File:Regulatory mechanisms in the lung during respiratory virus infection.jpeg

Summary
Nat Rev Immunol. 2012 Mar 9; 12(4): 295–305.

Molecules derived from both innate and adaptive immune cells contribute to the regulation of excessive pulmonary inflammation during acute respiratory virus infection. CD4+ T helper 1 (TH1) cells and type 1 CD8+ cytotoxic T cells (TC1 cells) express the transcription factors T-bet and BLIMP1 (B lymphocyte-induced maturation protein 1) and produce high levels of the regulatory cytokine interleukin-10 (IL-10), in addition to effector cytokines and cytolytic molecules, during respiratory virus infection. Regulatory T (TReg) cells in the lungs also express the ‘effector’ transcription factors T-bet and BLIMP1, produce various immunoregulatory cytokines (including IL-10 and transforming growth factor-β1 (TGFβ1)) and express the inhibitory receptor cytotoxic T-lymphocyte antigen 4 (CTLA4). Lung epithelial cells express CD200 and are required for the control of exuberant activation of classically activated macrophages. By contrast, alternatively activated macrophages contribute to the control of excessive pulmonary inflammation. Plasmacytoid dendritic cells (pDCs) also contribute to the suppression of excessive T cell-mediated inflammation through an unidentified mechanism. iNOS, inducible nitric oxide synthase; PPARγ, peroxisome proliferator-activated receptor-γ; TNF, tumour necrosis factor; TRAIL, TNF-related apoptosis-inducing ligand.