{'fraction_non_alphanumeric': 0.03856749311294766, 'fraction_numerical': 0.005509641873278237, 'mean_word_length': 5.770186335403727, '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}}
Tumor necrosis factor-alpha at the intersection of mycobacterial immunity and pathogenesis: an important new address in medicine.

TNF-a was first identified in 1975 as the host-produced molecule that caused tumors in an experimental murine model of necrosis [1]. Subsequently, TNF-a has been found to be a critical component in host defense against intracellular pathogens, such as Mycobacterium tuberculosisy and a major pro-inflammatory cytokine that is up-regulated in a variety of autoinflammatory diseases, including rheumatoid arthritis (RA), ankylosing spondylitis, inflammatory bowel disease, and psoriasis. Recognition of the central role of TNF-a in the pathophysiology of inflammation led to the development of TNF-a inhibitors, which have revolutionized the therapeutic approach to debilitating, lifealtering, autoinflammatory diseases. Currently, there are 3 therapeutic agents that operate by inhibiting TNF-cx: etanercept (Enbrel; a fusion protein that acts as a receptor antagonist), infliximab (Remicade; a chimeric [mouse/human] monoclonal antibody), and adalimumab (Hu-