Exploiting ECM remodelling to promote immune-mediated tumour destruction

2022 ◽  
Vol 74 ◽  
pp. 32-38
Ana Pires ◽  
Stephanie Burnell ◽  
Awen Gallimore
2001 ◽  
Vol 120 (5) ◽  
pp. A720-A720

2006 ◽  
Vol 175 (4S) ◽  
pp. 132-132 ◽  
Sean P. Hedican ◽  
Eric R. Wilkinson ◽  
Thomas F. Warner ◽  
Fred T. Lee ◽  
Stephen Y. Nakada

2018 ◽  
Vol 24 ◽  
pp. 240
Zaib Khan ◽  
Khawla Ali ◽  
Carmen Polanco ◽  
Vinni Makin

2015 ◽  
Vol 53 (12) ◽  
F Glaser ◽  
B Engel ◽  
C John ◽  
T Krech ◽  
A Carambia ◽  

2015 ◽  
Vol 53 (12) ◽  
K Karimi ◽  
K Neumann ◽  
J Meiners ◽  
R Voetlause ◽  
W Dammermann ◽  

2009 ◽  
Vol 37 (05) ◽  
pp. 314-318 ◽  
L. Keller ◽  
K. Meichner ◽  
S. Unterer ◽  
K. Hartmann ◽  
I. Zenker

Summary Objective: Severe thrombocytopenia is a common sequelae to heat stroke in dogs. So far it has been hypothezised that it is due to disseminated intravascular coagulation. We hypothezised that it is due to immune mediated destruction via antiplatelet antibodies. Material and methods: Prospective evaluation of dogs with heat stroke from May 2005 to August 2008. Dogs that developed severe thrombocytopenia within 5 days of admission were included in the study. All dogs were treated with a standardized treatment protocol. In addition, they received either immunoglobulins or prednisolone. Results: Six dogs were presented with heat stroke during that time period. Four developed a severe thrombocytopenia. All four dogs tested positive for antiplatelet antibodies and did not have elevated D-Dimers at that time. Platelet count in three dogs recovered fully, one dog was euthanized due to liver and renal failure. Conclusion: In those cases thrombocytopenia was due to immune mediated destruction not due to DIC. Clinical rele-vance: Due to the severity of the thrombocytopenia and the high risk for bleeding in those patients, immunosuppressive therapy in addition to DIC prophylaxis should be discussed.

1996 ◽  
Vol 76 (05) ◽  
pp. 774-779 ◽  
John T Brandt ◽  
Carmen J Julius ◽  
Jeanne M Osborne ◽  
Clark L Anderson

SummaryImmune-mediated platelet activation is emerging as an important pathogenic mechanism of thrombosis. In vitro studies have suggested two distinct pathways for immune-mediated platelet activation; one involving clustering of platelet FcyRIIa, the other involving platelet-associated complement activation. HLA-related antibodies have been shown to cause platelet aggregation, but the mechanism has not been clarified. We evaluated the mechanism of platelet aggregation induced by HLA-related antibodies from nine patients. Antibody to platelet FcyRIIa failed to block platelet aggregation with 8/9 samples, indicating that engagement of platelet FcyRIIa is not necessary for the platelet aggregation induced by HLA-related antibodies. In contrast, platelet aggregation was blocked by antibodies to human C8 (5/7) or C9 (7/7). F(ab’)2 fragments of patient IgG failed to induce platelet activation although they bound to HLA antigen on platelets. Intact patient IgG failed to aggregate washed platelets unless aged serum was added. The activating IgG could be adsorbed by incubation with lymphocytes and eluted from the lymphocytes. These results indicate that complement activation is involved in the aggregation response to HLA-related antibodies. This is the first demonstration of complement-mediated platelet aggregation by clinical samples. Five of the patients developed thrombocytopenia in relationship to blood transfusion and two patients developed acute thromboembolic disease, suggesting that these antibodies and the complement-dependent pathway of platelet aggregation may be of clinical significance.

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