Phases of myogenic cell activation and possible role of dermomyotome cells in teleost muscle formation

CD38 is a transmembrane glycoprotein that is widely expressed in a variety of human tissues and cells, especially those in the immune system. CD38 protein was previously considered as a cell activation marker, and today monoclonal antibodies targeting CD38 have witnessed great achievements in multiple myeloma and promoted researchers to conduct research on other tumors. In this review, we provide a wide-ranging review of the biology and function of the human molecule outside the field of myeloma. We focus mainly on current research findings to summarize and update the findings gathered from diverse areas of study. Based on these findings, we attempt to extend the role of CD38 in the context of therapy of solid tumors and expand the role of the molecule from a simple marker to an immunomodulator.

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Neuronal guidance proteins in cardiovascular inflammation

Basic Research in Cardiology ◽

10.1007/s00395-021-00847-x ◽

2021 ◽

Vol 116 (1) ◽

Author(s):

Marius Keller ◽

Valbona Mirakaj ◽

Michael Koeppen ◽

Peter Rosenberger

Keyword(s):

Cell Activation ◽

Immune Cell ◽

Vascular Endothelial ◽

Therapeutic Approaches ◽

Immune Cell Activation ◽

Cytokines And Chemokines ◽

The Future ◽

Cardiovascular Pathologies ◽

Neuronal Guidance

AbstractCardiovascular pathologies are often induced by inflammation. The associated changes in the inflammatory response influence vascular endothelial biology; they complicate the extent of ischaemia and reperfusion injury, direct the migration of immune competent cells and activate platelets. The initiation and progression of inflammation is regulated by the classical paradigm through the system of cytokines and chemokines. Therapeutic approaches have previously used this knowledge to control the extent of cardiovascular changes with varying degrees of success. Neuronal guidance proteins (NGPs) have emerged in recent years and have been shown to be significantly involved in the control of tissue inflammation and the mechanisms of immune cell activation. Therefore, proteins of this class might be used in the future as targets to control the extent of inflammation in the cardiovascular system. In this review, we describe the role of NGPs during cardiovascular inflammation and highlight potential therapeutic options that could be explored in the future.

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Role of IL-24 in NK cell activation and its clinical implication in systemic lupus erythematosus

Clinical Rheumatology ◽

10.1007/s10067-021-05618-6 ◽

2021 ◽

Author(s):

Yundi Tang ◽

Xiaotong Sun ◽

Yuxuan Wang ◽

Huijie Luan ◽

Ruijun Zhang ◽

...

Keyword(s):

Systemic Lupus Erythematosus ◽

Lupus Erythematosus ◽

Clinical Implication ◽

Cell Activation ◽

Nk Cell ◽

Systemic Lupus

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Infectious disease-associated encephalopathies

Critical Care ◽

10.1186/s13054-021-03659-6 ◽

2021 ◽

Vol 25 (1) ◽

Author(s):

Maria C. Barbosa-Silva ◽

Maiara N. Lima ◽

Denise Battaglini ◽

Chiara Robba ◽

Paolo Pelosi ◽

...

Keyword(s):

Infectious Disease ◽

Cognitive Deficits ◽

Brain Function ◽

Cell Activation ◽

Therapeutic Strategies ◽

Barrier Dysfunction ◽

Glial Cell Activation ◽

The Central Nervous System ◽

Underlying Mechanisms

AbstractInfectious diseases may affect brain function and cause encephalopathy even when the pathogen does not directly infect the central nervous system, known as infectious disease-associated encephalopathy. The systemic inflammatory process may result in neuroinflammation, with glial cell activation and increased levels of cytokines, reduced neurotrophic factors, blood–brain barrier dysfunction, neurotransmitter metabolism imbalances, and neurotoxicity, and behavioral and cognitive impairments often occur in the late course. Even though infectious disease-associated encephalopathies may cause devastating neurologic and cognitive deficits, the concept of infectious disease-associated encephalopathies is still under-investigated; knowledge of the underlying mechanisms, which may be distinct from those of encephalopathies of non-infectious cause, is still limited. In this review, we focus on the pathophysiology of encephalopathies associated with peripheral (sepsis, malaria, influenza, and COVID-19), emerging therapeutic strategies, and the role of neuroinflammation. Graphic abstract

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The Role of Coagulation and Complement Factors for Mast Cell Activation in the Pathogenesis of Chronic Spontaneous Urticaria

Cells ◽

10.3390/cells10071759 ◽

2021 ◽

Vol 10 (7) ◽

pp. 1759

Author(s):

Yuhki Yanase ◽

Shunsuke Takahagi ◽

Koichiro Ozawa ◽

Michihiro Hide

Keyword(s):

Mast Cells ◽

Cell Activation ◽

Coagulation Factors ◽

Chronic Spontaneous Urticaria ◽

Mast Cell Activation ◽

Coagulation Cascade ◽

Edema Formation ◽

Complement Components ◽

Complement Factors

Chronic spontaneous urticaria (CSU) is a common skin disorder characterized by an almost daily recurrence of wheal and flare with itch for more than 6 weeks, in association with the release of stored inflammatory mediators, such as histamine, from skin mast cells and/or peripheral basophils. The involvement of the extrinsic coagulation cascade triggered by tissue factor (TF) and complement factors, such as C3a and C5a, has been implied in the pathogenesis of CSU. However, it has been unclear how the TF-triggered coagulation pathway and complement factors induce the activation of skin mast cells and peripheral basophils in patients with CSU. In this review, we focus on the role of vascular endothelial cells, leukocytes, extrinsic coagulation factors and complement components on TF-induced activation of skin mast cells and peripheral basophils followed by the edema formation clinically recognized as urticaria. These findings suggest that medications targeting activated coagulation factors and/or complement components may represent new and effective treatments for patients with severe and refractory CSU.

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