So the poster gave more information about his condition on iHub.
Jaylimab Member Profile Jaylimab Thursday, October 29, 2020 12:14:08 PM
Re: GMC Silverado post# 127043 Post # of 127053
Hello All,
Thanks everyone for the well wishes. This condition is benign. It is an autoimmune condition where the immune system creates antibodies that attack the platelets. All other blood work is normal.
You can live a normal life with condition.
Symptoms include fatigue, bruising, and inflammation.
Worst case scenario is a brain bleed due to very low platelet levels usually under 10000 platelet count.
People usually remove the spleen as a curative effect. (Which I have done).
I figure that Dr. Patterson can tell me that this condition is caused by a CCL5 / CCR5 inbalance.
Remember, CCL5 promotes platelet formation.
See below: This will blow your mind: (P.S. - don't be upset because the study says Maraviroc. Shitty drug with liver toxicity. Think what Leronlimab can do and apply Leronlimab to this study. This is why I sent my blood to Dr. Patterson. See below.
In times of physiological stress, platelet count can transiently rise. What initiates this reactive thrombocytosis is poorly understood. Intriguingly, we found that treating megakaryocytes (MKs) with the releasate from activated platelets increased proplatelet production by 47%. Platelets store inflammatory cytokines, including the chemokine ligand 5 (CCL5, RANTES); after TRAP activation, platelets release over 25 ng/mL CCL5. We hypothesized that CCL5 could regulate platelet production by binding to its receptor, CCR5, on MKs. Maraviroc (CCR5 antagonist) or CCL5 immunodepletion diminished 95% and 70% of the effect of platelet releasate, respectively, suggesting CCL5 derived from platelets is sufficient to drive increased platelet production through MK CCR5. MKs cultured with recombinant CCL5 increased proplatelet production by 50% and had significantly higher ploidy. Pretreating the MK cultures with maraviroc prior to exposure to CCL5 reversed the augmented proplatelet formation and ploidy, suggesting that CCL5 increases MK ploidy and proplatelet formation in a CCR5-dependent manner. Interrogation of the Akt signaling pathway suggested that CCL5/CCR5 may influence proplatelet production by suppressing apoptosis. In an in vivo murine acute colitis model, platelet count significantly correlated with inflammation whereas maraviroc treatment abolished this correlation. We propose that CCL5 signaling through CCR5 may increase platelet counts during physiological stress.
Jaylimab Member Profile Jaylimab Thursday, October 29, 2020 12:14:08 PM
Re: GMC Silverado post# 127043 Post # of 127053
Hello All,
Thanks everyone for the well wishes. This condition is benign. It is an autoimmune condition where the immune system creates antibodies that attack the platelets. All other blood work is normal.
You can live a normal life with condition.
Symptoms include fatigue, bruising, and inflammation.
Worst case scenario is a brain bleed due to very low platelet levels usually under 10000 platelet count.
People usually remove the spleen as a curative effect. (Which I have done).
I figure that Dr. Patterson can tell me that this condition is caused by a CCL5 / CCR5 inbalance.
Remember, CCL5 promotes platelet formation.
See below: This will blow your mind: (P.S. - don't be upset because the study says Maraviroc. Shitty drug with liver toxicity. Think what Leronlimab can do and apply Leronlimab to this study. This is why I sent my blood to Dr. Patterson. See below.
In times of physiological stress, platelet count can transiently rise. What initiates this reactive thrombocytosis is poorly understood. Intriguingly, we found that treating megakaryocytes (MKs) with the releasate from activated platelets increased proplatelet production by 47%. Platelets store inflammatory cytokines, including the chemokine ligand 5 (CCL5, RANTES); after TRAP activation, platelets release over 25 ng/mL CCL5. We hypothesized that CCL5 could regulate platelet production by binding to its receptor, CCR5, on MKs. Maraviroc (CCR5 antagonist) or CCL5 immunodepletion diminished 95% and 70% of the effect of platelet releasate, respectively, suggesting CCL5 derived from platelets is sufficient to drive increased platelet production through MK CCR5. MKs cultured with recombinant CCL5 increased proplatelet production by 50% and had significantly higher ploidy. Pretreating the MK cultures with maraviroc prior to exposure to CCL5 reversed the augmented proplatelet formation and ploidy, suggesting that CCL5 increases MK ploidy and proplatelet formation in a CCR5-dependent manner. Interrogation of the Akt signaling pathway suggested that CCL5/CCR5 may influence proplatelet production by suppressing apoptosis. In an in vivo murine acute colitis model, platelet count significantly correlated with inflammation whereas maraviroc treatment abolished this correlation. We propose that CCL5 signaling through CCR5 may increase platelet counts during physiological stress.
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