Journal
ANNUAL REVIEW OF IMMUNOLOGY
Volume 27, Issue -, Pages 393-422Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev.immunol.021908.132703
Keywords
T cell; B cell; phagocyte; regulation; memory; inflammation
Categories
Funding
- Trudeau Institute, Inc.
- National Institutes of Health [AI067723, AI46530, AI069121, AG028878]
- American Lung Association
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [P01AI046530, R01AI069121, R01AI067723] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R21AG028878] Funding Source: NIH RePORTER
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Tuberculosis is primarily a disease of the lung, and dissemination of the disease depends on productive infection of this critical organ. Upon aerosol infection with Mycobacterium tuberculosis tuberculosis (Mtb), the acquired cellular immune response is slow to be induced and to be expressed within the lung. This slowness allows infection to become well established; thus, the acquired response is expressed in an inflammatory site that has been initiated and modulated by the bacterium. Mtb his a variety of surface molecules that interact with the innate response, and this interaction along with the autoregulation of the immune response by several mechanisms results in less-than-optimal control of bacterial growth. To improve current vaccine strategies, we must understand the factors that mediate induction, expression, and regulation of the immune response in the lung. We must also determine how to induce both known and novel immunoprotective responses without inducing immunopathologic consequences.
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