Rapid detection of mixed lymphocyte culture reactivity by 4F2 antigen appearance as detected by flow cytometry

1982 ◽  
Vol 5 (2) ◽  
pp. 180
Author(s):  
John M. Williams ◽  
Tom Cotner ◽  
Charles B. Carpenter ◽  
Howard M. Shapiro ◽  
Jack L. Strominger ◽  
...  
1977 ◽  
Vol 146 (2) ◽  
pp. 571-578 ◽  
Author(s):  
M E Dorf ◽  
J H Stimpfling

The ability of various B10 congenic resistant strains to respond to the alloantigen H-2.2 was tested. High and low antibody-producing strains were distinguished by their anti-H-2.2 hemagglutinating respones. However, these strains do not differ in their ability to respond to these antigenic differences in the mixed lymphocyte culture. The humoral response to the H-2.2 alloantigen was shown to be controlled by two interacting genes localized within the H-2 complex. Thus, F1 hybrids prepared between parental low responder strains could yield high level immune responses. In addition, strains bearing recombinant H-2 haplotypes were used to map the two distinct genes controlling the immune response. The alleles at each locus were shown to be highly polymorphic as evidenced by the asymmetric complementation patterns observed. The restricted interactions of specific alleles was termed coupled complementation. The significance of the results in the terms of mechanisms of Ir gene control are discussed.


1998 ◽  
Vol 75 (2-3) ◽  
pp. 295-306 ◽  
Author(s):  
Hideaki Endo ◽  
Junko Nakayama ◽  
Hideki Ushio ◽  
Tetsuhito Hayashi ◽  
Etsuo Watanabe

2002 ◽  
Vol 34 (2) ◽  
pp. 471-473 ◽  
Author(s):  
A Morgun ◽  
N Shulzhenko ◽  
I.D.C.G Silva ◽  
G.F Rampim ◽  
A.P Chinellato ◽  
...  

Blood ◽  
1980 ◽  
Vol 55 (4) ◽  
pp. 702-705
Author(s):  
ER Richie ◽  
MP Sullivan ◽  
J van Eys

A 5-yr-old girl with acute lymphocytic leukemia presented with moderate hepatomegaly, marked splenomegaly, but no evidence of a mediastinal mass. The peripheral blood white count was 270 x 10(9)/liter with 99% leukemic cells. Surface marker analysis showed the lymphoblasts to be E- rosette negative and complement receptor positive. The patient's leukemic cells were unreactive with anti-p23,30, which detects Ia-like antigens, and strongly reactive with A99 anti-T-cell serum, which reacts with normal human thymocytes and peripheral blood T cells. The percentage of leukemic cells bearing complement receptors diminished during relapse. The leukemic cells obtained at diagnosis and during relapse were nonreactive to mitogens and alloantigens and failed to stimulate proliferation of normal lymphocytes in mixed lymphocyte culture. There was no evidence for active suppression of normal lymphocyte reactivity mediated by the leukemic cells. The surface marker and functional profile of these leukemic cells is consistent with that of an early stage in T-cell maturation.


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