An Incomplete Antibody for Red Cells in Salmon Caviar

Vox Sanguinis ◽  
1967 ◽  
Vol 12 (6) ◽  
pp. 465-466 ◽  
Author(s):  
G. Uhlenbruck ◽  
O. Prokop
Blood ◽  
1952 ◽  
Vol 7 (8) ◽  
pp. 816-825 ◽  
Author(s):  
J. DAUSSET

Abstract 1. It is suggested that the incomplete antibody is essentially bivalent; one valence is nonreactive, and the other can become reactive under certain conditions. 2. The nonreactive valence of the incomplete antibody is believed to fix the antigen following trypsinization, or to fix nontrypsinized antigen with the aid of the colloid plasma factor. 3. The data obtained from our patients with acquired hemolytic anemia, further support the hypothesis presented; in addition, the data suggest the possibility of a special type of antibody, which acts essentially as a "doubly incomplete antibody," that is to say, that it possesses two nonreactive valences identical to the nonreactive valence of the incomplete antibody.


Blood ◽  
1959 ◽  
Vol 14 (10) ◽  
pp. 1079-1093 ◽  
Author(s):  
JEAN DAUSSET ◽  
JEAN MOULLEC ◽  
JEAN BERNARD

Abstract A case of acquired hemolytic anemia of 12 years’ duration showing a permanent polyagglutinability for at least 9 years, is presented. 1. Polyagglutinability is due to the presence on the surface of the patient’s erythrocytes of an antigen unknown up to the present time, which is independent of antigens T and H and does not behave like a normal antigen modified by proteolytic enzymes. It has been designated by the letters Tn. The Tn substance is not secreted in saliva. This antigen has not been found on the erythrocytes of 25 members of the patient’s family. 2. The substance which induces agglutination (natural anti-Tn) was found to be present in the serum of 473 white adults and 33 adult Negroes. It was absent or weak in 28 sera from cord’s blood. It acts like a complete antibody, being active in saline at the temperature of laboratory and then inducing massive clumping of Tn red cells. Through absorption and elution studies and through sensitization in rabbits, we have been able to demonstrate that anti-T and anti-Tn are distinct. 3. There are in our patient’s serum: (a) a substance specifically active against Tn erythrocytes treated by trypsin; this may be an immune anti-Tn; (b) a nonspecific incomplete antibody weaker than the anti-Tn and active against all varieties of red cells treated by trypsin; (c) an incomplete anti-E; (d) a cold antiplatelet substance; and (e) an immune antileukocyte antibody. These three last antibodies are very probably due to transfusions. 4. To explain the combination of an acquired hemolytic anemia and polyagglutinability, two hypotheses are presented: (a) The acquired hemolytic anemia has no relationship to the existence in the patient of a very rare group antigen, perhaps confined to one family. (b) The hemolytic anemia is directly related to the existence of the Tn antigen on our patient’s red cells and is due to the development of an immune anti-Tn antibody against the Tn antigen, this last antigen being either a group antigen or an antigen revealed or modified by the causal agent of the disease.


Vox Sanguinis ◽  
1967 ◽  
Vol 12 (6) ◽  
pp. 465-466 ◽  
Author(s):  
G. Uhlenbruck ◽  
O. Prokop

2015 ◽  
Vol 63 (S 01) ◽  
Author(s):  
W. Sommer ◽  
M. Avsar ◽  
J. Salman ◽  
C. Kühn ◽  
I. Tudorache ◽  
...  

1979 ◽  
Vol 41 (04) ◽  
pp. 804-810 ◽  
Author(s):  
Knut Nordstoga

SummaryThe composition of the occlusive material within dilated glomerular capillaries, following intravenous injections of Liquoid in blue foxes, was studied electron microscopically; it was found that it mainly consisted of a debris in which disintegrated red cells constituted the major component. Damaged platelets and necrotic endothelial remnants were other components. These observations were interpreted as a result of glomerular stasis, and it was concluded that stasis in glomerular capillaries is a basic event in the development of the renal lesions accompanying the generalized Shwartzman reaction.


