Sneller Michael C
Laboratory of Immunoregulation, National Institute of Allergy, Immunology, and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Cleve Clin J Med. 2002;69 Suppl 2:SII40-3. doi: 10.3949/ccjm.69.suppl_2.sii40.
The pathogenesis of granulomatous inflammation is complex and involves a variety of mechanisms acting in concert to bring about an inflammatory lesion that is able to contain and destroy intracellular pathogens. While this process is crucial to host defense, it is also a two-edged sword in that excessive or inappropriate granulomatous inflammation results in considerable damage to normal tissue. In recent years, there has been significant progress in dissecting the immunologic events involved in granuloma formation and maintenance. A better understanding of these events will allow us to more precisely modulate the granulomatous inflammatory response to the benefit of patients with both infectious and autoimmune diseases.
肉芽肿性炎症的发病机制复杂,涉及多种协同作用的机制,以形成能够容纳和破坏细胞内病原体的炎性病变。虽然这个过程对宿主防御至关重要,但它也是一把双刃剑,因为过度或不适当的肉芽肿性炎症会对正常组织造成相当大的损害。近年来,在剖析肉芽肿形成和维持过程中涉及的免疫事件方面取得了重大进展。对这些事件的更好理解将使我们能够更精确地调节肉芽肿性炎症反应,从而造福于患有感染性和自身免疫性疾病的患者。