Monoclonal antibody identification of mononuclear cells in endomyocardial biopsy specimens from a patient with rheumatic carditis

1985 ◽  
Vol 16 (4) ◽  
pp. 332-338 ◽  
Author(s):  
Charles C. Marboe ◽  
Daniel M. Knowles ◽  
Melvin B. Weiss ◽  
John J. Fenoglio
Keyword(s):  
Monoclonal Antibody ◽  
Endomyocardial Biopsy ◽  
Mononuclear Cells ◽  
Rheumatic Carditis ◽  
Biopsy Specimens

scholarly journals Differential Normalization of Mucosal Interleukin-8 and Interleukin-6 Activity after Helicobacter pyloriEradication

1998 ◽  
Vol 66 (10) ◽  
pp. 4742-4747 ◽  
Author(s):  
Takafumi Ando ◽  
Kazuo Kusugami ◽  
Masahiro Ohsuga ◽  
Kenji Ina ◽  
Masataka Shinoda ◽  
...  
Keyword(s):  
Mononuclear Cells ◽  
Eradication Therapy ◽  
Interleukin 8 ◽  
Biopsy Specimens ◽  
Mucosal Tissues ◽  
H Pylori ◽  
Triple Treatment

ABSTRACT There is differential resolution of mucosal infiltration with neutrophils and mononuclear cells following successfulHelicobacter pylori eradication. We investigated the effects of H. pylori eradication on mucosal interleukin-8 (IL-8) and IL-6 activity in relation to the resolution of H. pylori-associated gastritis. Eighty-one duodenal ulcer patients with H. pyloriinfection received dual- or triple-treatment eradication therapy, and mucosal biopsy specimens obtained at the initial and follow-up endoscopic examinations were cultured in vitro for 24 h. The levels of IL-8 and IL-6 were measured by enzyme-linked immunosorbent assays. In the 42 patients in whomH. pylori eradication failed, there was little change in the numbers of neutrophils and mononuclear cells infiltrating the mucosa and in IL-8 and IL-6 activity. In the 39 patients in whom H. pylori was eradicated, there was normalization both in the numbers of infiltrating neutrophils and in mucosal IL-8 activity, which was evident within 1 month following therapy. In contrast, there was a gradual resolution of mononuclear cell infiltration over a 6-month period, accompanied by a gradual normalization in IL-6 levels. Addition of H. pylori to cultures of mucosal tissues induced a significant increase in IL-8 activity in both uninfected control subjects and patients from whom H. pylori was eradicated. However, this introduction yielded a significant increase in IL-6 activity only in the latter group. This study indicates a dichotomy in the changes of mucosal IL-8 and IL-6 activity afterH. pylori eradication. The rapid normalization of IL-8 after H. pylori eradication and the ability of H. pylori cells to stimulate IL-8 in control tissues indicate that IL-8 induction is a part of the innate (nonimmune) responses to this organism. In contrast, the results of experiments analyzing IL-6 activity in cultured mucosal tissues suggest that the gradual resolution of mucosal IL-6 activity and mononuclear infiltration after successful eradication observed in vivo may reflect gradually diminishing residual immune responses against H. pylori.

scholarly journals Endomyocardial biopsy in Chagas' heart disease: pathogenetic contributions

1995 ◽  
Vol 113 (2) ◽  
pp. 821-825 ◽  
Author(s):  
Maria de Lourdes Higuchi
Keyword(s):  
Chagas Disease ◽  
Endomyocardial Biopsy ◽  
Clinical Stage ◽  
Myocardial Damage ◽  
Myocardial Inflammation ◽  
Biopsy Specimens ◽  
The World ◽  
Chagas Heart Disease ◽  
Myocardial Fibers

Endomyocardial biopsy procedure has been performed in many centers around the world, allowing a better treatment and follow up of the patients with myocardial disease. In Chagas' disease, it has been performed in São Paulo Heart Institute since 1978 and has brought important contributions to the understanding of the disease and consequently of the patient's clinical stage. In the present work we summarize the principal findings regarding the pathogenesis of Chagas' disease obtained mainly from the studies using endomyocardial biopsy specimens. Nowadays we do not have doubts that the inflammatory infiltrate aggressing myocardial fibers has fundamental role in the progression of the myocardial damage in Chagas' disease what culminates in chronic heart failure. The parasite seems to have active participation in the maintenance of such myocardial inflammation.

scholarly journals Monoclonal antibody T101 in T cell malignancies: a clinical, pharmacokinetic, and immunologic correlation

Blood ◽  
1986 ◽  
Vol 68 (3) ◽  
pp. 752-761 ◽  
Author(s):  
JH Bertram ◽  
PS Gill ◽  
AM Levine ◽  
D Boquiren ◽  
FM Hoffman ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
T Cells ◽  
T Cell ◽  
Complete Remission ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Rapid Infusion ◽  
Antigenic Modulation ◽  
T Cell Malignancies ◽  
Antibody Excess

