Immunomodulatory effect of sp. in mononuclear cells extracted from the blood of rheumatoid arthritis patients.

Background: Pathophysiological mechanisms of rheumatoid arthritis arise because of a proinflammatory environment, generated by the interaction of autoreactive lymphocytes and proinflammatory mediators. Current strategies to mitigate the progression of the disease produce adverse effects, so there is a need for new therapeutic strategies and molecular targets to treat this disease. In this context, evidence suggests that scorpion venoms could modulate the immune response and some important cellular mechanisms of pharmacological interest.

Prolonged chronic academic stress and its relationship with cytokine dysregulation in health science students.

Unlabelled: Academic stress is a problem that affects students due to a number of factors that are considered stressors. These include academic overload and completion of assignments and exams, exacerbated by such external conditions as family, social and economic problems. Together, these can affect emotional and physical health, which may lead in the long term to developing a number of pathologies, given the alteration of immunological homoeostasis with which they are related.

Scorpion Toxins and Ion Channels: Potential Applications in Cancer Therapy.

Apoptosis, a genetically directed process of cell death, has been studied for many years, and the biochemical mechanisms that surround it are well known and described. There are at least three pathways by which apoptosis occurs, and each pathway depends on extra or intracellular processes for activation. Apoptosis is a vital process, but disturbances in proliferation and cell death rates can lead to the development of diseases like cancer.

Low Frequency Of Regulatory B-Cells And Increased CD4+ and CD8+ Interferon-γ-producing cells in patients with tropical spastic paraparesis associated with human T-cell lymphotropic virus type.

Introduction: Tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM) is a disease caused by human T-cell lymphotropic virus type 1 (HTLV-I) that mainly infects CD4 T cells-for example, those of the CD4+CD25hiFOXP3+ [Treg] phenotype-where it inhibits forkhead box protein P3 (FOXP3) expression and promotes interferon-γ (IFN-γ) expression. However, the role it exerts on regulatory B cells (CD19+CD24hiCD38hi; Breg) is unknown.

Methods: The frequencies of Treg and Breg cells was evaluated and the Th1 profiles were assessed in TSP/HAM patients and healthy control subjects.