scholarly journals Characterization of T Lymphocyte and Monocyte Populations in HLA B8/DRw3 Normal Individuals and in Patients with Dermatitis Herpetiformis

1984 ◽  
Vol 82 (3) ◽  
pp. 231-234 ◽  
Author(s):  
Russell P. Hall ◽  
William M. Leiserson ◽  
Thomas M. Chused ◽  
Thomas J. Lawley
Cytotherapy ◽  
2002 ◽  
Vol 4 (1) ◽  
pp. 29-40 ◽  
Author(s):  
N. Hensel ◽  
J.J. Melenhorst ◽  
K. Bradstock ◽  
A.P. Schwarer ◽  
R. Eniafe ◽  
...  

1981 ◽  
Vol 153 (5) ◽  
pp. 1246-1259 ◽  
Author(s):  
M Fresno ◽  
G Nabel ◽  
L McVay-Boudreau ◽  
H Furthmayer ◽  
H Cantor

We have generated continuously propagatable T lymphocyte clones to study antigen-specific T cell functions. All Ly-2+ clones mediate suppressive activity and secrete a characteristic pattern of polypeptides that differs from Ly-2- T cell clones. Cells of one clone, Cl.Ly23/4, specifically bind glycophorin from sheep erythrocytes (SRBC). After incubation with [35S]methionine, supernate material from this clone also contains biosynthetically labeled 70,000-mol wt proteins that specifically bind to SRBC and this binding is inhibited by glycophorin from sheep but not other erythrocytes. These antigen-binding 70,000-mol wt peptides specifically and completely suppress primary anti-SRBC responses generated by mixtures of primed Ly-1+2- cells and B cells. Suppression by these antigen-binding peptides reflects direct inhibition of T-helper activity.


1987 ◽  
Author(s):  
Diane Nugent

Platelet membrane glycoproteins (GP) express anumber of antigenic determinants important in theetiology of autoimmune thrombocytopenia. Sensitization to GPIb, although not the most frequent cause of ITP, leads to a particularly severe form ofthe disease. We have identified a number of casesof ITP in which GPIb bears the relevant immunogen. Using GPIb-specific autoantibodies isolated from the plasma of one such patient, we have produced a number of rabbit polyclonal and murine monoclonal anti-idiotypic antibodies. These antibodies recognize an idiotype expressed on the IgM antibody of this patient as well as IgG or IgM antibodies from several other patients with ITP, all of which can be shown to bind specifically to GPIb. Statistical analysis of a series of plasmas from normal individuals and thrombocytopenic patients demonstrated that there is a very strong correlation between the presence of the idiotype and GPIb reactivity, (p < 0.00001). These anti-idiotypic antibodies are useful for the detection and characterization of GPIb-specific antibodies in the sera of patients with a clinically severe form of ITP. The classification of patients bearing this idiotype in their plasma may be useful in predicting disease outcome, thus identifying a group of ITP patients in whom more aggressive therapeutic regimens may be indicated. The use of these reagents and the development of human B lymphoblastoid cell lines producing monoclonal anti-GPIb antibodies will serve to elucidate the clonal origin and cellular regulation of autoantibody production in this disease


Blood ◽  
1989 ◽  
Vol 73 (2) ◽  
pp. 553-558 ◽  
Author(s):  
R O'Connor ◽  
JG Bradley ◽  
A O'Meara ◽  
TG Cotter

Abstract In this report we describe the production and characterization of a monoclonal antibody to the human promyelocytic leukemia cell line HL- 60. The antibody, NC-2, is of the IgG1 subclass and precipitates a 50- Kd protein from 125I-labeled HL-60 cells. The antigen is insensitive to treatment with trypsin, papain, or neuraminidase. NC-2 did not react with a number of established human cell lines, including Daudi, Molt-4, K562, U937, KG-1, CEM, Raji, and Gash-P. Neutrophils and monocytelike cells derived from HL-60 cells that were induced to differentiate continued to express the antigen. NC-2 reacted with all peripheral- blood cells except erythrocytes from eight (5%) of 150 normal individuals tested. Bone marrow samples from patients with myelogenous leukemias were more frequently reactive with NC-2 than were those from normal individuals (12/33 v 1/10). Family studies indicated that the antigen was inherited in an autosomal-dominant manner. These findings suggest that the expression of the above alloantigen is associated with an increased incidence of leukemia.


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