Phosphorylation at Y317 on Syk Negatively Regulates Both ITAM and hemITAM-Mediated Signaling and Function in Platelets.

Spleen tyrosine kinase (Syk) is expressed in a variety of hemopoietic cells. Its phosphorylation regulates downstream signaling events upon stimulation of receptors containing an immune tyrosine activation motif (ITAM), like glycoprotein VI (GPVI), or a hemITAM, including the C-type lectin-like receptor II-type (CLEC-2). This study focuses on the role of a specific phosphorylation site, Tyrosine 317, in the regulation of Syk function.

Autophagic Response of the Liver Cells to Schistosoma mansoni Infection and Praziquantel Treatment.

Purpose: The autophagy process is critical for cell survival, homeostasis, and functions. Autophagy deregulation was linked to several liver diseases; however, little is known about autophagy status during schistosomiasis and praziquantel (PZQ) treatment. This study is exploring autophagy status during schistosomiasis and praziquantel treatment in the hepatocytes, macrophages, and hepatic stellate cells (HSCs) in mice, and linking the variations in these levels to the parasitic parameters.

Phosphorylation of (Ser 291) in the linker insert of Syk negatively regulates ITAM signaling in platelets.

Receptor-induced tyrosine phosphorylation of spleen tyrosine kinase (Syk) has been studied extensively in hematopoietic cells. Metabolic mapping and high-resolution mass spectrometry, however, indicate that one of the most frequently detected phosphorylation sites encompassed S297 (S291 in mice) located within the linker B region of Syk. It has been reported that Protein kinase C (PKC) phosphorylates Syk S297, thus influencing Syk activity.

Association between toxoplasmosis and autoimmune rheumatic diseases in Egyptian patients.

Purpose: To explore the association between T. gondii and autoimmune rheumatic diseases (ARDs).

Methods: This study involved 82 patients with ARDs: 44 rheumatoid arthritis (RA), 28 systemic lupus erythematosus (SLE), and 10 systemic sclerosis (SSc) and 61 age- and sex-matched controls.

IL-11 induces NLRP3 inflammasome activation in monocytes and inflammatory cell migration to the central nervous system.

The objective of this study is to examine IL-11-induced mechanisms of inflammatory cell migration to the central nervous system (CNS). We report that IL-11 is produced at highest frequency by myeloid cells among the peripheral blood mononuclear cell (PBMC) subsets. Patients with relapsing-remitting multiple sclerosis (RRMS) have an increased frequency of IL-11 monocytes, IL-11 and IL-11R CD4 lymphocytes, and IL-11R neutrophils in comparison to matched healthy controls.

Therapeutic Effect of Anti-CD52 Monoclonal Antibody in Multiple Sclerosis and Its Animal Models Is Mediated via T Regulatory Cells.

The objective of this study is to determine the mechanism of action of anti-CD52 mAb treatment in patients with relapsing-remitting multiple sclerosis (RRMS). Experimental autoimmune encephalomyelitis (EAE), an animal model of the disease, was used to address the role of T regulatory cells (Tregs) in the anti-CD52 mAb-induced suppression of the disease. In vitro studies on PBMCs from RRMS patients and matched healthy controls determined the effect of IL-7 on the expansion of CD4CD25CD127 Tregs and induction of their suppressive phenotype.

Activity of isoflavone biochanin A in chronic experimental toxoplasmosis: impact on inflammation.

Toxoplasma gondii is a worldwide prevalent parasite. The infection has been linked to variable inflammatory effects including neuroinflammation. Biochanin A (BCA) is an isoflavone, known for its anti-inflammatory and anti-oxidative properties.

Fluconazole as Schistosoma mansoni cytochrome P450 inhibitor: In vivo murine experimental study.

Schistosomiasis is a chronic disease caused by blood flukes of the Schistosoma spp. New approaches against this morbid infection are needed. In this study, we investigated fluconazole (FLZ) as an inhibitor of Schistosoma mansoni cytochrome P450 (S.

Schistosomes Impede ATP-Induced T Cell Apoptosis In Vitro: The Role of Ectoenzyme SmNPP5.

Schistosomes (blood flukes) can survive in the bloodstream of their hosts for many years. We hypothesize that proteins on their host-interactive surface impinge on host biochemistry to help ensure their long-term survival. Here, we focus on a surface ectoenzyme of , designated SmNPP5.

Histopathological and ultrastructural assessment of atovaquone-proguanil hydrochloride combination in chronic murine toxoplasmosis.

Over one billion people worldwide are expected to have infection with anonymous health problems. Available therapies are ineffective for persistent chronic toxoplasmosis. So, there is an imperative need for effective therapies to eliminate chronic tissue stage.

Vitamin B6 Acquisition and Metabolism in .

Schistosomes are parasitic platyhelminths that currently infect >200 million people globally. The adult worms can live within the vasculature of their hosts for many years where they acquire all nutrients necessary for their survival and growth. In this work we focus on how parasites acquire and metabolize vitamin B6, whose active form is pyridoxal phosphate (PLP).

Rhinovirus and Innate Immune Function of Airway Epithelium.

Airway epithelial cells, which lines the respiratory mucosa is in direct contact with the environment. Airway epithelial cells are the primary target for rhinovirus and other inhaled pathogens. In response to rhinovirus infection, airway epithelial cells mount both pro-inflammatory responses and antiviral innate immune responses to clear the virus efficiently.

Schistosomes can hydrolyze proinflammatory and prothrombotic polyphosphate (polyP) via tegumental alkaline phosphatase, SmAP.

Schistosoma mansoni is a long-lived intravascular trematode parasite that can infect humans causing the chronic debilitating disease, schistosomiasis. We hypothesize that the action of host-interactive proteins found at the schistosome surface allows the worms to maintain a safe, anti-thrombotic and anti-inflammatory environment around them in the bloodstream. One such protein is the ˜60 kDa alkaline phosphatase SmAP which is known to be expressed in the outer tegument of all intravascular life stages.

Intravascular Cleave the Host Immune and Hemostatic Signaling Molecule Sphingosine-1-Phosphate Tegumental Alkaline Phosphatase.

Schistosomes are parasitic flatworms that infect the vasculature of >200 million people around the world. These long-lived parasites do not appear to provoke blood clot formation or obvious inflammation around them . Proteins expressed at the host-parasite interface (such as alkaline phosphatase, SmAP) are likely key to these abilities.

The Essential Ectoenzyme SmNPP5 from the Human Intravascular Parasite Schistosoma mansoni is an ADPase and a Potent Inhibitor of Platelet Aggregation.

Schistosomes are intravascular parasitic platyhelminthes infecting > 200 million people globally and causing a debilitating disease, schistosomiasis. Despite the relatively large size of the adult worms and their disruption of blood flow, surprisingly, they do not appear to provoke thrombus formation around them in vivo. We hypothesize that proteins expressed at the host-parasite interface are key to this ability.