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Can atopy help to clarify the role of Th2 mediated regulation in these diseases?
Amongst the heterogeneity of human immune responses T helper (Th) lymphocyte subsets have been shown to have an important role.1 Of these different subsets, Th1 cells mediate cellular immunity, including cytotoxicity and delayed-type hypersensitivity responses through the specific production of interferon γ (IFNγ) and interleukin (IL) 2. Th2 cells, characterised by IL4, IL5, and IL13 production, favour humoral immunity and down regulate Th1 mediated cellular immunity. Th2 responses are associated with IL4/IL13 mediated IgE production and IL5 mediated eosinophilia. Th1 activity in its turn inhibits these responses and results in effective immune responses against several infectious agents such as bacteria and viruses. Also, in several autoimmune diseases Th1 cells contribute to the induction and persistence of inflammation and inflammation-induced tissue damage.
Numerous studies have shown that Th1-induced immunity is inhibited by suppressive Th cells other than IL4+ Th2 cells. These suppressive cells are also distinguished by their particular cytokine secretion and/or function: transforming growth factor β (TGFβ)+ Th3 cells, IL10+ T regulatory 1 (Tr1) cells, and CD4+CD25+ anergic/suppressive cells.2,3 Although all these subsets may contribute to suppression of Th1 activity, the balance between Th1 and Th2 cells has been shown to strongly influence many inflammatory responses. Owing to the mutually antagonising abilities of Th1 and Th2 cells in many experimental animal and human in vitro studies, the Th1/Th2 balance in rheumatoid arthritis (RA) has been extensively studied.
“Balance between Th1 and Th2 cells strongly influences inflammatory responses”
Th1 predominance in RA and the impact of atopy-induced Th2 responses
In RA synovial tissue, synovial fluid, and serum, analysis of IFNγ and IL4 production to indicate Th1 and Th2 activity, showed that Th1 activity was clearly predominant and Th2 activity was absent compared with control subjects (table 1).4–6 …
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