scholarly journals The immune adherence receptor CR1-like existed on porcine erythrocytes membrane

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Wei Yin ◽  
Jiaoyan Cui ◽  
Junbing Jiang ◽  
Junxing Zhao ◽  
Kuohai Fan ◽  
...  
Keyword(s):  
1999 ◽  
Vol 189 (1) ◽  
pp. 25-35 ◽  
Author(s):  
Mercedes Domínguez ◽  
Alfredo Toraño

To mimic the sandfly pool feeding process and characterize the cellular and biochemical events that occur during the early stages of promastigote–host interaction, we developed an ex vivo model of human blood infection with Leishmania promastigotes. Within 30 s of blood contact, Leishmania promastigotes bind natural anti–Leishmania antibodies, which then activate the classical complement pathway and opsonization by the third component of complement. The opsonized promastigotes undergo an immune adherence reaction and bind quantitatively to erythrocyte CR1 receptors; opsonized Leishmania amastigotes also bind to erythrocytes. Progression of infection implies promastigote transfer from erythrocytes to acceptor blood leukocytes. After 10 min of ex vivo infection, 25% of all leukocytes contain intracellular parasites, indicating that blood cells are the early targets for the invading promastigotes. We propose that adaptation to the immune adherence mechanism aids Leishmania survival, promoting rapid promastigote phagocytosis by leukocytes. This facilitates host colonization and may represent the parasite's earliest survival strategy. In light of this mechanism, it is unlikely that infection-blocking vaccines can be developed.


2012 ◽  
Vol 86 (2) ◽  
pp. 146-148 ◽  
Author(s):  
Takao OZAKI ◽  
Naoko NISHIMURA ◽  
Kensei GOTOH ◽  
Shinji KAWABE ◽  
Keiji FUNAHASHI ◽  
...  

Immunobiology ◽  
2016 ◽  
Vol 221 (10) ◽  
pp. 1164
Author(s):  
Steven P. Broadley ◽  
Ann Plaumann ◽  
Raffaele Coletti ◽  
Christin Lehmann ◽  
Steffen Massberg ◽  
...  

Blood ◽  
1987 ◽  
Vol 69 (1) ◽  
pp. 211-218
Author(s):  
PJ McCaffery ◽  
AS Tan ◽  
MV Berridge

The presence of the Pgp-1 glycoprotein on mouse platelets is demonstrated by antibody-binding techniques, by immunoprecipitation, and by transblotting using the monoclonal antibody (MoAb) C71/26 against Pgp-1. C71/26 immunoprecipitates as a broad band of mol wt 87,000 to 100,000 as determined by radioiodination of the platelet cell surface and by the 3H-sodium borohydride labeling technique. Immunoblotting showed Pgp-1 expression on platelets to be quantitatively similar to its presence on macrophages and resolved platelet Pgp-1 into two bands of mol wt 87,000 and 97,000 whereas Pgp-1 on parasite-elicited peritoneal macrophages showed 82,000 and 87,000 mol wt species. Platelets and monocyte/macrophage cells from either peripheral blood or from the peritoneal cavity showed homogeneous binding of Pgp-1 antibody to greater than 97% of cells by flow cytometry. In contrast, lymphocytes from peripheral blood or from the spleen showed a heterogeneous binding pattern with 20% to 30% of cells being negative, and the majority weakly positive. In functional studies, MoAbs against CR1 and CR3 substantially inhibited platelet immune adherence, whereas C71/26 showed only marginal inhibitor. In contrast, C71/26 and other MoAbs against Pgp-1 inhibited platelet- dependent cytotoxicity of antibody-coated sheep erythrocytes in the presence of C5-deficient mouse plasma whereas M1/70 against CR3 showed no effect. In this assay, MoAbs against the alpha- and beta-subunits of leukocyte functional molecule LFA-1 also inhibited platelet cytotoxicity. These results show that the platelet cell surface moieties Pgp-1 and LFA-1 are involved in or closely associated with antibody-dependent cellular cytotoxicity by platelets.


1977 ◽  
Vol 28 (1) ◽  
pp. 211-223
Author(s):  
D.E. MacIntyre ◽  
A.P. Allen ◽  
K.J. Thorne ◽  
A.M. Glauert ◽  
J.L. Gordon

Endotoxin lipopolysaccharide (LPS) from Acinetobacter 199A induced aggregation of blood platelets from immune adherence-positive species (rat, rabbit) but not from immune adherence-negative species such as pig and man. Aggregation occurred in 2 phases: the first was not accompanied by secretion of platelet constituents, was apparently a consequence of C3 activation, and was selectively inhibited by EGTA. The second phase of aggregation was associated with secretion of platelet granule contents, and with a lesser amount of cytoplasmic leakage. Secondary aggregation was abolished by the sulphydryl alkylating agent N-ethylmaleimide, and by agents which increased the level of cyclic AMP in platelets, such as prostaglandin E1 (a stimulator of adenylate cyclase) and methyl xanthines (inhibitors of phosphodiesterase). Secondary aggregation was partly inhibited by agents which block platelet prostaglandin biosynthesis (e.g. aspirin, indomethacin). Primary aggregation was unaffected by these inhibitors at concentrations which blocked secondary aggregation.


PEDIATRICS ◽  
1980 ◽  
Vol 66 (2) ◽  
pp. 269-271
Author(s):  
William F. Balistreri ◽  
Edward Tabor ◽  
Robert J. Gerety

Serologic evidence of hepatitis A virus (HAV) or hepatitis B virus (HBV) infection was sought in 14 patients with biliary atresia and in four patients with neonatal hepatitis; maternal serum was also analyzed. Specific sensitive radioimmunoassays were used to detect HBV surface antigen (HBsAg) and antibody (anti-HBs); complement fixation was used to detect antibody to HBV core antigen (anti-HBc). Antibody to HAV (anti-HAV) was assayed by radioimmunoassay, as well as by immune adherence hemagglutination. There was no evidence of active or past HBV infection in any infant or mother studied. All three infants with detectable anti-HAV were born to mothers similarly anti-HAV positive; serial testing of sera from two of these infants documented disappearance of detectable anti-HAV by 9 months of age. It is unlikely, therefore, that either HAV or HBV had an etiologic role in neonatal cholestasis in these patients. The role of other (non-A, non-B) hepatitis viruses or nonviral etiologies must be investigated.


Vox Sanguinis ◽  
1971 ◽  
Vol 20 (2) ◽  
pp. 178-181 ◽  
Author(s):  
M. Mayumi ◽  
K. Okochi ◽  
K. Nishioka

1990 ◽  
pp. 173-181 ◽  
Author(s):  
H. Ishikura ◽  
Y. Kikuchi ◽  
O. Toyokawa ◽  
H. Hayasaka ◽  
K. Kikuchi

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