Experiments on Immunization of Guinea-Pigs with Normal and Leukemic Human White Blood Cells

1954 ◽  
Vol 12 (3) ◽  
pp. 188-192
Author(s):  
B. Landtman ◽  
Ruth Wegelius ◽  
Hilkka Tähkä
Keyword(s):  
Blood Cells ◽  
Guinea Pigs ◽  
White Blood Cells ◽  
Human White Blood Cells

Lead exposure affects inflammatory mediators, total and differential white blood cells in sensitized guinea pigs during and after sensitization

2013 ◽  
Vol 37 (3) ◽  
pp. 329-335 ◽  
Author(s):  
Tahereh Farkhondeh ◽  
Mohammad Hossein Boskabady ◽  
Mohammad Kazem Kohi ◽  
Goudarz Sadeghi-Hashjin ◽  
Mostafa Moin
Keyword(s):  
Lead Exposure ◽  
Inflammatory Mediators ◽  
Blood Cells ◽  
Guinea Pigs ◽  
White Blood Cells

A new group of glucocerebrosidase isozymes found in human white blood cells

1980 ◽  
Vol 97 (3) ◽  
pp. 1103-1107 ◽  
Author(s):  
Edward I. Ginns ◽  
Roscoe O. Brady ◽  
Daniel W. Stowens ◽  
F.Scott Furbish ◽  
John A. Barranger
Keyword(s):  
Blood Cells ◽  
White Blood Cells ◽  
Human White Blood Cells

scholarly journals Identification of phosphatidylserine-binding proteins in human white blood cells

1990 ◽  
Vol 269 (3) ◽  
pp. 723-728 ◽  
Author(s):  
M Wolf ◽  
M Baggiolini
Keyword(s):  
Protein Kinase C ◽  
Blood Cells ◽  
Binding Proteins ◽  
White Blood Cells ◽  
Human Neutrophils ◽  
Kinase C ◽  
Sds Page ◽  
Molecular Masses ◽  
Human White Blood Cells ◽  
Monocytes And Lymphocytes

Cytosol and membrane fractions from human neutrophils, monocytes, lymphocytes and platelets were separated by SDS/PAGE, blotted on to nitrocellulose and assayed for selective binding of phosphatidylserine (PS). Two PS-binding proteins with apparent molecular masses of 115 kDa and 100 kDa were identified in the cytosol of neutrophils, monocytes and lymphocytes. Corresponding bands along with other PS-binding proteins were detected in platelets in both cytosol and membrane fractions. These proteins were also found to bind protein kinase C (PKC) provided that PS was present. The 115 kDa and 100 kDa proteins (PS-p115/110) were partially purified from neutrophils and were used for the study of PS and PKC binding. The binding of PS did not require Ca2+ or Mg2+ and was inhibited by phosphatidic acid, by 1-alkyl-2-acetylphosphocholine and, to a lesser extent, by other lipids. The binding of PKC, however, was strictly PS- and Ca2(+)-dependent and seems to occur secondarily to PS binding.

Expression of CD80 (B7/BB-1) and CD28 in human white blood cells treated with urocanic acid

1996 ◽  
Vol 288 (10) ◽  
pp. 570-574 ◽  
Author(s):  
Jarmo K. Laihia ◽  
Jaakko Uksila ◽  
Marko Luhtala ◽  
Christer T. Jansén
Keyword(s):  
Blood Cells ◽  
White Blood Cells ◽  
Urocanic Acid ◽  
Human White Blood Cells

scholarly journals IMMUNOLOGICAL UNRESPONSIVENESS TO SENSITIZATION WITH SIMPLE CHEMICAL COMPOUNDS

1963 ◽  
Vol 118 (6) ◽  
pp. 1021-1035 ◽  
Author(s):  
Jack R. Battisto ◽  
Merrill W. Chase
Keyword(s):  
Specific Antibody ◽  
Blood Cells ◽  
Guinea Pigs ◽  
White Blood Cells ◽  
Chemical Compounds ◽  
Lymphoid Cells ◽  
Delayed Type Hypersensitivity ◽  
Simple Chemical ◽  
Picryl Chloride

Guinea pigs fed picryl chloride to induce specific immunologic unresponsiveness cleared small amounts of venously infused antipicryl antibody at a rate equal to that of normal guinea pigs. Catabolism of passively administered picryl-specific antibody did not alter the unresponsive state of picryl chloride-fed guinea pigs or the responsive state of normal guinea pigs. Lymphoid cells of picryl chloride immunized guinea pigs produced equal amounts of picryl-specific antibody in picryl chloride-fed and normal animals. Allergen-fed guinea pigs remained unresponsive to attempted sensitization with the allergen in excess of 10 months after the final feeding, though some became feebly sensitive between 9 and 11 months. Second attempts to make unresponsive animals hypersensitive were unsuccessful. White blood cells of guinea pigs unresponsive to picryl chloride were unable to transfer delayed-type hypersensitivity for picryl chloride to normal recipients yet readily transferred tuberculin hypersensitivity.

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