Abstract

EDITORIAL article Front. Immunol., 15 November 2013Sec. Inflammation Volume 4 - 2013 | https://doi.org/10.3389/fimmu.2013.00345

Highlights

  • Ehlers and Schaible (3) give an overview of the M.tb granuloma research and the host-pathogen interaction

  • The pathogen-induced strong TH1 type inflammation causes pathology: caseation, cavitation that allow the escape of the bacilli to infect a new host

  • Guirado and Schlesinger (7) confirm the protective role of the Th1-induced M.tb granuloma with strong M1 mediated bactericidal kill. They rightly stress the importance of the microenvironment in and around the granulomas that cause a variety of pulmonary pathologies in a single person and they acknowledge the changing dynamics between host and pathogen during the long course of the infection

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Summary

Introduction

Ehlers and Schaible (3) give an overview of the M.tb granuloma research and the host-pathogen interaction. The pathogen-induced strong TH1 type inflammation causes pathology: caseation, cavitation that allow the escape of the bacilli to infect a new host. Shaler et al (4) describe the stages of the M.tb granuloma development with the appearance within the lesions of the non-phagocytic macrophage derivatives: foam, epithelioid, and giant cells. Guirado and Schlesinger (7) confirm the protective role of the Th1-induced M.tb granuloma with strong M1 mediated bactericidal kill.

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