Complement factor 5 in asthma

Marsha Wills-Karp, Jörg Köhl, Christopher L. Karp


The worldwide prevalence and severity of allergic asthma have increased dramatically in recent decades. Therapeutic advances have unfortunately not kept pace, and asthma morbidity and mortality continue to rise. The cardinal features of allergic asthma include airway hyperresponsiveness (AHR) to a variety of specific and nonspecific stimuli, excessive airway mucus production, pulmonary eosinophilia, and elevated concentrations of serum immunoglobulin E (IgE). Although asthma is multifactorial in origin, it is generally accepted that it arises as a result of inappropriate immunological responses to common environmental antigens in genetically susceptible individuals (1). Specifically, a multitude of evidence suggests that CD4 T cells producing Th2 cytokines (IL-4, IL-5, IL-13) play a pivotal role in disease pathogenesis. Although extensive research is ongoing into the processes underlying the development of deleterious immune responses to the ubiquitous, otherwise harmless, antigens that drive the expression of allergic asthma, these mechanisms remain a mystery.

Original languageEnglish
Title of host publicationTherapeutic Targets in Airway Inflammation
Number of pages16
PublisherCRC Press
Publication date01.01.2003
ISBN (Print)9780824709563
ISBN (Electronic)9780203911471
Publication statusPublished - 01.01.2003

Research Areas and Centers

  • Academic Focus: Center for Infection and Inflammation Research (ZIEL)


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