{'fraction_non_alphanumeric': 0.02490566037735849, 'fraction_numerical': 0.022641509433962263, 'mean_word_length': 4.666666666666667, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Th-2 cytokines in allergic disease.

The Th-1/Th-2 paradigm The description of two subtypes of T helper cells based on cytokine profiles by Mosman and Coffman in 1986 was a major step forward in thinking on control of immune responses1. Building on previous divisions of responses into predominantly humoral or predominantly cellmediated2, they described murine T cells clones that could be divided into either Th-1 producing IFN-y and IL-2 but not IL-4 and IL-5 or Th-2 which produce IL-4 and IL-5 but not IFN-y1. The functional consequences of this division follow from the observation that IFN-y was required for activation of macrophage function and cytotoxic T-cell responses in cell mediated immunity3, whereas DL-4 unopposed by IFN-y was essential in switching B-cells to IgE synthesis4 and IL-5 was involved in eosinophil development and survival5. This was seen most elegantly in the response of different mouse strains to Leishmania infection which was shown to largely determined by the genetic tendency to mount either a healing Th1 response or an inappropriate Th-2 response leading to disseminated disease6"8. The potential relevance of Th-2 responses to atopic disease was rapidly apparent since IL-4 and EL-5 could explain both IgE and eosinophilic inflammation. These interactions are summarised in Figure 1.