Abstract
The human skin is increasingly exposed to haptens and environmental protein antigens. Because Langerhans cells represent the outermost network of MHC class II+ antigen presenting cells in mammalians, we investigated their interaction with CD4+ T cells. Hapten-modified Langerhans cells induced proliferation and IL-2 production in naive resting CD4+ T cells. T cells activated in this manner and subsequently cultured with IL-2 mediated contact sensitivity in vivo and produced IL-2 but no IL-4 upon restimulation in vitro. Thus they corresponded to Th1 cells. Repeated stimulation with Langerhans cells induced a modulation of the lymphokine pattern: IL-2- and IL-4-producing Th0-like cells were identified after 3 to 4 rounds of restimulation; after > 5 rounds, Th2-like cells with an IL-4+IL-2- pattern and the capacity for inducing IgE synthesis in B cells was identified. Th2 cells were also recently found to mediate inflammatory tissue lesions containing a cellular infiltrate. This demonstrates that Langerhans cells may activate resting CD4+ T cells, Th1-, Th0- and Th2-like cells. It further shows that Langerhans cells may promote the differentiation of postthymic CD4+ T cells into subsets with distinct immune functions: Th1 cells which have the potential to mediate inflammatory reactions such as allergic contact sensitivity and Th2 cells which may be responsible for abnormalities associated with atopic dermatitis, such as elevated IgE and inflammatory skin lesions containing a cellular infiltrate.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
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.