1. Getting the Bugs out of the Immune System: Do Bacterial Microbiota “Fix” Intestinal T Cell Responses? 
Janet Chow, Sarkis K. Mazmanian 
Cell Host & Microbe 
Volume 5, Issue 1, Pages 8-12 (January 2009)
DOI: /j.chom
Copyright © 2009 Elsevier Inc. Terms and Conditions

2. Figure 1
T Helper Lineage Differentiation Is a Dynamic Process that Is Influenced by the Intestinal Microbiota
CD4+ T helper cells can differentiate into proinflammatory (T helper 1 [Th1], Th2, or Th17) cells or anti-inflammatory regulatory T (Treg) cells. Th1 cells are characterized by their secretion of interferon-γ (IFNγ), and function to control infections by intracellular pathogens (i.e., viruses and bacteria). Th2 cells secrete IL-4, IL-5, and IL-13, and mediate immune responses to extracellular pathogens (i.e., parasites and bacteria). Th17 cells secrete IL-17, IL-21, and/or IL-22, and are believed to respond following infection by extracellular pathogens (i.e., fungi and bacteria). However, proinflammatory immune responses need to be regulated, as uncontrolled or elevated reactions will result in collateral damage to host tissues. Increased and prolonged Th1/Th17 responses are believed to drive autoimmune diseases such as multiple sclerosis, type 1 diabetes, rheumatoid arthritis, and psoriasis. Th2 responses, when left unchecked, may underlie the development of asthma and several allergic disorders. Proinflammatory immune reactions are controlled by regulatory T cells, which secrete factors such as IL-10 and TGFβ, and through other mechanisms that are still not well defined, limit T helper responses either following pathogen clearance or during the steady state. The current view of T helper differentiation posits that each of these lineages is distinct, and defined by gene regulatory networks encoded by the mammalian genome during T cell development. Recent studies are now suggesting that the distinction between each lineage fate is not predetermined, and may be adaptable. For example, the ratios between Th17 and Treg cell differentiation in the colon may be influenced by the intestinal microbiota, perhaps through modulation of their respective transcription factors, RORγt and Foxp3. Therefore, improper modulation of the balance between pro- and anti-inflammatory cell responses can lead to immune disorders, potentially linking the microbiota to noninfectious diseases.
Cell Host & Microbe 2009 5, 8-12DOI: ( /j.chom )
Copyright © 2009 Elsevier Inc. Terms and Conditions