestinal (GI) safety profile of this drug. These studies were designed to compare the therapeutic efficacy and upper GI effects of etodolac (600 mg/day) and naproxen (1000 mg/day) administered over 4 weeks in patients with active rheumatoid arthritis. In addition, the relative effects of the drugs on prostaglandin levels in the stomach and duodenum were assayed in one study. Fifteen patients were included in each study and received either 300 mg b.i.d. of etodolac or 500 mg b.i.d. of naproxen. In both studies, endoscopic examinations were performed on day 1 of the study and again 4 weeks later. In the second study, at the time of each endoscopy, samples of gastric and duodenal mucosa were taken for histologic study and prostaglandin assay. Endoscopy results from the first study showed significant differences in favor of etodolac between the two treatment groups. In the second study more naproxen-treated patients had abnormal endoscopy results than did etodolac-treated patients. Results from prostaglandin assays in gastric and duodenal mucosa showed no overall suppression of gastric or duodenal prostaglandin levels for etodolac-treated patients in contrast to naproxen-treated patients, who showed suppression of PGE2 and PGI2. The results of these studies show that etodolac therapy caused less gastric and duodenal injury than naproxen and also support the theory that the GI safety of etodolac may be due to selective sparing of cytoprotective prostaglandins.
2329322 Determination of cathepsins B and H in sera and synovial fluids of patients with different 1990 Mar Synovial fluids and sera of patients with inflammatory and metabolic joint diseases contain different cysteine proteinases. The quantities of cathepsins B and H were determined by newly developed specific enzyme-linked immunoassay tests (ELISA), with detection limits of 0.5 microgram/l for cathepsin B and 3 micrograms/l for cathepsin H. The values of cathepsin B in normal sera ranged from 0.6 microgram/l to 2 micrograms/l, whereas in sera of patients with joint diseases they ranged from 1.7 micrograms/l to 18 micrograms/l. Cathepsin H was not found in sera (values below 3 micrograms/l), but was measurable in patients' synovial fluids. Patients with rheumatoid arthritis have on average the highest values of cathepsin B in synovial fluids, whereas patients with undifferentiated arthritis have the highest values of cathepsin H. The results show that cathepsins B and H are present in arthritic synovial fluids, where they may be implicated in destructive processes. There is yet no clear correlation between the quantity of each cathepsin released in synovia and the clinical diagnosis or the stage of the disease.
1661164 The secretion of the tissue inhibitor of metalloproteinases (TIMP) by human synovial fibro 1991 Dec 3 The matrix metalloproteinases are a family of enzymes involved in the turnover of the connective tissues. The regulation of these enzymes is complex, involving the control of synthesis, the activation of proenzyme forms and the presence of specific inhibitors. Retinoids have been reported to inhibit the production of metalloproteinases by human and rabbit synovial fibroblasts and by human skin fibroblasts. The production of the highly specific tissue inhibitor of metalloproteinases (TIMP) by connective tissue cells may be crucial in the regulation of connective tissue breakdown and this present study was undertaken to determine if retinoic acid (RA) could modulate TIMP and collagenase production by synovial fibroblasts. The results show that RA at concentrations from 10(-7) to 10(-5) M significantly stimulated the secretion of TIMP by two of three human synovial cell lines. The effect of mononuclear cell factor (MCF) on TIMP and collagenase levels was also investigated. The apparent reduction of collagenase levels in the presence of RA, could result from a failure to accurately measure this enzyme in the presence of increased levels of TIMP.
