Characterization of specific T helper cell activity in mice bearing alloantigenic tumors in the anterior chamber of the eye

1991 ◽  
Vol 21 (8) ◽  
pp. 1923-1931 ◽  
Author(s):  
Yasuharu Bando ◽  
Bruce R. Ksander ◽  
J. Wayne Streilein
1988 ◽  
Vol 87 (4) ◽  
pp. 337-341 ◽  
Author(s):  
R. Standring ◽  
E.A. Lavender ◽  
A.W. Wheeler ◽  
V.M. Spackman ◽  
D.M. Moran

1990 ◽  
Vol 22 ◽  
pp. 53
Author(s):  
M.C. Caroleo ◽  
D. Frasca ◽  
C. Mancini ◽  
G. Nisticò ◽  
G. Doria

1996 ◽  
Vol 26 (3) ◽  
pp. 313-324 ◽  
Author(s):  
Harumi Jyonouchi ◽  
Sining Sun ◽  
Munetaka Mizokami ◽  
Myron D. Gross

1982 ◽  
Vol 155 (3) ◽  
pp. 831-838 ◽  
Author(s):  
J S McDougal ◽  
F W Shen ◽  
S P Cort ◽  
J Bard

The Qa-1 cell surface phenotype reportedly distinguishes two Ly-1 T cell subsets conjointly required for T helper effector activity. Ly-1 cells, obtained from several different priming regimens, were negatively selected with anti-Qa-1 plus complement and compared with unselected Ly-1 cells for helper cell activity. Priming isolated T cells on antigen-pulsed macrophages in the absence of B cells favors the generation of the Ly-1:Qa1- subset, which is capable of efficient helper activity in the absence of the Ly-1:Qa-1+ subset. Priming T cells in an environment containing B cells generates both Ly-1:Qa-1- helper effector cells and Ly-1:Qa-1+ cells which contribute to the helper effect. Whether Ly-1:Qa-1+ cells are capable of independent helper activity cannot be determined, and, as such, Ly-1:Qa-1+ cells are more appropriately termed "help associated" rather than "helper effector." Our results assign a membrane phenotype, Qa-1, which distinguishes an Ly-1 help-associated B cell requiring subset in our system and may prove to be a general marker in a number of systems of Ly-1 inducer cell subsets which functionally require or recognize B cells or their products.


Blood ◽  
1987 ◽  
Vol 69 (5) ◽  
pp. 1388-1393 ◽  
Author(s):  
EJ Sjamsoedin-Visser ◽  
CJ Heijnen ◽  
BJ Zegers ◽  
JW Stoop

Abstract The capacity of the peripheral blood lymphocytes (PBL) to generate an antibody response in vitro T cell-dependent antigen ovalbumin was studied in 12 severe hemophilia patients who were otherwise in good health. PBL from four of 12 patients were not capable of generating such a response after stimulation in vitro, whereas all controls were normal. This negative plaque-forming cell (PFC) response coincided with the presence of antibodies directed toward human T-lymphotropic virus III/lymphadenopathy-associated virus (HTLV-III/LAV). Only one patient with antibodies against HTLV-III/LAV had a normal PFC response. The negative PFC response was not due to a deficient T helper cell activity, nor to an excessive T suppressor cell function. However, in the peripheral blood of these four patients, the presence of activated B cells that are refractory to antigen-specific T helper cell signals and secrete specific antibodies spontaneously could be demonstrated. Most of the patients showed a hyperimmunoglobulinemia. No correlation between the T4/T8 ratio and the level of the PFC response was demonstrable. From the data obtained in these investigations we raise the hypothesis that infection with HTLV-III/LAV in hemophilia patients will lead to in vivo (pre)activation of B cells that results in unresponsiveness or decreased response to antigen-specific signals.


1990 ◽  
Vol 58 (9) ◽  
pp. 2785-2791 ◽  
Author(s):  
J Katz ◽  
S M Michalek ◽  
K W Beagley ◽  
J H Eldridge

1984 ◽  
Vol 85 (1) ◽  
pp. 34-44 ◽  
Author(s):  
Florence Tsui ◽  
Brian J. Underdown ◽  
Michel Klein ◽  
Barry Zimmerman

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