File:Innate immunity to respiratory virus infection.jpeg

Summary
Regulating the adaptive immune response to respiratory virus infection. Nat Rev Immunol. 2012 Mar 9; 12(4): 295–305.

Virus infection of respiratory epithelial cells is first detected by cytosolic and/or endosomal innate sensors in the infected epithelial cells (not shown). Recognition of the invading virus by these innate immune receptors leads to the production of pro-inflammatory cytokines such as interleukin-1β (IL-1β) and IL-18, and chemokines such as CC-chemokine ligand 2 (CCL2). These soluble mediators that are released by infected cells activate adjacent CD45− parenchymal cells, such as fibroblasts and epithelial cells, and neighbouring innate immune cells. Following activation, these cells convert latent transforming growth factor-β (TGFβ) to an active form, resulting in increased secretion of the chemokines CCL2 and CCL20 by parenchymal stromal cells and of cytokines such as IL-12 and tumour necrosis factor (TNF) by inflammatory cells. This enhanced production of chemokines and cytokines facilitates the maturation of tissue-resident CD103+ and CD11b+ dendritic cells (DCs) and the recruitment and maturation of monocyte-derived DCs. Antigen acquisition and activation of immature antigen-bearing respiratory DCs results in their mobilization and migration out of the infected lungs along chemokine gradients of CCL21 and sphingosine-1-phosphate (S1P) to the lymph nodes draining the infected lung. Once in the lymph nodes, these DCs participate in initiating adaptive immune responses to the respiratory virus (not shown).