2891468 Possible mode of action of 5-aminosalicylic acid. 1987 Dec Despite the extensive use of sulfasalazine (SAS) and/or 5-aminosalicylic acid (5-ASA) in patients with inflammatory bowel disease and, more recently, rheumatoid arthritis, their mode of action has not been elucidated so far. None of the numerous pharmacological and biochemical effects described, including immunosuppressive, antifolate, and modulatory actions on lymphocyte and leukocyte functions, could be defined unequivocally as mediating their beneficial activity. Recently, interest has focused on actions of SAS and 5-ASA on the various enzymes of the arachidonic acid cascade. Mucosa of patients with inflammatory bowel disease generates excessive amounts of cyclooxygenase products such as prostaglandins (PG) as well as 5-lipoxygenase products such as leukotriene (LT) B4 and sulfidopeptide-LT. Both PG and LT exert proinflammatory actions and are potentially important mediators of mucosal inflammation. SAS and 5-ASA, however, have been found to inhibit PG synthesis under certain experimental conditions only, while increasing PG formation under other conditions. While SAS was found to inhibit colonic LTB4 synthesis, 5-ASA was reported to selectively affect the cyclooxygenase pathway of arachidonate metabolism in this tissue. Our results demonstrate that, like the parent compound, the metabolite 5-ASA in a dose-dependent manner inhibits release of LTB4 and sulfidopeptide-LT from normal human colonic mucosa (IC50 3.5 and 3.7 mmol/liter, respectively). Indomethacin, which has no efficacy in the treatment of patients with inflammatory bowel disease, on the other hand, selectively inhibited PGE2 formation in normal and inflamed colonic mucosa (IC50 1.7 and 1.0 mmol/liter, respectively) without reducing synthesis of LTB4 or sulfidopeptide-LT.(ABSTRACT TRUNCATED AT 250 WORDS)
2198156 Multicentre double-blind study of the efficacy, safety and tolerance of pirazolac compared 1990 Of the 160 patients (80 pirazolac/80 sulindac) who entered the study through 14 investigators, three-quarters completed a 12-weeks therapy and three-fifths completed the entire 24-weeks therapy. In the pirazolac group 15% of the patients and in the sulindac group 11% dropped out from the study due to adverse clinical experience. The drop-out rates due to unsatisfactory therapeutic response were respectively 15% and 16% in the pirazolac and the sulindac groups. Both treatment groups showed significant improvement from baseline for all parameters except for the erythrocyte sedimentation rate at weeks 4, 8, 12 and 16 for the sulindac group and weeks 4 and 8 for the pirazolac group. The two treatment groups were comparable as to effectiveness; however, the improvement rates in 36 out of 41 efficacy measurements based on the definition of clinically relevant changes in relation to baseline were estimated to be superior for the group under pirazolac therapy. The rate of improvement for the American Rheumatism Association functional class at the end of the study was 23% in the pirazolac group and 9% in the sulindac group (p less than 0.05). Of the patients in the pirazolac and sulindac groups, 45% and 44% respectively reported no adverse effects at all throughout the whole 24-weeks study. The rates of patients reporting at least one adverse reaction in a body system were not different between the two groups. An exception was the body as a whole where ten patients (12.5%) in the sulindac group and only two (2.5%) in the pirazolac group reported adverse reactions (p = 0.03). No differences occurred between the two treatment groups with regards to intensity, causality or the number of occurrences of adverse clinical experiences. One death in the sulindac treatment group was reported during the study. In both treatment groups, alterations in laboratory tests were minor or negligible or associated with abnormal pre-treatment values and, generally speaking, without any clinical relevance. There were some patients, who had increases from baseline in alkaline phosphate in both treatment groups. However, these were usually transient, occasionally complemented by a slight increase of serum glutamic oxaloacetic acid transaminase.
2612116 Anticardiolipin antibodies in patients with autoimmune diseases: isotype distribution and 1989 Dec A prospective study of IgG and IgM isotypes of anticardiolipin antibodies (aCL) was performed in a series of 167 patients with various autoimmune diseases, including rheumatic and nonrheumatic disorders, and in a group of 100 healthy blood donors. The IgG aCL serum was regarded as positive if a binding index (BI) greater than 2.85 (3.77 SD) was detected and a BI greater than 4.07 (3.90 SD) was defined as positive for IgM aCL. Forty patients (24%) were found to be positive for IgG and/or IgM aCL. IgG aCL were detected in 23% of patients with systemic lupus erythematosus (SLE), in 9% with idiopathic thrombocytopenic purpura, in 7% with progressive systemic sclerosis, and in 6% with dermatomyositis-polymyositis. IgM aCL were present in 43% patients with primary biliary cirrhosis, in 33% with rheumatoid arthritis, in 22% with SLE, and in 8% with giant-cell arteritis. IgG aCL were found to have a significant association with thrombosis and thrombocytopenia, and IgM and aCL with haemolytic anaemia and neutropenia, in SLE but not in the other autoimmune diseases. The identification of these differences in the aCL isotype associations, depending on the autoimmune disorder, may improve the clinical usefulness of these tests.
2319518 Atlantoaxial subluxation in systemic lupus erythematosus: further evidence of tendinous al 1990 Feb We prospectively determined the frequency of atlantoaxial subluxation in a group of patients with systemic lupus erythematosus (SLE) and analyzed its relationship with tendinous laxity, Jaccoud's syndrome and other features of the disease. Five of 59 patients (8.5%) had atlantoaxial subluxation. No patient presented atlantoaxial subluxation in neutral lateral cervical radiographs but all 5 had anterior atlantoaxial subluxation in full flexion films; one patient also had lateral subluxation. The 5 patients with atlantoaxial subluxation were compared with the remaining 54. Mean SLE disease duration was longer in patients with atlantoaxial subluxation (12 years) than in those without (6.6 years) (p less than 0.01). Jaccoud's syndrome, patellar tendon elongation and articular hypermobility were significantly more frequent in patients with atlantoaxial subluxation. The presence or history of arthritis failed to distinguish patients with and without atlantoaxial subluxation, while chronic renal failure and increased serum parathyroid hormone levels were significantly associated to the presence of atlantoaxial subluxation. We suggest that atlantoaxial subluxation is further evidence of tendinous alterations seen in patients with SLE.
