12/2/15
Micro 204: Allergic inflammation
Although we know a lot about pathways and mechanisms, we also are lacking a
clear understanding of how this immune pathway functions in normal biology and
how this pathway has come to be so dysregulated in persons growing up in
industrialized countries.
Questions for discussion (first in small groups, then in general format with
instructors):
1. The Medzhitov paper presents arguments that allergic inflammation arose to
protect us against noxious environmental agents, perhaps by establishing adversive
behaviors. Discuss pros and cons to such arguments and suggest experimental
approaches in animal models or human systems to assess your alternative
hypotheses. Where do you think allergic immunity arose in evolution?
2. Epithelial cytokines remain all the rage in allergic immunity, since the receptors
for these cytokines tend to be highly expressed on innate and adaptive immune cells
implicated in allergic inflammation. Despite this, relatively little is known regarding
the cells that produce or release IL-33, TSLP or IL-25. What kinds of tools and/or
models and what kinds of human studies might help you more clearly define roles
for these cytokines upstream of allergic inflammation?
3. The Fahy paper points out that human asthma can be heterogeneous, at least as
revealed by differences in responses to different classes of anti-inflammatory
therapeutics. Leaving out obvious potential reasons for this (non-adherence to
drugs; pharmacogenomics differences in drug clearance), think about research
approaches in animal models or among human populations that might help you
discern whether this disease is many different diseases or a single disease
expressed across a range of phenotypes.