Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease resulting from a loss of tolerance to multiple self antigens, and characterized by autoantibody production and inflammatory cell infiltration in target organs, such as the kidneys and brain. T cells are critical players in SLE pathophysiology as they regulate B cell responses and also infiltrate target tissues, leading to tissue damage. Abnormal signaling events link to defective gene transcription and altered cytokine production, contributing to the aberrant phenotype of T cells in SLE. Study of signaling and gene transcription abnormalities in SLE T cells has led to the identification of novel targets for therapy.

Highlights

  • T cells and systemic lupus erythematosus Systemic lupus erythematosus (SLE) is an autoimmune disease that afflicts mainly women in the reproductive years

  • These results show that statins may have therapeutic value in restoring signaling defects in SLE T cells and potentially disease [10]

  • Activation induces changes in the expression of lymphocyte kinase (Lck), CD3ζ, FcRγ, zeta associated protein of 70 kDa (ZAP70), and spleen tyrosine kinase (Syk), phosphorylation of intermediates, and calcium fluxing, many of which are observed in SLE T cells

Read more

Summary

Introduction

T cells and systemic lupus erythematosus Systemic lupus erythematosus (SLE) is an autoimmune disease that afflicts mainly women in the reproductive years. TCR activation restored the ERK phosphorylation and decreased their production of the cytokines IL6 and IL10, which are implicated in SLE pathogenesis These results show that statins may have therapeutic value in restoring signaling defects in SLE T cells and potentially disease [10]. Despite interesting preclinical data on the therapeutic potential of the disruption of the CD40-CD40L interaction, clinical efforts so far have not met the predictions Another co-stimulatory molecule - inducible T cell costimulator (ICOS) - is required for controlling the local inflammatory effector functions of T cells infiltrating the kidneys in MRL/lpr lupus-prone mice [37].

II III IV V VI VII
Conclusion
64. Richardson B
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.