2939116 The effect of etodolac administration on renal function in patients with arthritis. 1986 Apr The effect of etodolac 50-600 mg/d on renal function was assessed in four- to 52-week trials in 1,382 patients with arthritides. No patient was withdrawn from treatment due to an abnormal renal function test related to etodolac administration. There were no significant differences in the incidence of definite renal function abnormalities between patients receiving etodolac and those receiving placebo. Both etodolac and placebo groups had a significantly lower incidence of deviant BUN results than either aspirin- or sulindac-treated patients. Fewer than 2% of patients receiving etodolac showed either a persistent or variably persistent pattern of deviant renal function tests. The results in these studies indicate that chronic etodolac therapy did not adversely affect renal function in patients with arthritis.
3259883 B cells expressing CD5 are increased in Sjögren's syndrome. 1988 May In this investigation of B cells expressing the CD5 (Leu-1) cell surface marker, we found increased numbers of these cells in 13 of 19 patients with primary Sjögren's syndrome (SS) (68%), as well as in the rheumatoid arthritis patients. The percentage of B cells that demonstrated increased expression of CD5 was 46% in SS patients, 47% in rheumatoid arthritis patients, 24% in systemic lupus erythematosus patients, and 26% in normal subjects. Over a 2-year period, CD5 expression on B cells was a stable finding in several patients, except for 2 who required either steroid therapy or combined chemotherapy and irradiation for malignant lymphoma. Both of these patients had clinical remissions and their levels of CD5+ B cells returned to normal. The first patient had a clinical picture of SS/systemic lupus erythematosus overlap, associated with polyclonal B cell activation and decreased production of interleukin-2 in response to stimulation with phytohemagglutinin. These cellular immune abnormalities returned to normal after the institution of corticosteroids. Our observations suggest a relationship between the CD5+ B cell abnormality and disease activity. The results are discussed in relation to immunoregulatory properties of CD5+ B cells in autoimmune mice and the characteristic predisposition to malignant lymphoma among SS patients.
1899362 T cell activation by mycobacterial antigens in inflammatory synovitis. 1991 Mar To define which mycobacterial antigens were responsible for the activation of synovial fluid T lymphocytes, acetone-precipitated Mycobacterium tuberculosis (AP-MT) antigens were separated into five fractions following polyacrylamide gel electrophoresis and added to the mononuclear cell cultures of patients with inflammatory synovitis. Fractions 2 (50 to 70 kDa) and 5 (less than 28 kDa) resulted in significantly more proliferation than that of fractions 1, 3, and 4. The response to a purified mycobacterial 65-kDa heat shock protein (hsp), which migrated in fraction 2, was highly correlated (r = 0.89, P less than 0.001) with the response to the crude AP-MT. The proliferative response to a different hsp. the Escherichia coli DnaK, by synovial fluid lymphocytes was marginal. Analysis of the synovial fluid T cell response to mycobacterial culture filtrates by T cell Western blotting revealed dominant responses to antigen(s) in the range of 31 to 21 kDa in each responding patient, although no other consistent pattern of T cell activation was noted. Three lines of evidence suggested that the response to the low molecular weight fractions was directed against degradation fragments of the 65-kDa protein. These observations suggest that the activation of T lymphocytes obtained from inflammatory synovial fluids by crude mycobacterial antigens was due in large part to recognition of the 65-kDa mycobacterial hsp.
2820319 Evidence for both histamine H1 and H2 receptors on human articular chondrocytes. 1987 Jun Using specific histamine H1 and H2 receptor antagonists, evidence is presented for the existence of both H1 and H2 receptors on human articular chondrocytes in vitro. Stimulation of the H1 receptor by histamine (range 0.18 to 17.8 mumol/l) significantly increased prostaglandin E (PGE) production, while activation of the histamine H2 receptor increased intracellular cyclic adenosine-5'-monophosphate (AMP). The histamine H1 antagonists mepyramine and tripelennamine blocked the histamine induced increase in PGE production, and the H2 antagonists cimetidine and ranitidine prevented the increase in intracellular cyclic AMP. These observations suggest that mast cell-chondrocyte interactions mediated via histamine may contribute to some of the pathophysiological changes observed in joint disease.