Semin Respir Crit Care Med 2010; 31(4): 375-379
DOI: 10.1055/s-0030-1262205
© Thieme Medical Publishers

The Etiologic Role of Infectious Antigens in Sarcoidosis Pathogenesis

Kyra A. Oswald-Richter1 , Wonder P. Drake1 , 2 , 3
  • 1Department of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee
  • 2Division of Infectious Diseases, Vanderbilt University Medical School, Nashville, Tennessee
  • 3Department of Medicine, Vanderbilt University Medical School, Nashville, Tennessee
Further Information

Publication History

Publication Date:
27 July 2010 (online)

Preview

ABSTRACT

Sarcoidosis is a disease of unknown etiology, characterized pathologically by noncaseating granulomas that most commonly involve the lung, skin, lymph nodes, and eyes. Syndromes with similar pathological and immunologic features to sarcoidosis such as chronic beryllium disease, hypersensitivity pneumonitis, and tuberculosis illustrate that granulomatous diseases may or may not have an infectious etiology. Although the etiology of sarcoidosis remains unknown, recent molecular, genetic, and immunologic studies strengthen the association of sarcoidosis with infectious antigens. Currently, the strongest agents considered include Propionibacterium and Mycobacterium species. Independent studies report the presence of microbial nucleic acids and proteins within sarcoidosis specimens. Th-1 immune responses to mycobacterial proteins have been detected within sarcoidosis diagnostic bronchoalveolar lavage (BAL). These proteins are actively secreted by the mycobacterial SecA 2 secretion system and are important to evade the host immune system. Recent discoveries regarding MHC class II alleles provide additional insight regarding the role of microbial antigens in sarcoidosis pathogenesis. Although further investigation is warranted, the recent progress of independent laboratories, using complementary techniques, strengthens the role of microbial antigens in sarcoidosis pathogenesis. These studies lay a strong foundation toward identifying therapeutic targets.

REFERENCES

Kyra A Oswald-RichterPh.D. 

Division of Infectious Diseases, Vanderbilt University Medical School, 1161 21st Avenue South, Medical Center North

Rm. A-3314, Nashville, TN 37232-2363

Email: Kyra.Richter@vanderbilt.edu