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. In addition, platelets can directly influence adaptive immune responses via secretion of, for example, CD40 and CD40L molecules. Platelets are also the source of most of the microvesicles in the circulation and these miniscule elements further enhance the platelet’s ability to communicate with the immune system. More recently, it has been demonstrated that platelets and their parent cells, the MK, can also uptake, process and present both foreign and self-antigens to CD8+ T-cells conferring on them the ability to directly alter adaptive immune responses. This review will highlight several of the non-hemostatic attributes of platelets that clearly and rightfully place them as integral players in immune reactions.

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. Recent findings The most recent pathophysiologic irregularities associated with ITP relate to abnormal T-cell responses, particularly, defective T regulatory cell activity and how therapeutics can restore these responses. The robust literature on T cells in ITP points to the notion that ITP is a disease initiated by faulty self-tolerance mechanisms very much like that of other organ-specific autoimmune diseases. There is also a large literature on new and existing animal models of ITP and these will be discussed. It appears that understanding how to specifically modulate T cells in patients with ITP will undoubtedly lead to effective antigen-specific therapeutics. Conclusions ITP is predominately a T cell disorder which leads to a breakdown in self tolerance mechanisms and allows for the generation of anti-platelet autoantibodies and T cells. Novel therapeutics that target T cells may be the most effective way to perhaps cure this disorder.

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Desloratadine exerted anti-inflammatory and antioxidant effects on CSU patients revealed by CRP. Patients' remission was synergistic to CRP attenuation emphasizing CRP relevance for CSU clinical assessment.

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. Objective: This study aimed to investigate the efficacy of a first-line treatment: desloratadine 5 mg/day on antioxidant status and clinical assessment in Tunisian patients with CSU and to identify possible associations between GSTT1 and GSTM1 genotypes and susceptibility to CSU. Methods: Sixty patients with CSU and 60 age- and gender-matched healthy controls were included in the study. We calculated the urticaria activity score (UAS) and assessed the antioxidant parameters (total antioxidant status [TAS], glutathione S-transferase [GST], SOD, CAT, GPx]). Multiplex PCR was performed to find the relationship between GSTM1 and GSTT1 polymorphisms with CSU susceptibility. Results: At baseline, GST, GPx, CAT, SOD activities, and TAS were significantly lower in CSU patients compared to healthy controls ( P < 0.05). After treatment, GST, GPx, CAT, SOD activities and TAS were significantly increased in patients compared to those before treatment ( P < 0.001). We observed a significant association in null alleles of GSTM1. Before treatment, GST activity was significantly lower in patients having GSTM1 + genotype than those having GSTM1 - genotype ( P = 0.001). After treatment, TAS and antioxidant enzymes GST, GPx, SOD, and CAT were significantly elevated in patients having GSTM1 - genotype than those having GSTM1 + genotype ( P < 0.05). Conclusion: These results suggest the impact of GSTM1 and GSTT1 on CSU susceptibility and desloratadine efficacy in Tunisian patients.