CpG oligonucleotides induce acute murine thrombocytopenia dependent on toll-like receptor 9 and spleen tyrosine kinase pathways.

Background: CpG oligonucleotides (ODNs) are synthetic single-stranded DNA sequences that act as immunostimulants. They have been increasingly used to treat several cancers; however, thrombocytopenia is a potential recognized side effect of some sequences.

Objectives: We tested the ability of 2 CpG ODNs (ODN 2395 and ISIS 120704) to induce thrombocytopenia when administered to BALB/c mice and determined mechanisms associated with thrombocytopenia.

Desloratadine Efficacy in Relation to GSTM1 and GSTT1 Polymorphic Genes in Chronic Spontaneous Urticaria.

Background: The etiopathogeny of chronic spontaneous urticaria (CSU) is not well defined. Allelism in glutathione S-transferase GSTM1 and GSTT1 has been suggested as a risk factor. Desloratadine is the first-line treatment for this disease.

The Immune Nature of Platelets Revisited.

Platelets are the primary cellular mediators of hemostasis and this function firmly acquaints them with a variety of inflammatory processes. For example, platelets can act as circulating sentinels by expressing Toll-like receptors (TLR) that bind pathogens and this allows platelets to effectively kill them or present them to cells of the immune system. Furthermore, activated platelets secrete and express many pro- and anti-inflammatory molecules that attract and capture circulating leukocytes and direct them to inflamed tissues.

An update on the pathophysiology of immune thrombocytopenia.

Unlabelled: : Immune thrombocytopenia (ITP) is an autoimmune bleeding disorder mediated by antiplatelet autoantibodies and antigen-specific T cells that either destroy platelets peripherally in the spleen or impair platelet production in the bone marrow. There have been a plethora of publications relating to the pathophysiology of ITP and since January of 2019, at least 50 papers have been published on ITP pathophysiology.

Purpose Of Review: To summarize the literature relating to the pathophysiology of ITP including the working mechanisms of therapies, T-cell and B-cell physiology, protein/RNA/DNA biochemistry, and animal models in an attempt to unify the perceived abnormal immune processes.