1987 ◽  
Vol 58 (03) ◽  
pp. 936-942 ◽  
Author(s):  
Lindsey A Miles ◽  
Edward F Plow

SummaryGlu-plasminogen binds to platelets; the monocytoid line, U937, and the human fetal fibroblast line, GM1380 bind both plasminogen and its activator, urokinase. This study assesses the interaction of these fibrinolytic proteins with circulating human blood cells. Plasminogen bound minimally to red cells but bound saturably and reversibly to monocytes, granulocytes and lymphocytes with apparent Kd values of 0.9-1.4 μM. The interactions were of high capacity with 1.6 to 49 × 105 sites/cell and involved the lysine binding sites of plasminogen. Both T cells and non-rosetting lymphocytes and two B cell lines saturably bound plasminogen. Urokinase bound saturably to gianulocytes, monocytes, non-rosetting lymphocytes and a B cell line, but minimally to T cells, platelets and red cells. Therefore, plasminogen binding sites of high capacity, of similar affinities, and with common recognition specificities are expressed by many peripheral blood cells. Urokinase receptors are also widely distributed, but less so than plasminogen binding sites. The binding ol plasminogen and/ or urokinase to these cells may lead to generation of cell- associated proteolytic activity which contributes to a variety of cellular functions.


1975 ◽  
Vol 34 (01) ◽  
pp. 115-126 ◽  
Author(s):  
Kiyoake Watanabe ◽  
Francis C Chao ◽  
James L Tullis

SummaryAntithrombin activity has been identified in intact washed human platelets. An apparent activity was demonstrated at platelet concentrations above 0.31 × 109/ml, when platelet suspensions were incubated with 2.0 NIH units/ml of thrombin. Neither red cells nor white cells revealed antithrombin activity. No significant loss of the platelet antithrombin activity was observed after ten successive washings or after treatment of platelets with antibodies to antithrombin III or α2-macroglobulin. Almost the same amount of antithrombin activity as normal platelets was demonstrated in the platelets from an afibrinogenemic patient. Pre-treatment of platelets with trypsin, papain, and neuroaminidase reduced the activity significantly, whereas lipase was without effect. The platelet antithrombin reacted with thrombin in less than 3 seconds, and this rapid reaction of platelet antithrombin was different from that of plasma antithrombin III or fibrinogen. The thrombin-like clotting activity of ancrod was inhibited by fibrinogen but not platelets. Also, unlike plasma antithrombin III or fibrinogen, brief exposure to heat (56° C or 60° C) reduced considerable amounts of platelet antithrombin activity. These results suggest that platelets possess a specific antithrombin with different characteristics from other known antithrombins.


1968 ◽  
Vol 20 (03/04) ◽  
pp. 384-396 ◽  
Author(s):  
G Zbinden ◽  
S Tomlin

SummaryAn in vitro system is described in which adhesion of blood platelets to washed and tannic acid-treated red cells was assayed quantitatively by microscopic observation. ADP, epinephrine and TAME produced a reversible increase in platelet adhesiveness which was antagonized by AMP. With Evans blue, polyanetholsulfonate, phthalanilide NSC 38280, thrombin and heparin at concentrations above 1-4 u/ml the increase was irreversible. The ADP-induced increase in adhesiveness was inhibited by sodium citrate, EDTA, AMP, ATP and N-ethylmaleimide. EDTA, AMP and the SH-blocker N-ethylmaleimide also reduced spontaneous platelet adhesion to red cells. No significant effects were observed with adenosine, phenprocoumon, 5-HT, phthalanilide NSC 57155, various estrogens, progestogens and fatty acids, acetylsalicylic acid and similarly acting agents, hydroxylamine, glucose and KCN. The method may be useful for the screening of thrombogenic and antithrombotic properties of drugs.


1964 ◽  
Vol 47 (3_Suppl) ◽  
pp. S28-S36
Author(s):  
Kailash N. Agarwal
Keyword(s):  

ABSTRACT Red cells were incubated in vitro with sulfhydryl inhibitors and Rhantibody with and without prior incubation with prednisolone-hemisuccinate. These erythrocytes were labelled with Cr51 and P32 and their disappearance in vivo after autotransfusion was measured. Prior incubation with prednisolone-hemisuccinate had no effect on the rate of red cell disappearance. The disappearance of the cells was shown to take place without appreciable intravascular destruction.


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