Journal
CELLULAR IMMUNOLOGY
Volume 258, Issue 1, Pages 29-37Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.cellimm.2009.03.008
Keywords
Toll-like receptor 2; Lipoprotein; Mycobacterium tuberculosis; CD14; CD36; Antigen presenting cell
Categories
Funding
- NIH [A1069085, A1034343, A1035726, A127243, HL55967, T32 A1007024, T32 GM007250, HHSN266200700022C/NOI-AI-70022]
- Tuberculosis Research Unit
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL055967] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI035726, R01AI069085, R01AI027243, R01AI034343, T32AI007024] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [T32GM007250] Funding Source: NIH RePORTER
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Mycobacterium tuberculosis (Mtb) signals through Toll-like receptor 2 (TLR2) to regulate antigen presenting cells (APCs). Mtb lipoproteins, including LpqH, LprA, LprG and PhoS1, are TLR2 agonists, but their coreceptor requirements are unknown. We studied Mtb lipoprotein-induced responses in TLR2(-/-), TLR1(-/-), TLR6(-/-), CD14(-/-) and CD36(-/-) macrophages. Responses to LprA, LprG, LpqH and PhoS1 were completely dependent on TLR2. LprG, LpqH, and PhoS1 were dependent on TLR1, but LprA did not require TLR1. None of the lipoproteins required TLR6, although a redundant contribution by TLR6 cannot be excluded. CD14 contributed to detection of LprA, LprG and LpqH, whereas CD36 contributed only to detection of LprA. high/Studies of lung APC subsets revealed lower TLR2 expression by CD11b(high)/CD11c(low) lung macrophages than CD11b(low)/CD11c(high) alveolar macrophages, which correlated with hyporesponsiveness of lung macrophages to LpqH. Thus, lung APC subsets differ in TLR expression, which may determine differences in responses to Mtb. (C) 2009 Elsevier Inc. All rights reserved
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