Journal of Cellular Immunology

Early-stage NSCLC, encompassing resectable stage I-III  are curable, and represents 25% of all lung cancers. The management of non-metastatic NSCLC is a rapidly changing area of clinical oncology, where utilization of molecular biomarkers has become a cornerstone in informing appropriate management. In current clinical practice, adjuvant chemotherapy is recommended after surgical resection for tumors ≥ 4 cms in size (AJCC 7th stage IB, AJCC 8th stage IIA, and higher stage groups thereafter).

Alzheimer’s disease (AD) is a leading cause of death and morbidity in the United States [1]. The hallmarks of AD are β-amyloid (Aβ) and tau. However, studies have indicated that metabolic dysfunction may play a more pivotal role in the progression of AD [2]. Glucose hypometabolism and mitochondrial dysfunction are well-known features of AD [2].

Approximately 1.6-3.8 million people sustain a mild traumatic brain injury (mTBI) in the US annually. This amounts to the hospitalization of 100-300 per 100,000 young adults. The Centers for Disease Control and Prevention reports that around 5.3 million people live with a permanent disability after mTBI, and there are currently no known restorative therapies.

Alzheimer’s disease (AD) research has long been dominated with communications regarding the amyloid hypothesis and targeting amyloid clearance through pharmacological therapies from the brain [1]. 

The maturation of the immune system is a complex process that undergoes major transitions during fetal and neonatal development [1]. Throughout this developmental window, the response to liver injury is dependent on the nature and timing of the insult [2].

Neuroblastoma is derived from the developing sympathetic nervous system and is the most common extracranial solid tumor of childhood.

Alzheimer’s disease (AD) is a leading cause of death and morbidity in the United States [1]. The hallmarks of AD are β-amyloid (Aβ) and tau. However, studies have indicated that metabolic dysfunction may play a more pivotal role in the progression of AD [2]. Glucose hypometabolism and mitochondrial dysfunction are well-known features of AD [2].

Mutations in ELANE, the gene for neutrophil elastase (NE), are the most common cause of cyclic and severe congenital neutropenia

Approximately 1.6-3.8 million people sustain a mild traumatic brain injury (mTBI) in the US annually. This amounts to the hospitalization of 100-300 per 100,000 young adults. The Centers for Disease Control and Prevention reports that around 5.3 million people live with a permanent disability after mTBI, and there are currently no known restorative therapies.

Alzheimer’s disease (AD) research has long been dominated with communications regarding the amyloid hypothesis and targeting amyloid clearance through pharmacological therapies from the brain [1]. 

Low-molecular weight proteins, cofactors, amino acids, metabolites and many bioactive signaling molecules are filtered through the glomeruli. Evolution has yielded highly conserved pathways in proximal tubule epithelium for the reabsorption of filtered molecules;

Back in 2017, I published a review on the immunotherapy options for dogs with cancer. Somewhat provocatively the paper was entitled: Immunotherapy for dogs: Running behind humans. 

This study aimed to investigate the role of the renin-angiotensin system (RAS) in COVID-19, particularly focusing on key components such as ACE, ACE2, and their related peptides, angiotensin-(1-7) and angiotensin-(1-9). Using serum samples from healthy controls and both non-severe and severe COVID-19 patients, ELISA assays revealed no significant differences in these RAS components between the groups.

Polyamines are small organic molecules ubiquitously present in all living organisms and function as crucial regulators of biological processes ranging from fundamental cellular metabolism to immune regulation. Dysregulation of polyamine metabolism has been implicated in numerous diseases, including neurodegenerative disorders, inflammatory conditions, autoimmune diseases, and cancer. This review provides an overview of pathophysiology of these conditions, highlighting polyamines’ role in immunometabolic alterations in the context of immune regulation.

Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease reflecting an imbalance between regulatory and effector immune responses. With the rapid development of molecular biology and multi-omics, the pathogenesis of SLE has been gradually elucidated. In particular, imbalances and abnormalities in immune cell function have been shown to play an important role in the development of SLE. Understanding the specific pathogenesis of SLE is the basis for targeted therapy against specific targets. 

Background: Chikungunya virus (CHIKV) is an alphavirus spread by mosquitos that causes arthralgias and arthritis that may last for years. The objective of this study was to describe the arthritis progression and T cell immunology over a two-year period. Methods: A cohort of 40 cases of serologically confirmed CHIKV from Magdalena and Atlántico, Colombia were followed in 2019 and again in 2021. Arthritis disease severity, disability, pain, stiffness, physical function, mobility, fatigue, anxiety, sleep disturbances and depression were assessed. 

Chimeric antigen receptor (CAR)-T cell therapy has shown potential in improving outcomes for individuals with hematological malignancies. However, achieving long-term full remission for blood cancer remains challenging due to severe life-threatening toxicities such as limited anti-tumor efficacy, antigen escape, trafficking restrictions, and limited tumor invasion. Furthermore, the interactions between CAR-T cells and their host tumor microenvironments have a significant impact on CAR-T function.

Hyperglycemia in diabetes induces impairment of hematopoiesis, an important consequence in bone marrow (BM) that contributes to chronic complications in advanced diabetes. The alterations to blood cells associated with diabetes mellitus (DM) pathologies have been carefully and extensively documented, but the underlying mechanism(s) is still unclear. Our recent publication indicates that aberrant intracellular synthesis of hyaluronan (HA) by hyperglycemic dividing BM progenitors is the central mechanism involved.