Abstract Eight patients with cutaneous T cell lymphomas (CTCL) and five with various other T cell malignancies were treated with mouse monoclonal antibody (MoAb) T101. Doses of 1 to 500 mg were administered weekly over a two-hour period and resulted in one complete remission (convoluted T cell lymphoma) and one partial remission (CTCL). Remission duration was 6 weeks and 3 months, respectively. Frequent toxicities were pruritus, hives, flushing, and shortness of breath. Supraventricular arrhythmias and blood pressure instability were also observed. Complete targeting of peripheral blood T cells was achieved with 1 mg of MoAb in the nonleukemic patients (WBC less than 10,000/microL), and free, bioavailable antibody was present at the next (10-mg) dose level. Even higher doses resulted in substantial antibody excess that persisted for as long as 6 weeks. Serum concentrations of MoAb decreased with increasing number of peripheral blood T cells, and 25 to 35 mg of T101 were required for induction of antibody excess in leukemic patients. Excess antibody induced antigenic modulation, which was of consequence only if MoAb excess persisted to the next treatment. In the original treatment, the rapidly administered MoAb was able to target and remove peripheral blood T cells before the development of antigenic modulation. Antimouse antibodies developed in three patients. Their presence rendered further therapy ineffective and was associated with an anaphylactic reaction in one patient. Development of these antibodies could not be predicted by lymphoproliferative assays. In these assays, however, the T101 protein strongly stimulated the mononuclear cells of the patient who reached the only complete remission of this trial. Immunologic stimulation by the MoAb thus might have played a role in this patient's antitumor response. In summary, therapy with MoAb T101 was specific but only modestly efficacious. Rapid infusion of nonmodulating doses of antibody provided excellent targeting and removal of peripheral blood T cells and might be a valid approach in future trials with immunoconjugated T101.

scholarly journals Identification and characterization of a novel monocyte subpopulation in human peripheral blood

Blood ◽  
1989 ◽  
Vol 74 (7) ◽  
pp. 2527-2534 ◽  
Author(s):  
B Passlick ◽  
D Flieger ◽  
HW Ziegler-Heitbrock
Keyword(s):  
Monoclonal Antibody ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Peritoneal Macrophages ◽  
Monocyte Subset ◽  
Light Scatter ◽  
Oxygen Intermediates ◽  
Average Cell Size ◽  
Average Cell

Abstract With the aid of two-color immunofluorescence and flow cytometry, a new subset of cells coexpressing CD14 and CD16 antigens can be identified in human peripheral blood. Using the monoclonal antibody My4, these CD14+/CD16+ cells account for 2.2% of the mononuclear cells and form about 13% of all cells identified by the monocyte-specific CD14 monoclonal antibody. The CD14+/CD16+ cells can be assigned to the monocyte lineage based on typical morphology, on expression of additional monocyte-associated molecules, on the ability to form reactive oxygen intermediates and on the expression of monocyte- specific NaF-sensitive esterase. Light scatter analysis revealed lower forward angle and right angle light scatter for the CD14+/CD16+ cells compared with the regular monocytes, and the average cell size was determined to be 13.8 and 18.4 microns, respectively. Expression of class II antigens on these “small monocytes” was twofold higher compared with the regular monocytes. By contrast, the capacity to perform adherence to plastic surfaces, as well as the ability to phagocytize antibody-coated erythrocytes was clearly reduced in the CD14+/CD16+ monocyte subset as compared with the regular monocytes. Hence the CD14+/CD16+ cells appear to represent a new monocyte subset with a distinct functional repertoire. A survey of various tissues revealed that a large proportion of the alveolar macrophages, but not of the peritoneal macrophages, express the CD14+/CD16+ phenotype.

scholarly journals Production and regulation of interleukin-2 in human lymphoblastic leukemias studied with T-cell monoclonal antibodies

Blood ◽  
1983 ◽  
Vol 61 (4) ◽  
pp. 781-789 ◽  
Author(s):  
S Venuta ◽  
R Mertelsmann ◽  
K Welte ◽  
SP Feldman ◽  
CY Wang ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
T Cells ◽  
T Cell ◽  
Mononuclear Cells ◽  
Lymphoblastic Leukemia ◽  
Interleukin 2 ◽  
Gel Filtration ◽  
Lymphatic Leukemia ◽  
Daudi Cells ◽  
Self Replication

Abstract Human leukemias are illnesses of hemopoietic stem cells that go through processes of self-replication and partial differentiation under the control of as yet largely unknown growth and differentiation factors. IL-2 is a powerful factor controlling proliferation of normal T cells. We report that acute lymphoblastic leukemias of T and non-B, non-T phenotypes produce a growth factor after mitogen stimulation. This factor is able to support the proliferation of human and murine IL-2- dependent cytotoxic cells, has a mol wt of 26,000 daltons by gel filtration, an isoelectric point of 6.6, and its biologic activity is inhibited by an anti IL-2 monoclonal antibody. This factor is, therefore, by all parameters studied very similar to IL-2 produced by normal lymphocytes. A recently developed monoclonal antibody, Pan T2, binds to normal T cells, renders T cells responsive to IL-2, and induces the release of IL-2, which in turn provides the second signal for T-cell proliferation. Mononuclear cells from acute lymphoblastic leukemia do not respond to the addition of this monoclonal antibody unless cocultured with irradiated Daudi cells. Since normal T cells do not require Daudi to produce IL-2 and since Daudi cells do not produce IL-2 under any conditions, we conclude that the cell responsible for IL- 2 production in acute lymphatic leukemia is a leukemic T cell with an altered mechanism of IL-2 production at the level of the Pan T2 binding site.

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