{'fraction_non_alphanumeric': 0.033361847733105215, 'fraction_numerical': 0.00427715996578272, 'mean_word_length': 5.724137931034483, '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}}
Increased adherence to keratinocytes of peripheral blood mononuclear leucocytes of a patient with drug‐induced erythema multiforme

Summary The pathogenetic mechanisms involved in the development of drug‐induced erythema multiforme (EM) are still largely unknown. The observation that epidermal keratinocytes (KC) in EM express intercellular adhesion molecule‐1 (ICAM‐1) points to a putative role for T‐cell/KC adhesion in the pathogenesis of EM. In this study, the binding of peripheral blood mononuclear leucocytes (PBML) from a patient with carbamazepine‐induced EM and of normal control PBML to autologous and heterologous KC was investigated, using two different binding assays. Patient PBML obtained at the time of disease (tO) showed an increased binding to ICAM‐1‐positive heterologous KC, which could be inhibited completely by anti‐LFA‐1. Adhesion of patient PBML‐tO to autologous KC, and to carbamazepine‐pretreated heterologous KC in sections of skin biopsies, was also increased, but was found to be only partially LFA‐1 ‐dependent. These findings support the view that PBML/KC adherence plays an important role in the pathogenesis of this drug‐induced EM.