Th1 and Th2 Lymphocytes in Autoimmune Disease

Abstract

This review reconsiders how the Th1/Th2 paradigm can be applied to Th1-mediated autoimmune disease. Although there is evidence that autoimmune diseases such as multiple sclerosis, type 1 insulin-dependent diabetes mellitus, and posterior uveitis are Th1 mediated and that in some cases reduction of the Th1 response or a Th2 type shift may alleviate disease, many apparent exceptions are now well documented. These exceptions center around the contradictory actions of the Th1 cytokine IFN-gamma and the evidence that Th2 lymphocytes can also cause disease. Recent information on the regulation of Th1 and Th2 lymphocytes in terms of the innate immune response and by other T cells helps to clarify the reasons for some of these discrepancies and enables the Th1/Th2 concept to be accepted as an integral part of the complex interactions occurring as autoimmune disease develops.

Toxicological Implications and Inflammatory Response in Human Lymphocytes Challenged with Oxytetracycline

“…Immunity, which has the fundamental role to protect and defend the organism from the disease 16, 17, 18, is also involved in the homeostasis and health maintenance against autoimmunity diseases and tumors 17. The exacerbation of cytotoxic CD8+ T lymphocytes 18 and CD4+ T Helper 1 (T H 1) 19 responses were associated with inflammatory diseases and autoimmunity disorders 20. T H 1 activity is mainly based on the production of interferon‐gamma (IFN)‐γ, which optimizes the antimicrobial responses and fosters CD8+ T lymphocyte activity, and also appears to play a fundamental role in triggering autoimmune responses 21, 22, 23, 24, 25, 26, 27, 28, 29.…”

Neutralization of mitogenic lectins by intravenous immunoglobulin (IVIg) prevents T cell activation: does IVIg really have a direct effect on T cells?

“…T cells are important players in normal immunity, but also play a critical role in the development and persistence of autoimmunity [7][8][9]. Clinical studies conducted on IVIgtreated patients have revealed significant modulations of T cell functions in these patients.…”

Single-Nucleotide Polymorphism at CYP27B1-1260, but Not VDR Taq I, Is Possibly Associated with Persistent Hepatitis B Virus Infection

“…The reaction of such an immune response may benefit autoimmune diseases, but exacerbate chronic viral infections such as chronic HCV and HBV infections, because the balance of Th1/Th2 response is shifted toward Th1 in autoimmune reaction (Crane and Forrester, 2005;Afzali et al, 2007) and skewed toward Th2 in the immune response of chronic HBV and HCV infections (Bertoletti et al, 1997;Rossol et al, 1997;Tsai et al, 1997). The explanation for this scenario remains elusive.…”

“…The explanation for this scenario remains elusive. The Th1/Th2 imbalance is regarded as an integral part of the complex interactions in the development of autoimmune disease (Crane and Forrester, 2005), and this may also apply for viral infections with various characteristics (Bertoletti et al, 1997). Other pathophysiological processes possibly involved in the complex multifactorial genetic regulation and the action of vitamin D in the autoimmune and viral disorders may also be responsible for this scenario.…”