Lymphocyte surface molecules as immune activation biomarkers

2016 ◽  
Vol 49 (4-5) ◽  
pp. 347-354 ◽  
Author(s):  
Eberhard Wieland ◽  
Maria Shipkova
1980 ◽  
Vol 17 (12) ◽  
pp. 1575-1583 ◽  
Author(s):  
Charles L. Sidman ◽  
Tuvia Bercovici ◽  
Carlos Gitler

1978 ◽  
Vol 79 (2) ◽  
pp. 419-426 ◽  
Author(s):  
J Braun ◽  
K Fujiwara ◽  
T D Pollard ◽  
E R Unanue

In the previous study, lymphocyte surface molecules were separated into two subsets depending on whether capping was associated was associated with redistribution of cytoplasmic myosin. In the present study, the effects of the local anesthetic chlorpromazine and of the Ca2+ ionophore A23187 were compared. Both drugs affected the surface redistribution of immunoglobulin (Ig), Fc receptors, and the TL antigen--molecules that appear to cap by association with microfilaments--but had no effect on the Thy.1 (theta) and H2 antigens--molecules that cap slowly, apparently unlinked to microfilament function. The capping of Ig, Fc receptor, and TL was inhibited while that of H2 and theta was not. Both drugs reversed the Ig Fc receptor, and TL caps but not the H2 and theta caps. In the former group, the reversal of caps was accompanied by a parallel reversal of the myosin segregated to the cap area. The appearance of myosin after drug treatment varied: chlorpromazine resulted in a diffuse pattern similar to that of normal lymphocytes, whereas A23187 produced an array of aggregates and coarse filaments. The results are compatible with the view that two mechanisms for capping exist in the lymphocyte. The Ca2+ ionophore may affect capping of microfilament-dependent caps by producing a systemic activation of contractile proteins while chlorpromazine may act by disrupting a Ca2+-dependent link between surface complexes and the contractile proteins.


Parasitology ◽  
1996 ◽  
Vol 113 (3) ◽  
pp. 267-277 ◽  
Author(s):  
M. K. Shaw

SUMMARYSporozoite invasion of bovine lymphocytes byTheileria parvais a pH-dependent process that occurs without the need forde novoprotein synthesis. The process was inhibited by RGD(S) peptides, fibronectin and, in the presence of serum, by antibodies reactive with fibronectin. Invasion was also blocked by a range of sulphated glycoconjugates, but treatment of lymphocytes with heparitinase did not inhibit entry. Enzymic modifications of the lymphocyte surface demonstrated that trypsin-insensitive glycoproteins containingO- andN-linked carbohydrates as well as phospholipase-sensitive molecules on the host cell surface were critical to sporozoite entry. Modification of the lymphocyte surface with NEM and DTT had only marginal effects on sporozoite binding but blocked parasite internalization. Invasion was also blocked by several antibodies which cross-reacted with sporozoite surface molecules. While only a few experimental conditions specifically blocked sporozoite binding, a wider range of reagents and treatments inhibited parasite entry. The reasons for this are discussed in terms of the nature of the zippering process that facilitates sporozoite internalization.


Nature ◽  
1982 ◽  
Vol 298 (5871) ◽  
pp. 284-286 ◽  
Author(s):  
Koussay Dellagi ◽  
Jean-Claude Brouet

1978 ◽  
Vol 79 (2) ◽  
pp. 409-418 ◽  
Author(s):  
J Braun ◽  
K Fujiwara ◽  
T D Pollard ◽  
E R Unanue

A detailed kinetic analysis of the distribution of cytoplasmic myosin during the capping of various lymphocytic surface molecules revealed two distinct capping mechanisms. (a) Some cell surface molecules, including immunoglobulin, Fc receptor, and thymus leukemia antigen, all cap spontaneously in a small fraction of lymphocytes during locomotion. Cytoplasmic myosin becomes concentrated in the cytoplasm underlying these spontaneous caps. Exposure to specific antibodies causes all three of these surface molecules to cap rapidly with a concomitant redistribution of cytoplasmic myosin to the area of the cap. These antibodies also stimulate cell locomotion. (b) Other lymphocyte surface molecules, including H2 and Thy.1, do not cap spontaneously. Moreover, exposure to antibodies to these molecules causes them to cap slowly without a redistribution of cytoplasmic myosin or stimulation of cell locomotion. Exposure to concanavalin A gives a response intermediate between these two extremes. We believe that the first type of capping is active and may involve a direct link between the surface molecules and the cytoplasmic contractile apparatus. The second type of capping appears to result simply from aggregation of cross-linked molecules in the plane of the membrane.


1995 ◽  
Vol 25 (5) ◽  
pp. 1306-1311 ◽  
Author(s):  
Umberto Dianzani ◽  
Manuela Bragardo ◽  
Donatella Buonfiglio ◽  
Valter Redoglia ◽  
Ada Funaro ◽  
...  

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